I AIR QUALITY CRITERIA
1 FOR
i
I CARBON MONOXIDE
eg
®i
U. S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE
Public Health Service
Environmental Health Service
-------
AIR QUALITY CRITERIA
FOR
CARBON MONOXIDE
U. S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE
Public Health Service
Environmental Health Service
National Air Pollution Control Administration
Washington, D. C.
March 1970
-------
National Air Pollution Control Administration Publication No. AP-62
For sale by the Superintendent of Documents, U.S. Government Printing Office, Washington, D.C., 20402 - Price $1.50
-------
PREFACE
Air quality criteria tell us what science has
thus far been able to measure of the obvious
as well as the insidious effects of air pollution
on man and his environment. Such criteria
provide the most realistic basis that we pres-
ently have for determining to what point pol-
lution levels must be reduced if we are to
protect the public health and welfare.
The criteria we can issue at the present
time do not tell us all that we would like to
know; but taking all of man's previous experi-
ence in evaluating environmental hazards as a
guide, we can conclude that improved knowl-
edge will show that there are identifiable
health and welfare hazards associated with air
pollution levels that were previously thought
to be innocuous. As our scientific knowledge
grows, air quality criteria will have to be re-
viewed and, in all probability, revised. The
Congress has made it clear, however, that we
are expected, without delay, to make the
most effective UF ^f the knowledge we now
have.
The 1967 amendments to the Clean Air
Act require that the Secretary of Health, Ed-
ucation, and Welfare". . .from time to time,
but as soon as practicable, develop and issue
to the States such criteria of air quality as in
his judgment may be requisite for the protec-
tion of the public health and welfare . . . Such
criteria shall . . . reflect the latest scientific
knowledge useful in indicating the kind and
extent of all identifiable effects on health and
welfare which may be expected from the pres-
ence of an air pollution agent . . . ."
Under the Act, the issuance of air quality
criteria is a vital step in a program designed to
assist the States in taking responsible techno-
logical, social, and political action to protect
the public from the adverse effects of air pol-
lution.
Briefly, the Act calls for the Secretary of
Health, Education, and Welfare to define the
broad atmospheric areas of the Nation in
which climate, meteorology, and topography,
all of which influence the capacity of air to
dilute and disperse pollution, are generally ho-
mogeneous.
Further, the Act requires the Secretary to
define those geographical regions in the coun-
try where air pollution is a problem—whether
interstate or intrastate. These air quality con-
trol regions will be designated on the basis of
meteorological, social, and political factors
which suggest that a group of communities
should be treated as a unit for setting limita-
tions on concentrations of atmospheric pol-
lutants. Concurrently, the Secretary is re-
quired to issue air quality criteria for those
pollutants he believes may be harmful to
health or welfare, and to publish related infor-
mation on the techniques which can be em-
ployed to control the sources of those pollut-
ants.
Once these steps have been taken for any
region, and for any pollutant or combination
of pollutants, then the State or States re-
sponsible for the designated region are on no-
tice to develop ambient air quality standards
applicable to the region for the pollutants in-
volved, and to develop plans of action for im-
plementing the standards.
The Department of Health, Education, and
Welfare will review, evaluate, and approve
these standards and plans and, once they are
approved, the States will be expected to take
action to control pollution sources in the
manner outlined in their plans.
At the direction of the Secretary, the Na-
tional Air Pollution Control Administration
has established appropriate programs to carry
in
-------
out the several Federal responsibilities speci-
fied in the legislation. Previously, on February
11,1969, air quality criteria and control tech-
niques information were published for sulfur
oxides and particulate matter.
This publication, Air Quality Criteria for
Carbon Monoxide, is the result of extensive
and dedicated effort on the part of many
persons-so many that it is not practical to
name each of them.
In accordance with the Clean Air Act, a
National Air Quality Criteria Advisory Com-
mittee was established, having a membership
broadly representative of industry, universi-
ties, conservation interests, and all levels of
government. The committee provided invalu-
able advice on policies and procedures under
which to issue criteria, and provided major
assistance in drafting this document.
With the help of the committee, expert
consultants were retained to draft portions of
this document, while other segments were
drafted by staff members of the National Air
Pollution Control Administration. After the
initial drafting, there followed a sequence of
review and revision by the committee, as well
as by individual reviewers especially selected
for their competence and expertise in the
many fields of science and technology related
to the problems of atmospheric pollution by
carbon monoxide. These efforts, without
which this document could not have been
completed successfully, are knowledge indi-
vidually on the following pages.
As also required by the 1967 amendments
to the Clean Air Act, appropriate Federal de-
partments and agencies, also listed on the fol-
lowing pages, were consulted prior to issuing
this criteria document. A Federal consultation
committee, comprising members designated
by the heads of 17 departments and agencies,
reviewed the document, and met with staff
personnel of the National Air Pollution Con-
trol Administration to discuss their com-
ments.
This Administration is pleased to acknowl-
edge the efforts of each of the persons specifi-
cally named, as well as the many not named
who have contributed to the publication of
this volume. In the last analysis, however, the
National Air Pollution Control Administra-
tion is responsible for its content.
JOHN T. MIDDLETON
Commissioner
National Air Pollution Control Administration
IV
-------
NATIONAL AIR QUALITY CRITERIA ADVISORY COMMITTEE
Dr. Delbert S. Earth, Chairman
Bureau of Criteria and Standards
National Air Pollution Control Administration
Dr. Herman R. Amberg*
Manager, Manufacturing Services Dept.
Central Research Division
Crown Zellerbach Corp.
Camas, Washington
Dr. Nyle C. Brady*
Director, Agricultural Experiment
Station
Cornell University
Ithaca, New York
Dr. Seymour Calvert
Dean
School of Engineering
University of California - Riverside
Riverside, California
Dr. Adrian Ramond Chamberlain
Vice President
Colorado State University
Fort Collins, Colorado
Mr. James R. Garvey*
President and Director
Bituminous Coal Research, Inc.
Monroeville, Pennsylvania
Dr. David M. Gates
Director
Missouri Botanical Gardens
St. Louis, Missouri
Dr. Neil V. Hakala
President
Esso Research & Engineering Company
Linden, New Jersey
Dr. Ian T. Higgins
Professor, School of Public Health
The University of Michigan
Ann Arbor, Michigan
Mr. Donald A. Jensen
Director, Automotive Emissions
Office
Engineering Staff
Ford Motor Company
Dearborn, Michigan
Dr. Herbert E. Klarman
Department of Environmental
Medicine and Community Health
Downstate Medical Center
State University of New York
Brooklyn, New York
Dr. Leonard T. Kurland*
Professor of Epidemiology
Mayo Graduate School of Medicine
Head, Medical Statistics
Epidemiology and Population Genetics
Section, Mayo Clinic
Rochester, Minnesota
Dr. Frederick Sargent II
Dean, College of Environmental
Sciences
University of Wisconsin - Green Bay
Green Bay, Wisconsin
Mr. William J. Stanley*
Director, Chicago Department of
Air Pollution Control
Chicago, Illinois
*Membership expired June 30, 1969.
-------
CONTRIBUTORS AND REVIEWERS
Dr. David M. Anderson
Assistant Manager
Environmental Quality Control
Bethlehem Steel Corporation
Bethlehem, Pennsylvania
Dr. Bruce Armstrong
Associate Professor of Medicine
University of Southern California
School of Medicine
Los Angeles, California
Dr. Poul Astrup
Professor of Clinical Chemistry
Rigshospitalet
University Hospital
Cophenhagen, Denmark
Dr. Stephen M. Ayres
Director, Cardiopulmonary Laboratory
St. Vincent's Hospital and
Medical Center
New York, New York
Mr. Francis E. Blacet
Department of Chemistry
University of California,
Los Angeles
Los Angeles, California
Mr. F. W. Bowditch
Director, Emission Control
General Motors Technical Center
Warren, Michigan
Professor R. A. Bryson
Center for Climatic Research
Department of Meteorology
The University of Wisconsin
Madison, Wisconsin
Dr. Bertram W. Carnow
Associate Professor of Preventive
Medicine and Community Health
University L ' T'linois College
of Medicine
Chicago, Illinois
Dr. Donald Bartlett, Jr.
Department of Physiology
Dartmouth Medical School
Hanover, New Hampshire
Dr. P. Chovin
Prefecture de Police
Laboratoire Municipal
Paris, France
Dr. Mario C. Battigelli
The School of Medicine
Department of Medicine
The University of North Carolina
at Chapel Hill
Chapel Hill, North Carolina
Dr. Rodney Beard
Department of Preventive Medicine
Stanford University School of Medicine
Palo Alto, California
George D. Clayton, President
George D. Clayton and Associates, Inc.
Air Pollution and Industrial Health
Consultants
Detroit, Michigan
Dr. Seymour Cohen
Environmental Epidemiology Unit
California Department of Public
Health
Berkeley, California
VI
-------
Mr. C. G. Cortelyou
Coordinator
Air and Water Conservation
Mobil Oil Corporation
New York, New York
Miss Margaret Deane
Environmental Epidemiology Unit
California Department of Public Health
Berkeley, California
Dr. Arthur B. DuBois
Department of Physiology
School of Medicine
University of Pennsylvania
Philadelphia, Pennsylvania
Dr. Robert Eckhart
Director, Medical Research Division
Esso Research and Engineering Company
Linden, New Jersey
Dr. Hans L. Falk
Associate Director for Laboratory
Research
National Institute of Environmental
Health Sciences
Research Triangle Park, North Carolina
Mr. J. L. Gilliland
Ideal Cement Company
Denver, Colorado
Dr. John R. Goldsmith, Chief
Environmental Epidemiology Unit
California Department of Public
Health
Berkeley, California
Dr. Harold H. Golz
Medical Director
American Petroleum Institute
New York, New York
Dr. Robert J. Gordon
School of Medicine
University of Southern California
Los Angeles, California
Dr. A. J. Haagen-Smit
Chairman
California Air Resources Board
Sacramento, California
Mr. C. M. Heinen, Chief Engineer
Emission Control and Chemical Development
Product Planning & Development Staff
Chrysler Corporation
Detroit, Michigan
Dr. Margaret Hitchcock
Air and Industrial Hygiene Laboratory
California Department of Public Health
Berkeley, California
Dr. Kenneth D. Johnson
Staff Engineer
Manufacturing Chemists' Association
Washington, D. C.
Mr. John Kinosian
Bureau of Air Sanitation
California Air Resources Board
Sacramento, California
Dr. Leonard I. Kleinman
Department of Environmental Health
College of Medicine
University of Cincinnati
Cincinnati, Ohio
Dr. Paul Kotin, Director
National Institute of Environmental
Health Sciences
Research Triangle Park, North Carolina
Mr. J. F. Kunc
Senior Research Associate
Petroleum Staff
Esso Research and Engineering Company
Linden, New Jersey
Mr. Philip A. Leighton
Consultant', Atmospheric Chemistry
Solvany, California
Vll
-------
Dr. H. N. MacFarland
Professor and Director
Centre of Research on Environmental Quality
Faculty of Science
York University
Downsview, Ontario
Mr. Herbert C. McKee
Assistant Director
Department of Chemistry and
Chemical Engineering
Southwest Research Institute
Houston, Texas
Dr. George McNew
Director
Boyce Thompson Institute of
Plant Research, Inc.
Yonkers, New York
Mr. Hezekiah Moore
Air and Industrial Hygiene Laboratory
California Department of Public Health
Berkeley, California
Mr. V. W. Moore
Vice President
Research-Cottrell, Inc.
Bound Brook, New Jersey
Dr. Peter K. Mueller
Air and Industrial Hygiene Laboratory
California Department of Public Health
Berkeley, California
Mr. William Munroe
Chief, Air Pollution Control Program
State of New Jersey Department of
Health
Trenton, New Jersey
Dr. Thaddeus J. Murawski
Bureau of Epidemiology
New York State Department of Health
Albany, New York
Dr. Peter B. Peacock
Professor and Chairman
Department of Public Health and
Epidemiology
University of Alabama Medical School
Birmingham, Alabama
Mr. Norman Perkins
Environmental Epidemiology Unit
California Department of Public
Health
Berkeley, California
Dr. Emil A. Pfitzer
Head, Toxicology Division
Department of Environmental Health
College of Medicine
University of Cincinnati
Cincinnati, Ohio
Dr. Alexander Rihm, Jr.
Assistant Commissioner
Division of Air Resources
New York State Department of Health
Albany, New York
Mr. Elmer Robinson, Chairman
Environmental Research Department
Stanford Research Institute - Washington
Arlington, Virginia
Dr. Stanley Rokaw
Chief, Pulmonary Research Section
Rancho Los Amigos Hospital
Los Angeles, California
Mr. Jean J. Schueneman, Chief
Division of Air Quality Control
Environmental Health Services
Maryland Department of Health
Baltimore, Maryland
Dr. John H. Schulte
Professor - Director
Division of Occupational Medicine
Department of Preventive Medicine
Ohio State University
Columbus, Ohio
Vlll
-------
Dr. R. W. Scott
Coordinator for Conservation Technology
Esso Research and Engineering Company
Linden, New Jersey
Professor Arthur C. Stern
Department of Environmental Sciences and
Engineering, School of Public Health
The University of North Carolina
Chapel Hill, North Carolina
Dr. Raymond R. Suskind
Director, Department of Environmental
Health
College of Medicine
University of Cincinnati
Cincinnati, Ohio
Mr. Victor H. Sussman
Director
Bureau of Air Pollution Control
Pennsylvania Department of Health
Harrisburg, Pennsylvania
Mr. O. Clifton Taylor
Acting Director
Statewide Air Pollution Research Center
University of California, Riverside
Riverside, California
Mr. William Tuddenham
Environmental Epidemiology Unit
California Department of Public Health
Berkeley, California
Mr. Hans Ury
Environmental Hazards Evaluation Unit
California Department of Public Health
Berkeley, California
Dr. Ralph C. Wands, Director
Advisory Center on Toxicology
National Research Council
National Academy of Sciences
Washington, D. C.
Dr. Eugene Weaver
Product Development Group
Ford Motor Company
Dearborn, Michigan
Mr. Leonard H. Weinstein
Program Director
Environmental Biology
Boyce Thompson Institute for Plant
Research, Inc.
Yonkers, New York
Dr. Bernard Weinstock
Manager and Senior Scientist
Fuel Sciences Department
Ford Motor Company
Dearborn, Michigan
Mr. Harmon Wong-Woo
California Air Resources Board
Sacramento, California
Mr. John E. Yocom
Director, Engineering and Technical
Programs
The Travelers Research Company
Hartford, Connecticut
Mr. Roland S. Yunghans
Environmental Scientist
State of New Jersey
Department of Health
Trenton, New Jersey
IX
-------
FEDERAL AGENCY LIAISON REPRESENTATIVES
Department of Agriculture
Dr. Theodore C. Byerly
Assistant Director of Science
and Education
Department of Commerce
Mr. James R. Hibbs
Advisor on Environmental Quality
Department of Defense
Mr. Thomas R. Casberg
Office of the Deputy Assistant
Secretary (Properties and Installations)
Department of Housing & Urban Development
Mr. Samuel C. Jackson
Assistant Secretary for Metropolitan
Development
Department of the Interior
Mr. Harry Perry
Mineral Resources Research Advisor
Department of Justice
Mr. Walter Kiechel, Jr.
Assistant Chief
General Litigation Section
Land and Natural Resources Division
Department of Labor
Dr. Leonard R. Linsenmayer
Deputy Director
Bureau of Labor Standards
Post Office Department
Mr. W. Norman Meyers
Chief, Utilities Division
Bureau of Research & Engineering
Department of Transportation
Mr. William H. Close
Assistant Director for Environmental
Research
Office of Noise Abatement
Department of the Treasury
Mr. Gerard M. Brannon
Director
Office of Tax Analysis
Atomic Energy Commission
Dr. Martin B. Biles
Director
Division of Operational Safety
Federal Power Commission
Mr. F. Stewart Brown
Chief
Bureau of Power
General Services Administration
Mr. Thomas E. Crocker
Director
Repair and Improvement Division
Public Buildings Service
National Aeronautics and Space
Administration
Major General R. H. Curtin, USAF
(Ret.)
Director of Facilities
National Science Foundation
Dr. Eugene W. Bierly
Program Director for Meteorology
Division of Environmental Sciences
Tennessee Valley Authority
Dr. F. E. Gartrell
Assistant Director of Health
Veterans Administration
Mr. Gerald M. Hollander
Director of Architecture and Engi-
neering
Office of Construction
-------
TABLE OF CONTENTS
Chapter Page
LIST OF FIGURES xv
LIST OF TABLES xvi
1. INTRODUCTION 1-1
2. OCCURRENCE, PROPERTIES, AND FATE OF ATMOSPHERIC CARBON
MONOXIDE 2-1
A. INTRODUCTION 2-1
B. CARBON MONOXIDE IN HISTORY 2-1
C. OCCURRENCE 2-1
1. Technological Sources 2-1
2. Natural Sources 2-2
a. Nonbiological 2-2
b. Biological 2-2
D. PROPERTIES AND GASEOUS REACTIONS OF CARBON MONOXIDE 2-2
1. Physical Properties 2-2
2. Gaseous Chemical Reactions of Carbon Monoxide 2-2
a. Lower Atmospheric Reactions 2-2
b. Upper Atmospheric Reactions 2-4
E. BACKGROUND LEVELS AND FATE OF CARBON MONOXIDE 2-4
1. Background Levels and Estimated Mean Life-Time of Carbon Monoxide .... 2-4
2. Possible Processes for Carbon Monoxide Removal 2-5
a. Atmospheric Migration 2-5
b. Biological Removal 2-5
c. Biochemical Removal 2-6
d. Absorption in Oceans 2-6
e. Adsorption on Surfaces 2-6
F. SUMMARY 2-6
G. REFERENCES 2-7
3. PRINCIPLES OF FORMATION AND CONTROL OF CARBON MONOXIDE 3-1
A. INTRODUCTION 3-1
B. FORMATION OF CARBON MONOXIDE BY COMBUSTION 3-1
1. General Combustion Processes 3-1
2. Internal Combustion Engines 3-1
3. Stationary Combustion Sources 3-3
C. SUMMARY 3-3
D. REFERENCES 3-3
4. ESTIMATION OF CARBON MONOXIDE EMISSIONS 4-1
A. INTRODUCTION 4-1
B. RECENT CARBON MONOXIDE EMISSION LEVELS 4-1
1. National Emission Levels 4-1
2. Regional Emission Levels 4-1
xi
-------
C. EMISSIONS AND EMISSION FACTORS BY SOURCE TYPE 4-1
1. Mobile Combustion Sources 4-1
a. Motor Vehicles 4-1
b. Aircraft 4-8
c. Other Nonhighway Mobile Sources 4-9
2. Carbon Monoxide from Combustion for Power and Heat 4-9
3. Industrial Processes Producing Carbon Monoxide 4-10
4. Solid Waste Combustion ' 4-10
5. Miscellaneous Combustion 4-10
D. PROJECTIONS OF CARBON MONOXIDE EMISSION LEVELS 4-11
E. SUMMARY 4-11
F. REFERENCES 4'1 J
5. MEASUREMENT OF CARBON MONOXIDE CONCENTRATIONS IN AMBIENT AIR 5-1
A. INTRODUCTION 5-1
B. PREPARATION OF CARBON MONOXIDE GAS STANDARDS 5-1
1. VolumetriC'.Gas Dilution Techniques 5-1
2. Gravimetric Methods for Standardizing Carbon Monoxide Gas Mixtures 5-1
3. Chemical Assay of Carbon Monoxide Gas Standards 5-2
C. MEASURING CARBON MONOXIDE IN ATMOSPHERE 5-2
1. Continuous Measurement of Carbon Monoxide 5-2
a. Definitions of Terms Describing Instrument Performance 5-2
b. Nondispersive Infrared Analyzers 5-2
c. Electrochemical Analyzers 5-4
(1) Galvanic Analyzer 5-4
(2) Coulometric Analyzer 5-4
d. Mercury Vapor Analyzer 5-4
e. Gas Chromatographic Analyzer 5-5
f. Catalytic Analysis 5-5
2. Intermittent Analysis 5-5
a. Collection of Spot or Integrated Samples 5-5
b. Nondispersive Infrared Analysis 5-5
c. Infrared Spectrophotometric Analysis 5-5
d. Gas Chromatographic Analysis 5-6
e. Colorimetric Analysis 5-6
(1) Colored Silver Sol Method 5-6
(2) National Bureau of Standards Colorimetric Indicating Gel 5-6
(3) Length-of-Stain Indicator Tube 5-6
D. SUMMARY 5-6
E. REFERENCES 5-7
6. ATMOSPHERIC CARBON MONOXIDE CONCENTRATIONS 6-1
A. INTRODUCTION 6-1
B. TEMPORAL VARIATIONS IN CARBON MONOXIDE CONCENTRATIONS ... 6-1
1. Diurnal Patterns 6-1
2. Seasonal Patterns 6-3
3. Annual Variations 6-3
C. EFFECTS OF METEOROLOGICAL FACTORS 6-3
xii
-------
D. OBSERVED URBAN CARBON MONOXIDE CONCENTRATIONS 6-5
1. Sources of Data 6-5
2. Techniques of Data Analysis 6-5
a. Introduction 6-5
b. Averaging Time 6-17
c. Frequency Distribution 6-17
d. An Air Quality Model 6-19
3. Eight-Hour 0.1 Percentile Averages 6-19
a. CAMP Observations 6-19
b. California Observations 6-20
4. Special Carbon Monoxide Exposure Situations 6-21
a. Variations With Type of Vehicle Traffic 6-21
b. Car Passenger Exposure to Carbon Monoxide 6-23
c. Severe Carbon Monoxide Exposure Locations 6-23
d. Indoor Levels of Carbon Monoxide 6-23
e. Projected Future Trends 6-25
E. METEOROLOGICAL DIFFUSION MODELS 6-26
F. SUMMARY 6-28
G. REFERENCES 6-28
7. EFFECTS OF CARBON MONOXIDE ON PLANTS AND CERTAIN 7-1
MICROORGANISMS
A. GENERAL DISCUSSION 7-1
B. SUMMARY 7-2
C. REFERENCES 7-2
8. TOXICOLOGICAL APPRAISAL OF CARBON MONOXIDE 8-1
A. INTRODUCTION 8-1
B. THEORETICAL CONSIDERATIONS 8-1
C. MEASUREMENT OF CARBOXYHEMOGLOBIN IN BLOOD 8-3
1. Nondestructive Methods 8-3
2. Destructive Methods 8-6
a. Carbon Monoxide Detector Tubes 8-6
b. Reduction of Palladium Chloride by the Microdiffusion Technique 8-6
c. Monometric and Volumetric Methods 8-6
d. Spectrophotometric Determination of Released CO by NDIR (Nondispersive 8-7
Infrared) Method 8-7
e. Gas-Phase Chromatography 8-7
3. Equilibrium Methods—Analysis of Expired Air 8-7
4. Discussion 8-7
D. UPTAKE OF CARBON MONOXIDE BY HUMANS 8-7
E. EFFECT OF CARBON MONOXIDE ON THE CENTRAL NERVOUS SYSTEM . . 8-10
1. Animal Data 8-10
a. Morphological Changes 8-10
b. Behavioral Changes 8-11
2. Human Data 8-14
3. Discussion 8-24
xiii
-------
F. EFFECTS OF CARBON MONOXIDE ON CARDIOVASCULAR SYSTEM 8-24
1. Animal Data 8"24
Q 94
a. Short-Term Exposure
b. Long-Term Exposure
2. Human Data 8'27
a. Studies of Oxygen Debt • 8'27
b. Studies of Hemodynamic Responses 8-27
G. NON-HEMOGLOBIN ABSORPTIVE SYSTEMS 8-34
1. Myoglobin j|-34
2. Cytochrome Oxidases °~^'
H. EFFECTS OF CARBON MONOXIDE AT HIGH ALTITUDE 8-37
I. ADAPTATION 8'42
J. ENDOGENOUS FORMATION OF CARBON MONOXIDE 8'43
K. SUMMARY 8'45
L. REFERENCES 8-52
9. EPIDEMIOLOGICAL APPRAISAL OF CARBON MONOXIDE 9-1
A. INTRODUCTION 9-1
B. SOURCES AND MAGNITUDE OF EXPOSURE TO CARBON MONOXIDE .... 9-1
1. Community and Residential Exposures 9-2
2. Occupational Exposures 9-3
3. Cigarette, Pipe, and Cigar Smoking 9-7
C. DEFINITION OF SENSITIVE GROUPS 9-7
D. STUDIES AND INTERPRETATION 9-10
1. Mortality Studies 9-10
2. Morbidity Studies 9-14
3. Possible Relevance of Carbon Monoxide Exposure to Motor Vehicle Accidents . 9-17
E. SUMMARY 9-18
F. REFERENCES 9-19
10. SUMMARY AND CONCLUSIONS 10-1
A. OCCURRENCE, PROPERTIES, AND FATE OF ATMOSPHERIC
CARBON MONOXIDE 10-1
B. FORMATION OF CARBON MONOXIDE 10-1
C. ESTIMATION OF CARBON MONOXIDE EMISSIONS 10-1
D. MEASUREMENT OF CARBON MONOXIDE CONCENTRATIONS
IN AMBIENT AIR 10-1
E. ATMOSPHERIC CARBON MONOXIDE CONCENTRATIONS 10-2
F. EFFECTS OF CARBON MONOXIDE ON VEGETATION AND
MICROORGANISMS 10-3
G. TOXICOLOGICAL APPRAISAL OF ATMOSPHERIC CARBON MONOXIDE . . . 10-3
H. EPIDEMIOLOGICAL APPRAISAL OF CARBON MONOXIDE 10-4
I. AREAS FOR FUTURE RESEARCH 10-5
J. CONCLUSIONS 10-5
K. RESUME 10-6
APPENDIX A-l
SUBJECT INDEX M
xiv
-------
LIST OF FIGURES
Figure Page
3-1 Effect of Air-Fuel Ratio on Exhaust Gas Carbon Monoxide Concentrations
From Three Test Engines 3-2
4-1 Carbon Monoxide Emissions By Source Category for Various U.S. Metro-
politan Areas in 1968 4-6
4-2 Forecast of Total Carbon Monoxide Emissions From Motor Vehicles 4-7
4-3 Effect of Average Route Speed on Carbon Monoxide Emission by Weight. . 4-7
4-4 Carbon Monoxide Emissions by Individual Vehicles, Los Angeles 4-8
5-1 Typical Nondispersive Infrared Analyzer Response to Water Vapor 5-3
6-1 Diurnal Variation of Carbon Monoxide Levels on Weekdays in Detroit. . . . 6-2
6-2 Diurnal Variation of Carbon Monoxide levels on Weekdays in Los Angeles. . 6-3
6-3 Hourly Average Carbon Monoxide Concentration and Traffic Count in Mid
Town Manhattan 6-4
6-4 Diurnal Variation of Carbon Monoxide Levels on Weekdays, Saturdays, and
Sundays in Chicago, 1962-1964 6-4
6-5 Correlation of Carbon Monoxide Concentration and Traffic Density 6-4
6-6 Concentration Versus Averaging Time and Frequency for Carbon Monoxide
From December 1, 1961, to December 1, 1967, Chicago CAMP Station. . . 6-18
6-7 Eight-Hour-Averaging-Time Carbon Monoxide Concentrations (ppm) Ex-
ceeded 0.1 Percent of the Time at CAMP Sites, 1962 through 1967 6-20
6-8 Eight-Hour-Averaging-Time Carbon Monoxide Concentrations (ppm) Ex-
ceeded 0.1 Percent of the Time at Various California Sites, 1963 through
1967 6-20
6-9 Eight-Hour-Averaging-Time Carbon Monoxide Concentrations (ppm) Ex-
ceeded 0.1 Percent of the Time in Los Angeles Area, 1956 through 1967. . . 6-21
6-10 Maximum Annual 8-Hour-Averaging-Time Concentrations of Carbon Mon-
oxide Expected at Various Types of Sites 6-22
6-11 Hourly Average CO Levels Inside and Outside Gas-Heated House With Gas-
Burning Kitchen Stove 6-25
6-12 Hourly Average CO Levels Inside and Outside House Heated With Hand-
Fired Coal-Burning Furnace 6-26
8-1 Oxyhemoglobin Dissociation Curves of Human Blood Containing Varying
Amounts of Carboxyhemoglobin, Calculated From Observed ©2 Dissocia-
tion Curve of CO-Free Blood (pH = 7.4, T = 37°C, PCO2 = 40 mm Hg). . . 8-2
8-2 Effect of CO Administration on Arterial Oxygen Tension, Compared With
O^ Dissociation Curves in Figure 8-1, Based On Data in Table 8-1 8-5
8-3 Uptake of CO at Various Concentrations and Rates of Ventilation 8-8
8-4 Average Values of Percent Carboxyhemoglobin in Seven Nonsmokers Ex-
posed to 35 mg/m3 (30 ppm) CO 8-10
8-5 Concentration and Duration of Continuous CO Exposure Required to Pro-
duce Blood COHb Concentrations of 1.25, 2.0, 2.5, 5.0, 7.5, and 10 Percent
in Healthy Male Subjects Engaging in Sedentary Activity 8-11
8-6 Effect of CO on Mean DRL Response Rate in Rats 8-12
8-7 Effect of Small Concentrations of COHb on Certain Psychomotor Tests. . . 8-16
xv
-------
8-8 Mean Percent Correct Responses (± One Standard Deviation) to 1,000-Hertz
Tone by 18 Human Subjects During Exposure to CO 8-17
8-9 Time After Initial Exposure to Each Concentration of CO That Mean Correct
Response Fell Two Standard Deviations From the Mean Performance Level
in Absence of CO 8-18
8-10 Relation Between COHb and Visual Threshold 8-21
8-11 Effect of Progressive Increases of Blood COHb on Visual Threshold, and of
Oxygen and Carbogen (93% ©2 + 7% CO2> in Counteracting This Effect. . . g-23
8-12 Myocardial Metabolic Measurements in Three Representative Patients Be-
fore and After CO Inhalation 8-33
8-13 Diagrammatic Summary of Current Concepts Regarding Variables That Influ-
ence Body CO Stores 8-38
9-1 Carbon Monoxide Levels of Environmental Air and of Expired Air of
Smoker and Nonsmoker, Los Angeles and Pasadena, August 1962 9-2
9-2 Carbon Monoxide Levels of Environmental Air and COHb Levels of Smoker
and Nonsmoker, Los Angeles County, 1963 9-3
9-3 Distribution of COHb Among Individuals Involved in Traffic Accidents. . . 9.5
9-4 COHb Levels of Policemen Who Smoke Before and 5 Hours After Exposure
to Between 12 and 23 mg/m3 (10 and 12 ppm) CO, Paris, 1963 9.5
9-5 COHb Levels of Policemen Who Do Not Smoke Before and 5 Hours After
Exposure to Between 12 and 23 mg/m3 (10 and 12 ppm) CO, Paris, 1963. . 9.7
9-6 Distribution of Expired-Air CO, According to Smoking History and Cor-
rected for Ambient-Air CO 9.9
9-7 Percentage of Hemoglobin Saturated With CO in Cord and Maternal Blood
Specimens of Smokers and Nonsmokers 9-10
9-8 Comparison of Maximum Concentrations of Oxidant and Carbon Monoxide,
Maximum Temperature, and Daily Death Rate for Cardiac and Respiratory
Causes, Los Angeles County, 1956-1958 9-11
9-9 Fourier Curves Fitted to Data in Figure 9-8 9-12
9-10 COHb Levels of Coroner Cases, by Smoking Status and Atmospheric CO
Concentration, Los Angeles County, 1961 9-13
9-11 COHb Levels in Myocardial Infarction Deaths and in Other Cardiovascular
Disease Deaths, Los Angeles County, 1961 9-14
9-12 Cumulative Distribution of Blood CO Concentrations, Based on 5-Year Study
of Car Drivers, Workmen With CO Exposure, and Private Individuals Sus-
pected of Accidental CO Exposure 9-18
LIST OF TABLES
Table
1-1 Factors To Be Considered in Developing Air Quality Criteria j_2
2-1 Physical Properties of Carbon Monoxide 2-3
4-1 Carbon Monoxide Emission Estimates By Source Category-1968 4_2
4-2 Carbon Monoxide Emission Estimates -1968 4.3
xvi
-------
4-3 Summary of Total Emissions From Metropolitan Areas Throughout United
States-1967-1968 4-5
6-1 Carbon Monoxide Concentration at CAMP Sites, by Averaging Time and
Frequency, 1962 through 1967 6-6
6-2 Carbon Monoxide Concentration by Averaging Time and Frequency, 1962
through 1967, in California 6-7
6-3 Carbon Monoxide Concentration by Averaging Time and Frequency, 1956
through 1967, in Los Angeles County 6-11
6-4 Carbon Monoxide Concentration by Averaging Time and Frequency, from
December 1, 1961, to December 1, 1967, Chicago CAMP Station 6-16
6-5 In-Traffic 20- to 30-Minute Carbon Monoxide Exposures for Various Driv-
ing Routes 6-24
8-1 Blood and Gas Studies (Averages of Two Measurements Taken 30 Minutes
Apart) After Administration of Carbon Monoxide and Air Until Attainment
of Carboxyhemoglobin Equilibrium 8-4
8-2 Percent Carboxyhemoglobin in Blood of Subjects Exposed to 35 mg/m3 (30
ppm) CO 8-9
8-3 Results of Physiological and Psychological Tests on Subjects Exposed to 345
mg/m3 (300 ppm) CO 8-15
8-4 Effects of Varying CO Exposure on Visual Performance 8-22
8-5 Percent Change in Blood Values of Individual Dogs in Response to 58
mg/m3 (50 ppm) CO Inhalation Daily for 3 Months 8-26
8-6 Total Increased Oxygen Uptake (Vc<2)> Oxygen Debt (O2o)» and Ratio of
O2 D Before and After CO Inhalation by Ten Nonsmokers 8-28
8-7 Heart Rate and Pulmonary Diffusing Capacity (DL^o) Before and After CO
Inhalation by Ten Nonsmokers 8-28
8-8 Mean Pulmonary Function Studies Before and After CO Inhalation by Ten
Nonsmokers 8-29
8-9 Hemodynamic and Respiratory Responses of Five Subjects to CO Inhalation. 8-30
8-10 Systemic Cardiorespiratory Measurements in 26 Subjects Before and After
CO Inhalation 8-32
8-11 Myocardial Metabolic Measurements in 11 Subjects Before and After CO
Inhalation 8-34
8-12 Effect of CO on Alveolar-Arterial Oxygen Difference (A-aDQ2) m Nine Sub-
jects After Exposure Sufficient to Increase COHb About 10 Percent 8-35
8-13 Extravascular CO Capacities, Half-Times, and Equilibrium Times For Trans-
fer of CO from Intravascular Pool to Extravascular Pool, and Levels of
Blood COHb at End of Transfer 8-38
8-14 Average Data for Eight Subjects (Divided Into Two Groups of Four) to Com-
pare Effects of CO and High Altitudes on Various Physiological Parameters 8-40
8-15 Summary of Effects of Carbon Monoxide in Animals 8-47
8-16 Summary of Effects of Carbon Monoxide in Humans 8-49
9-1 COHb Levels of Smokers and Nonsmokers in Exposed and Control Groups. . 9-4
9-2 Frequency Distribution of CO Blood Analyses of Individuals Involved in
Traffic Accidents 9-5
9-3 COHb Levels of 108 Smokers and 92 Nonsmokers Before Work 9-8
xvii
-------
9-4 Proportion of Smokers and Median Values of Expired CO Among Longshore-
men 9-8
9-5 COHb Levels for Cardiovascular Disease Categories by Age, Smoking Habits,
and Sex, Los Angeles County, 1961 9-15
9-6 Relationship Between Number of Hospital Admissions for Myocardial Infarc-
tion, Myocardial Infarction Case Fatality Rates, and Ambient CO Levels by
Day of Week, Los Angeles County, 1958 9-16
10-1 Effects of Carbon Monoxide 10-7
XVlll
-------
CHAPTER 1.
INTRODUCTION
Pursuant to authority delegated to the
Commissioner of the National Air Pollution
Control Administration, Air Quality Criteria
for Carbon Monoxide is issued in accordance
with Section 107(b) of the Clean Air Act (42
U.S.C. 1857-18571).
Air quality criteria are an expression of the
scientific knowledge of the relationship
between various concentrations of pollutants
in the air and their adverse effects on man and
his environment. Criteria are issued to assist
the states in developing air quality standards.
Air quality criteria are descriptive; that is,
they describe the effects that have been
observed to occur when the concentration of
a pollutant in the ambient air has reached or
exceeded a specific level for a specific time
period. In the development of criteria, many
factors have to be considered. The chemical
and physical characteristics must be consider-
ed, along with exposure time and conditions
of the environment. The criteria must also in-
clude consideration of the contributions of all
such variables to the effects of air pollution
on human health, agriculture, materials, vis-
ibility, and climate. Futher, the individual
characteristics of the receptor must be taken
into account. Table 1 1 is a list of the major
factors considered in developing criteria.
Air quality standards are prescriptive. They
prescribe pollutant exposure or levels of ef-
fect that a political jurisdiction determines
should not be exceeded in a specified
geographic area, and are used as one of several
factors in designing legally enforceable pol-
lutant emission standards.
This document focuses on carbon mon-
oxide (CO) as it is found in the ambient air;
therefore, literature on extremely high levels
of CO has not been extensively cited. The
occurrence, properties, and fate of atmospher-
ic CO and principles of formation and control
are reviewed in the earlier chapters; these are
followed by a discussion of estimation of CO
emissions and measurement of atmospheric
CO. The effects of CO are considered in
relation to (1) vegetation, (2) toxicological
studies on animals and man, and (3) epidemi-
ological studies.
The National Air Pollution Control Admin-
istration is currently advocating the use of the
metric system to express atmospheric con-
centrations of air pollutants, e.g., micrograms
per cubic meter Oug/m^). In most instances,
gaseous pollutants have hitherto been re-
ported on a volume ratio basis, i.e., parts per
million (ppm).. In this document, wherever
possible, both types of units are given.
Conversion from volume (ppm) to mass
(jug/m^) units requires a knowledge of the gas
density at the temperature and pressure of
measurement, since gas density varies with
changes in these two parameters. In this
document 25°C (77°F) has been taken as
standard temperature and 760 mm Hg
(atmospheric pressure at sea level) as standard
pressure.
Because of the magnitude of the numbers
involved, concentrations of CO are given in
milligrams per cubic meter rather than in
micrograms per cubic meter. The factor for
converting CO from volume (ppm) to mass
(mg/m^) units is given in Chapter 2. The Ap-
pendix includes information of the derivation
of this factor.
In general, the terminology employed fol-
lows usage recommended in the publications
style guide of the American Chemical Society.
1-1
-------
The scientific literature has been generally
reviewed through March 1969, with addition-
al sources from reports as recent as January
1970. The results and conclusions of
foreign investigations are evaluated for their
possible application to the air pollution
problem in the United States. This document
is not intended as a complete, detailed
literature review, and it does not cite every
published article relating to CO in the
ambient atmosphere. The literature has, how-
ever, been reviewed thoroughly for informa-
tion related to the development of criteria;
and the document not only summarizes the
current scientific knowledge of CO air pol-
lution, but also attempts to point up the
major deficiencies in that knowledge and the
presently recognized needs for further
research.
Methods and techniques for controlling the
sources of CO emissions as well as the costs of
applying these techniques are described in AP-
65, Control Techniques for Carbon Monoxide
from Stationary Sources and AP-66, Control
Techniques for Carbon Monoxide, Nitrogen
Oxide, and Hydrocarbon Emissions from
Mobile Sources.
Table 1-1. FACTORS TO BE CONSIDERED IN DEVELOPING AIR QUALITY CRITERIA81
Properties of pollution
Concentration
Chemical composition
Mineralogical structure
Adsorbed gases
Coexisting pollutants
Physical state of pollutant
Solid
Liquid
Gas
Kinetics of formation
Residence time
Measurement methods
Spectroscopic
Chemical
Exposure parameters
Duration
Concomitant conditions
Temperature
Pressure
Humidity
Characteristics of receptor
Physical characteristics
Individual susceptibility
State of health
Rate and site of transfer to receptor
Responses
Effects on health (diagnosable effects, latent
effects, and effects predisposing the organism
to diseases)
Human health
Animal health
Plant health
Effects on human comfort
Soiling
Other objectionable surface deposition
Corrosion of materials
Deterioration of materials
Effects on atmospheric properties
Effects on radiation and temperature
aAdapted from S. Calvert. Statement for air quality criteria hearings held by the Subcommittee on Air and Water.
Pollution of the U.S. Senate Committee on Public Works. July 30, 1968. Published in "Hearings Before the
Subcommittee on Air and Water Pollution of the Committee on Public Works, United State Senate (Air Pollu-
tion-1968, Part 2)."
1-2
-------
CHAPTER 2.
OCCURRENCE, PROPERTIES, AND FATE
OF ATMOSPHERIC CARBON MONOXIDE
A. INTRODUCTION
Carbon monoxide (CO) is the most widely
distributed and the most commonly occurring
air pollutant. Total emissions of CO to the
atmosphere exceed those of all other pollut-
ants combined.
Most atmospheric CO is produced by the
incomplete combustion of carbonaceous
materials used as fuels for vehicles, space heat-
ing, and industrial processing or burned as ref-
use. Man's activities are, therefore, largely re-
sponsible for CO contamination, and his tech-
nological advances have contributed to the
present atmospheric concentrations.
No large natural source of CO has been
positively identified, but a number of geo-
physical and biological sources of CO are
known. Their ultimate contribution to urban
atmospheric concentrations is thought to be
relatively small.1
This document explores the fundamental
knowledge on CO in the context of its role as
an air pollutant; there are many other aspects
of CO of collateral interest. In addition to the
references to be found in this document, a
bibliography2 on CO compiled in 1966 gives
sources of further information.
B. CARBON MONOXIDE IN HISTORY
Human experience with CO probably began
during prehistoric times when man first dis-
covered fire. CO poisoning has been traced
through Greek and Roman literature; in fact,
this form of poisoning has been closely as-
sociated with the history of mankind.
Materials used for making fire in prehistoric
times were probably wood, grasses, and other
organic matter. Lewin3 cites many cases of
CO poisoning due to the incomplete com-
bustion of such fuels. He also includes ref-
erences to the effects of CO on the health of
man in the writings of Greek physicians of the
Third Century.
With the increased use of coal for domestic
heating in the Fifteenth Century, CO
poisoning increased greatly. This increase was
due to inhalation of CO formed in incomplete
combustion in the heating of homes and to
the exposure of men in mines where the
deadly "white damp" was encountered after
explosions and mine fires. The) introduction
of illuminating gas (a mixture of hydrogen,
carbon monoxide, methane, and other hydro-
carbons) for domestic heating (still used ex-
tensively in Europe but largely replaced by
natural gas in the United States) further in-
creased this hazard.
The introduction of the internal com-
bustion engine for transportation and the de-
velopment of a number of technological proc-
esses wherein CO is produced have greatly in-
creased the production of CO and its release
to the atmosphere.
Over the past few centuries, therefore, the
problem of dealing with CO has spread from
individual dwellings and work environments
to include the ambient air in cities. Concern
has now broadened from the acute and often
lethal effects of high concentrations of the gas
to encompass as well those effects that may
occur as a result of considerably longer ex-
posures to much lower concentrations.
C. OCCURRENCE
1. Technological Sources
Carbon monoxide is found among the com-
bustion products of organic materials used as
fuels. Transportation activities represent the
2-1
-------
largest source category. Other major techno-
logical sources of CO emissions are stationary
heat-generating facilities, industrial processes,
and solid-waste combustion. CO is also
formed in explosions and in the firing of
weapons. It occurs in high concentrations in
cigarette smoke. The major technological
sources of CO are discussed in greater detail in
Chapter 4.
2. Natural Sources
a. Nonbiological
Some CO is reported to be produced in vol-
canos and is formed in natural gases (e.g.,
gases found in coal mines).4 It has also been
reported to be formed during electrical
storms.5 Forest fires caused by lightning
sometimes make a considerable contribution
to atmospheric CO.6 A small amount of CO is
also formed as a photochemical degradation
product of various reactive organic com-
pounds in the process involving the formation
of photochemical smog.7-8 Some CO is be-
lieved to be formed in the upper atmosphere
above 70 kilometers (km) by photodissocia-
tion of carbon dioxide (CO2).9
b. Biological
Small quantities of CO are formed by vege-
tation during seed germination and seedling
growth of plants,10 and it has been observed
in injured, cut, or dried plants.1! Some CO is
found in marsh gases and it is also formed by
certain brown algae (kelps).12'13 Carbon
monoxide concentrations of up to 900 milli-
grams per cubic meter (mg/m^) (786 ppm)
have been found in the floats of Nereocyctis,
a familiar kelp or seaweed.14 Mature leaves
of green plants have been shown to produce
CO.11 Microorganisms also have shown to
produce CO from plant flavonoids.15
Carbon-monoxide-producing colonies of
marine hydrozoan jellyfish (siphonophores)
are widespread and make up a large portion of
the plankton in the warmer oceans of the
world.16'17 CO is also produced in the float
cells of the surface-dwelling Physalia physalis
(Portugese Man-of-War).18 In addition to the
generation of CO by ocean-dwelling biological
2-2
specimens, other mechanisms may exist
through which CO is generated in the ocean.
Another biological source of CO is endog-
enous CO, which is produced in measurable
quantities in man and animals as a by-product
of heme catabolism.19'21 This endogenous
Co is produced in larger amounts in hemolytic
disease states.
D. PROPERTIES AND GASEOUS REAC -
TIONS OF CARBON MONOXIDE
1. Physical Properties
Carbon monoxide is a colorless, odorless,
tasteless gas, slightly lighter than air.22 Quite
flammable, it burns with a bright blue flame,
but does not support combustion.
Physical properties of CO are outlined in
Table 2-1.
2. Gaseous Chemical Reactions of Carbon
Monoxide
The likely gaseous reactions wherein CO
might be oxidized to CO2 have been reviewed
by Bates and Witherspoon.9 The reaction
with molecular oxygen:
2 CO + O2 -> 2 CO2
(D
is possible in the lower atmosphere, but is
apparently unimportant. Both dry and moist
experimental mixtures of CO and oxygen
have remained unchanged after 7 years of ex-
posure to sunlight.23 The possibilities of reac-
tions between CO and atomic oxygen have
been reviewed by Leighton,8 and he has con-
cluded that they are unimportant; Bates and
Witherspoon have come to a similar conclu-
sion.9
a Lower A tmospheric Reactions
Two oxidation reactions, although very
slow, do occur in the lower atmosphere.24'26
CO + O2 -» CO2 + O (2)
and in the presence of moisture
CO + H2O -> CO2 + H2. (3)
Both of these reactions have appreciable en-
ergy barriers, 51 and 56 kilocalories per mole
-------
Table 2-1. PHYSICAL PROPERTIES OF CARBON MONOXIDE
Molecular weight
Melting point
Boiling point
Specific gravity relative to air
Density
At 0°C, 760 mm Hg
At 25°C, 760 mm Hg
Explosive limits in air
Solubility2
AtO°C
At 25°C
Conversion factors
At 0°C, 760 mm Hg
At 25°C, 760 mm Hg
28.01
-207°C
-192°C
0.968
1.25g/liter
1.15g/liter
12.5 to 74.2% (volume)
3.54 ml/100 ml water
2.14 ml/100 ml water
1 mg/m3 = 0.800 ppm
1 ppm = 1.250 mg/m3
1 mg/m3 = 0.874 ppm
1 ppm = 1.145 mg/m3
aVolume of CO indicated is at 0°C, 760 mm Hg.
(kcal/mole), respectively. Direct chemical re-
actions between CO and oxygen or water oc-
cur at a frequency of less than one reaction
per 101 s molecular collisions at room temper-
ature. These reactions become important as
gas-phase processes primarily at temperatures
above 500°C and even more so above 1000°C.
These reactions occur more readily and at
lower temperatures on the surfaces of certain
catalysts, usually metal oxides. For example,
oxidation is catalyzed at room temperatures
by metallic catalysts, such as Hopcalite, which
is a mixture of the oxides of manganese and
copper, and by palladium on silica gel.27
Ozone will oxidize CO to CO2,but the rate
of this reaction is extremely slow at atmos-
pheric temperatures and concentrations.28'29
A high activation energy of about 20 kcal for
the oxidation of CO by ozone has been
found.30
Oxidation by NO2 in the reaction
NO2 + CO -» CO2 + NO
(4)
has an even higher activation energy than does
the oxidation of CO by ozone. The activation
energy of 28 kcal essentially precludes the
occurrence of this process in the atmos-
phere.3 1
Consideration has also been given to the
possibility that some very rapid reactions may
occur between CO and certain intermediates
of photochemical smog reactions. One pos-
sible intermediate is the hydroxyl radical,
which may occur when the photolysis of alde-
hydes produces perhydroxyl, which can then
be reduced to the hydroxyl radical. Hydroxyl
appears to react very rapidly with CO, and
there is some indication that perhydroxyl also
reacts with CO.32 Such reactions involve
chain-type mechanisms, and Doyle33 has
calculated that a global average hydroxyl con-
centration of only 10'9 to 10"^ part per mil-
lion (ppm) would be sufficient to convert all
emitted CO to CO2.
Methane, which is found in the troposphere
at concentrations one order of magnitude
higher than CO concentrations, can also be
oxidized by hydroxyl radicals. The rate of re-
action is slow, however, and the extent to
which methane competes with CO for the
hydroxyl radicals in the atmosphere has not
been defined.
Although future research with hydroxyl
radicals may be rewarding, at present one
must conclude that significant gaseous oxida-
tion reactions of CO in the ambient atmos-
phere have not been proved.
2-3
-------
b. Upper A tmospheric Reactions
Short-wavelength ultraviolet radiation
(about 1700A) dissociates CO2 into CO and
atomic oxygen9 according to the reaction:
CO-, + hv -> CO + O.
(5)
The yield of CO from the photodissociation
of COo in the upper atmosphere, however, is
considered to be relatively small at levels be-
low 100 kilometers since the intensity of ac-
tive ultraviolet radiation falls off rapidly at
that level.
Carbon dioxide may be reformed by a
three-body collision:
CO + O + M -* CO2 + M
(6)
where M represents the third body. The third
body absorbs excess energy by collision from
the energy-rich combination of a CO molecule
and an oxygen atom. In the absence of such a
collision, no stable CO2 can be formed. The
probability of this collision occurring is small,
however, because of the low concentration of
such third bodies at higher altitudes.
From the foregoing information, it must be
concluded that no gaseous reactions have
been shown to be important scavengers of CO
in the atmosphere.
E. BACKGROUND LEVELS AND FATE
OF ATMOSPHERIC CARBON
MONOXIDE
1. Background Levels and Estimated Mean
Lifetime of Carbon Monoxide
The amount of CO measurable in relatively
unpolluted ("clean") air is small. Junge has
estimated the background level of CO in the
lower atmosphere to be in the range of 0.01
to 0.2 mg/m3 (0.01 to 0.2 ppm).34 Studies of
background levels of CO using solar spectral
techniques at Mt. Wilson, California;
Ottawa, Canada; Jungfraujoch, Switzerland;
and Columbus, Ohio, confirmed that such
levels average about 0.1 mg/m3 (0.1
ppm).35"37 There appears to be no significant
variation in such levels with geographical loca-
2-4
tions.37 Robbins et al.,38 using an experi-
mental, continuous-measurement HgO
method sensitive in parts per billion (ppb),
have recently determined that North Pacific
marine air mass concentrations may contain
as little as 0.029 mg/m3 (0.025 ppm) and the
clean (nonurban) air mass over continental
California contains 0.06 to 1.2 mg/m3 (0.05
to 1.0 ppm). These investigators have also de-
termined, on the basis of a 12-day sample,
that typical background levels of CO at Inge
Lehmann Station in northern Greenland range
from 0.06 to 0.75 mg/m3 (0.05 to 0.65
ppm).39 The variability of CO in nonpolluted
areas appears to be a characteristic of the air
mass in transit and reflects its prior history.
Robinson and Robbins estimate that arctic air
masses passing over Greenland have CO con-
centrations of between 0.11 and 0.23 mg/m3
(0.10 and 0.20 ppm) and that concentrations
of 0.6 to 1.2 mg/m3 (0.5 to 1.0 ppm) can
occur when the air mass has recently traversed
a heavily populated area.39 Measurements at
Point Barrow, Alaska, gave clear air CO levels,
ranging from 0.063 to 0.299 mg/m3 (0.055 to
0.260 ppm) and averaging 0.104 mg/m3 (0.90
ppm).40
The exact turnover time of CO in the
atmosphere is not known with certainty. A
recent estimate, derived from radioactive
measurements, of the residence time of CO in
the lower atmosphere has a lower limit of 0.1
year.41 Another estimate based on different
technique is 3 years.34 (The published esti-
mate of 0.3 year given in reference 34 is based
on a miscalculation)42 Robbins et al. esti-
mate a mean residence time of about 5 years,
and have tentatively concluded that the back-
ground levels of CO are not rising significantly
at the persent time.38
The previously discussed relative inertness
of CO in reactions with the normal gaseous
atmospheric constituents and its photon
transparency43 effectively eliminate the pos-
sibility of chemical reactions as a mechanism
for CO removal in the lower atmosphere with
the possible exception of the still speculative
reaction with the hydroxyl radical.
-------
In spite of the above, calculations have
shown that in the absence of removal proc-
esses, the estimated world-wide emissions of
CO from technological sources (estimated to
be on the order of 1.8 to 2.1 x 1011 kg or
198 to 231 million tons per year1 3-40) would
be sufficient to raise the atmospheric back-
ground concentration of CO by 0.03 mg/rn^
(0.03 ppm) per year creating a current back-
ground level of 1 mg/m^ (1 ppm).9'38'44 It is
therefore postulated that some "sink" or re-
moval process for atmospheric CO exists.
2. Possible Processes for Carbon
Monoxide Removal
The following discussion represents a re-
view of possible CO removal processes. Some
of the CO "sinks" discussed below are highly
speculative, however; in fact, they may actual-
ly contribute CO rather than remove it from
the atmosphere.
a. Atmospheric Migration (Upper
Atmospheric Sink).
Conceivably CO in the lower atmosphere
may eventually migrate by atmospheric mix-
ing to a potential sink in the upper atmos-
phere, where it is oxidized to CO2 in the
presence of high-intensity ultraviolet solar
radiation. A recent laboratory study by
Harteck and Reeves45 confirmed that CO, in
the presence of NO2 or other absorbing mole-
cules, when subjected to high-intensity, ultra-
violet radiation in an evacuated chamber, was
oxidized to CO 2-
b. Biological Removal (Terrestrial and
Marine Biosphere Sink).
Another possible removal agent of atmos-
pheric CO is the presence, in significant
numbers, of plants and microorganisms that
can metabolize CO. The earth's surface is a
possible vector for the removal of CO from
the atmosphere. Carbon monoxide in contact
with the soil may be oxidized to CO2 and
converted to methane (CH^.) by common
specific anaerobic methane-producing soil
microorganisms, Methanosarcina barkerii and
Methanobacterium formicum, in the presence
of moisture.
This action has been demonstrated in the
laboratory by Schnellen,46 who showed that
pure cultures of these bacteria convert CO in-
to methane. Schnellen has found that Ms.
barkerii is capable of converting CO to Qfy
according to the equation:
4 CO + 2 H2O -* CH4 + 3 CO2 (7)
Stephenson,4 7 however, indicates that CO,
in the absence of H2, reacts with water in
these bacteria in two stages as follows:
4 CO + 4 H2O -> 4 CO2 + H2 (8)
and
CO2 + 4 H2 -* CH4 + 2 H20.
(9)
In the presence of H2, these bacteria convert
CO directly into methane and water:
CO + 3 H2 -* CH4 + H2O.
(10)
An aerobic soil bacterium, Bacillus oligo-
carbophilus (Carboxydomonas oligocarbo-
phila), found in and isolated from arable soil,
has also been demonstrated to oxidize CO to
CO2- When cultivated on simple organic
media free from other carbon sources, this
organism oxidizes CO to CO2, which is then
utilized as a source of energy.48 Another
bacterium, Clostridium welchii, when grown
in the presence of CO, has been reported to
produce lactic acid as a fermentation prod-
uct.49
Although these soil bacteria utilize CO in
their fermentation or metabolic processes, it
is difficult to estimate global destruction rates
of CO on the basis of such laboratory experi-
ments.
Within the biosphere, the process of plant
respiration may serve as a potential removal
process; but this concept has not been firmly
established, even though it is recognized that
plants are scavengers for a wide variety of
atmospheric materials. Chapter 7 of this docu-
ment treats this subject in greater detail.
2-5
-------
c. Biochemical Removal (Biochemical
Sink).
A potential biochemical removal process
for CO is the binding of CO to the porphyrin-
type compounds that are widely distributed
in plants and animals. In particular, the heme
compounds such as hemoglobin, which are
analogous to porphyrin compounds found in
plants are known to bind CO. It must be
noted, however, that practically all of the CO
absorbed by the heme compounds found in
man and animals is eventually discharged
from the blood, and only a small fraction is
retained.5 ° This type of process in vegetation
may have an important potential for scaveng-
ing atmospheric CO.Permanent removal from
the environment, however, would depend on
whether CO subsequently enters into some re-
action process to form CO2 when the porphy-
rin compound is degraded.
d. Absorption in Oceans (Oceanic Sink).
While absorption in the world's oceans is a
recognized sink process for atmospheric CO 2,
there is no evidence at present that the oceans
are a sink for CO because no process or
reaction that would remove CO has been
discovered.1-14 The solubility of CO at 1
atmosphere (atm) pressure in sea water ranges
from about 17 to 32 milliliters CO (0°C, 1
atm)/liter water over a water temperature and
chloriniry range of -2° to 30°C and 15 to 21
grams of chlorine per kilogram of water, re-
spectively.5 1 This solubility is too low for the
oceans to accumulate CO or for precipitation
washout to be an effective scavenging agent.
An apparent daily cycle for CO concentra-
tions over ocean areas seems to indicate some
involvement of the ocean in the fate of CO.34
The high CO concentrations in some, marine
plants14 may also be indicative of some com-
plex system in the ocean involving CO.
Swinnerton et al. simultaneously sampled
the CO content of the air and the surface
waters at 29 different points along the path
of an oceanographic cruise between Washing-
ton, D.C., and Puerto Rico.52 These investiga-
tors found that the measured concentrations
of CO in the water exceeded by 7 to 90 times
2-6
the concentrations of CO theoretically ex-
pected to be present based on solubility calcu-
lations. Apparently, man-made pollution is
not the principal source of CO in sea water,
since the highest ratios were found in the
open ocean. The ocean, therefore, may be a
source rather than a sink for atmospheric CO,
as discussed previously.
e. Adsorption on Surfaces.
Kummler et al. indicate that the gas-phase
oxidation of CO by nitrous oxide (N2O),
considered too slow to be of importance in
the atmosphere, is catalyzed in the presence
of certain surfaces (such as charcoal, carbon
black, and glass) at 300°C and above.5 3 These
investigators have extrapolated these reported
high-temperature reaction rates to 27°C and
consider that such a catalytic reaction is
feasible at ambient temperatures. This con-
clusion is supported by laboratory studies of
Gardner and Petrucci, where the chemisorp-
tion of CO on metallic films (such as copper,
cobalt, and nickel oxides) at room tempera-
tures have been measured by infrared spec-
troscopy.5 4
The necessary data for evaluation of the
catalytic efficiency of common surfaces such
as metals, soil, and atmospheric particles are
presently unavailable; therefore, the possibil-
ity of such surfaces serving as a sink by ad-
sorption of atmospheric CO is uncertain.
F. SUMMARY
Carbon monoxide constitutes the largest
single fraction of the pollutants found in
urban atmospheres. It is produced primarily
by the incomplete combustion of organic
materials used as fuels for transportation and
in the heating of buildings; it also results from
industrial processes, refuse burning, and agri-
cultural burning. Several natural sources of
CO of both biological and nonbiological
origin have also been identified, but their con-
tributions to urban atmospheric concentra-
tions are thought to' be small. Background
levels of CO (resulting from natural and tech-
nological sources) found in relatively unpol-
luted air range from 0.029 to 1.15 mg/m3
(0.025 to 1.0 ppm).
-------
Carbon monoxide is colorless, tasteless, and
odorless; although flammable, it does not sup-
port combustion. Oxidation reactions with
both oxygen and water vapor are known to
involve CO in the lower atmosphere, but the
rate of these reactions is very slow.
Worldwide emissions of CO from techno-
logical sources have been estimated to be
more than 1.8 x 1011 kg (200 million tons)
annually. In the absence of any removal proc-
esses, this large tonnage would be sufficient to
raise the background level of CO by 0.03
mg/m^ (0.03 ppm) per year; yet these back-
ground levels do not appear to be rising. The
mean residence time of atmospheric CO has
been estimated to be between 1 month and 5
years.
Several "sinks", or removal processes, have
been postulated in an attempt to explain the
apparent constancy of the background CO
levels. These processes include: the migration
of CO to the upper atmosphere, where oxida-
tion to CO2 may subsequently take place; the
removal of CO by the terrestrial and marine
biospheres, through processes such as the
metabolic conversion of CO to CO2 and
methane by soil microorganisms; the binding
of CO to porphyrin compounds in plants and
animals, with subsequent oxidation of the CO
to CO2; an interaction between CO and ocean
water, or some agent in ocean water; and the
adsorption and subsequent oxidation of CO
on various surfaces. Although the biosphere
provides several potential mechanisms involv-
ing both land and marine plant and animal
communities, the precise mechanism of re-
moval of CO from the atmosphere cannot at
present be identified with any certainty. In
fact, some of the CO sinks discussed above are
highly speculative and may actually contri-
bute rather than remove CO from the atmos-
phere.
G. REFERENCES
1. Jaffe, L. S. Ambient Carbon Monoxide and Its
Fate in the Atmosphere. J. Air Pollution Control
Assoc. 75:534-540, August 1968.
2. Cooper, A. G. Carbon Monoxide. A Bibliography
with Abstracts. U. S. DHEW, PHS. Division of
Air Pollution. Washington, B.C. PHS Publication
Number 1503; Bibliography No. 68. 1966. 440
P-
3. Lewin, L. Carbon Monoxide Poisoning: A Man-
ual for Physicians, Engineers, and Accident In-
vestigators. Berlin, Julius Springer-Verlag, 1920.
4. Flury, F. and F. Zernik. Noxious Gases-Smoke,
Fog, Fumes and Dust. Berlin, Julius Springer-
Verlag, 1931.
5. White, J. J. Carbon Monoxide and Its Relation to
Aircraft. U. S. Naval Med. Bull. 30(2): 151-165,
April 1932.
6. National Air Pollution Control Administration,
Reference Book of Nationwide Emissions. U.S.
DREW, PHS, CPEHS, NAPCA. Durham, N.C.
7. Altshuller, A. P. and J. J. Bufalini. Photo-
chemical Aspects of Air Pollution: A Review.
Photochem. Photobiol. 4(2):97-146, March
1965.
8. Leighton, P. A. Photochemistry of Air Pollution.
New York, Academic Press, 1961. 300 p.
9. Bates, D. R. and A. E. Witherspoon. The Photo-
chemistry of Some Minor Constiuents of the
Earth's Atmosphere (CO2, CO, CH4, N2O).
Monthly Notices of the Roy. Astron. Soc.
(London). 772:101-124, January 1952.
10. Siegel, S. M., G. Renwick, and L. A. Rosen.
Formation of Carbon Monoxide During Seed
Germination and Seedling Growth. Science.
7J7(3531):683-684, August 31, 1962.
11. Wilks, S. S. Carbon Monoxide in Green Plants.
Science. 729(3354):964-966, April 10, 1959.
12. Loewus, M. W. and C. C. Delwiche. Carbon Mon-
oxide Production by Algae. Plant Physiol.
JS(4):371-374, July 1963.
13. Chapman, D. J. and R. D. Tocher. Occurrence
and Production of Carbon Monoxide in Some
Brown Algae. Can. J. Botany. 44:1438-1442,
October 1966.
14. Robinson, E. and R. C. Robbins. Sources,
Abundance and Fate of Gaseous Atmospheric
Pollutants. Stanford Research Institute., Menlo
Park, Calif. Final Report. SRI Project PR-6755.
February 1968. 124 p.
15. Westlake, D. W. S.," J. M. Roxburgh, and G.
Talbot. Microbial Production of Carbon Mon-
oxide from Flavonoids. Nature.
189(4163):510-511, February 11, 1961.
16. Barham, E. G. Siphonophores and the Deep
Scattering Layer. Science. 740(3568):826-828,
May 17, 1963.
17. Barham, E. G. and J. W. Wilton. Carbon Mon-
oxide Production by a Bathypelagic Siphono-
phore. Science. 144(3620):860-862, May 15,
1964.
18. Wittenberg, J. B. The Source of Carbon Mon-
oxide in the Float of the Portugese Man-of-War,
Physalia physalis L. J. Exp. Biol. 57(4):698-705,
December 1960.
2-7
-------
19. White, P. et al. Carbon Monoxide Production As-
sociated with Ineffective Erythropoiesis. Blood.
24(6): 845, December 1964.
20. Middelton, V. et al. Carbon Monoxide Accumula-
tion in Closed Circle Anesthesia Systems. Anes-
thesiology. 25(6):715-719, November-December
1965.
21. Landaw, S. A. and H. S. Winchell. Endogenous
Production of Carbon'14 Labeled Carbon
Monoxide: An In Vivo Technique for the Study
of Heme Catabolism. J. Nucl. Med. 7:696-707,
September 1966.
22. Hygienic Guide Series: Carbon Monoxide. Amer.
Ind. Hyg. Assoc. J. 2<5(4):431-434, July-August
1965.
23. Mellor, J. W. Carbon. In: A Comprehensive
Treatise on Inorganic and Theoretical Chemistry,
Vol. V. London, Longmans, Green and Co.,
1924. p. 926-950.
24. Tunder, R. et al. Compilation of Reaction Rate
Data for Non-Equilibrium Performance and Re-
entry Calculation Programs. Aerospace Corp. El
Segundo, Calif. Aerospace Report Number
TR-1001(9210-02)-!. January 1967.
25. Fischer, E. R. and M. McCarty, Jr. Study of the
Reaction of Electronically Excited Oxygen
Molecules with Carbon Monoxide. J. Chem.
Phys. 45(3):781-784, August 1, 1966.
26. Graven, W. M. and F. J. Long. Kinetics and
Mechanisms of the Two Opposing Reactions of
the Equilibrium CO + H2O = CO2 + H2. J. Amer.
Chem. Soc. 75(10):2602-2607, May 20, 1954.
27. Carbon Monoxide. In: The Merck Index of
Chemicals and Drugs. Stecher, P. G. (ed.). Rah-
way, N. J., Merck and Co., 1960. p. 212.
28. Garvin, D. The Oxidation of Carbon Monoxide in
the Presence of Ozone. J. Amer. Chem. Soc.
76(6): 1523-1527, March 20, 1954.
29. Harteck, P. and S. Dondes. Reaction of Carbon
Monoxide and Ozone. J. Chem. Phys.
26:1734-1737, June 1957.
30. Zatsiorskii, M., V. Kondratev, and S. Solnish-
kova. Radiation of the Flame of CO + Og and
the Mechanism of this Reaction. Zh. Fiz. Khim.
(Leningrad). 14(12):1521-1527. 1940.
31. Brown, F. B. and R. H. Crist. Further Studies on
the Oxidation of Nitric Oxide; The Rate of the
Reaction Between Carbon Monoxide and Nitro-
gen Dioxide. J. Chem. Phys. 9:840-846, Decem-
ber 1941.
32. Greiner, N. R. Hydroxyl-Radical Kinetics by
Kinetic Spectroscopy. I. Reactions with H2, CO,
and CH4 at 300°K. J. Chem. Phys.
46(7):2795-2799, April 1, 1967.
33. Doyle, G. J. Unpublished Data. Stanford Re-
search Institute. Menlo Park, Calif. 1968.
34. Junge, C. E. Air Chemistry and Radioactivity.
New York, Academic Press, 1963. 382 p.
35. Migeotte, M. and L. Neven. Recent Progress in
the Observation of the Solar Infrared Spectrum
at the Scientific Station at Jungfraujoch, Switzer-
land [Recents Progres Dans L'Observation du
Spectre Infrarouge du Soleil a la Station Scientif-
2-8
ique du Jungfraujoch (Suisse)]. Mem. Soc. Roy.
Sci. Liege. 72(1-11): 165-178, 1952.
36. Benesch, W., M. Migeotte, and L. Neven. Investi-
gations of Atmospheric CO at the Jungfraujoch.
J. Opt. Soc. Amer. 45:1119-1123, November
1953.
37. Locke, J. L. and L. Herzberg. The Absorption
Due to Carbon Monoxide in the Infrared Solar
Spectrum. Can. J. Phys. J7(4): 504-516, May
1953.
38. Robbins, R. C., K. M. Borg, and E. Robinson.
Carbon Monoxide in the Atmosphere. J. Air Pol-
lution Control Assoc. 75:106-110, February
1968.
39. Robinson, E. and R. C. Robbins. "Atmospheric
CO Concentrations on the Greenland Ice Cap."
Jour. Geophysical Research. 74(8): 1968-1973,
April 15, 1969.
40. Cavanagh, L. A. C. F. Schadt, and E. Robinson.
Atmospheric Hydrocarbon and Carbon Mon-
oxide Measurements at Point Barrow, Alaska.
Environ. Sci. Technol. 5:251-257, March 1969.
41. Weinstock, B. Carbon Monoxide: Residence
Time in the Atmosphere. Science.
766(3902):224-225, October 10, 1969.
42. Private communication with R. C. Robbins.
Menlo Park, Calif. September 24, 1969.
43. Penndorf, R. The Vertical Distribution of
Atomic Oxygen in the Upper Atmosphere. J.
Geophys. Res. 5<4(l):7-38, March 1949.
44. Haagen-Smit, A. J. and L. G. Wayne. Atmos-
pheric Reactions and Scavenging Processes. In:
Air Pollution, Stern, A. C. (ed.), Vol. I, 2d ed.
New York, Academic Press, 1968, p. 149-186.
45. Harteck, P. and R. E. Reeves, Jr. Some Specific
Photochemical Reactions in the Atmosphere.
Presented at the Symposium on the Chemistry of
the Natural Atmosphere, American Chemical
Society Annual Meeting. Chicago. September
1967.
46. Schnellen, C. G. T. P. Research on Methane
Fermentation [Onderzoekingen Over de Metha-
angisting]. Doctoral Thesis, Technische Wet-
enschap de Delft. Rotterdam, Drukkerij de Ma-
asstad, 1947. 137 p.
47. Stephenson, M. Bacterial Metabolism. 3rd ed.
New York, Longmans, Green and Co., 1949. 398
P.
48. Kaserer, H. The Oxidation of Hydrogen by
Microorganisms [Die Oxydation des Wasser-
stoffes durch Mikroorganismen]. Zentr. Bakter-
iol. Parasitenk, Abt. II. 76(14-16):681-696,
1906.
49. Waksman, S. A. Principles of Soil Microbiology.
2d ed. Baltimore, Williams & Wilkins Co., Jan-
uary 1932. 894 p.
50. Luomanmaki, K. Studies on the Metabolism of
Carbon Monoxide. Ann. Med. Exp. Biol. Fenniae
(Helsinki). 44(Suppl 2): 1-55, 1966.
51. Douglas E. Carbon Monoxide Solubilities in Sea
Water. J. Phys. Chem. 77(6): 1931-1933 May
1967.
-------
52. Swinnerton, J. W., V. J. Linnenbom, and C. H. trie Co. and Barringer Research Ltd. Presented at
Cheek. Distribution of Methane and Carbon the 50th Annual Meeting of the American Geo-
Monoxide Between the Atmosphere and Natural physical Union. Washington, D. C. April 21-25,
Waters. Environ. Sci. Technol. 3:836-838, Sep- 1969.
tember 1969. 54. Gardner, R. A. and R. H. Petrucci. The Chem-
53. Kummler, R. H. et al. Satellite Solution of the isorption of Carbon Monoxide on Metals. J.
Carbon Monoxide Sink Anomaly. General Elec- Amer. Chem. Soc. &2(19):5051-5053, October 5,
1960.
2-9
-------
CHAPTER 3.
PRINCIPLES OF FORMATION AND
CONTROL OF CARBON MONOXIDE
A. INTRODUCTION
Carbon monoxide formation results direct-
ly from the incomplete combustion of a gase-
ous, liquid, or solid carbon-containing fuel;
therefore, the CO found in urban air generally
has its origin in one of the many combustion
processes associated with man's day-to-day
activities, industry, and commerce. It is the
purpose of this chapter to discuss the general
mechanisms of combustion leading to the for-
mation of CO and their specific involvement
in CO formation in mobile and stationary
sources.
A more detailed discussion of the informa-
tion presented in this chapter may be found
in AP-65, Control Techniques for Carbon
Monoxide Emissions from Stationary Sources,
and AP-66, Control Techniques for Carbon
Monoxide, Nitrogen Oxide, and Hydrocarbon
Emissions from Mobile Sources.
B. FORMATION OF CARBON MONOXIDE
BY COMBUSTION
1. General Combustion Processes
Incomplete combustion of carbon or car-
bon-containing compounds creates varying
amounts of CO. The chemical and physical
processes that occur during this combustion
are complex, because they depend not only on
the type of carbon compound reacting with
oxygen, but also on the conditions existing in
the combustion chamber. Despite the com-
plexity 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 re-
acts with hydroxyl radicals to form carbon
dioxide (CO2). This second reaction is ap-
proximately ten 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.
Consideration of this mechanism leads to
four basic variables that control the concen-
tration of CO in all combustion of hydro-
carbon gases. These are (1) oxygen concentra-
tion, (2) flame temperature, (3) gas residence
time at high temperature, and (4) combustion
chamber turbulence. Oxygen concentration
affects the formation of both CO and CO2
because oxygen is required in the initial reac-
tions with the fuel molecule and in the forma-
tion of the hydroxyl radical. As the availabil-
ity of oxygen increases, more complete con-
version of monoxide to dioxide results. Flame
temperature affects both the formation of
monoxide and the conversion of monoxide to
dioxide because both reaction rates increase
exponentially with increasing temperature.
The conversion of CO to CO2 is also enhanced
by longer residence time because this is a rela-
tively slow reaction compared to CO forma-
tion. Increasing combustion-gas turbulence in-
creases the actual reaction rates by by-passing
the relatively slower gaseous diffusion mixing
process.
2. Internal Combustion Engines
The two factors that effectively determine
total CO emissions from internal combustion
engines are the concentration of CO in the
exhaust and the exhaust volume. The exhaust
3-1
-------
concentration depends mainly on the air-to-
fuel (A/F) ratio entering the combustion
cylinder; the exhaust volume depends on the
power output.
Exhaust concentrations of CO increase
with lower (richer) A/F ratios, decrease with
higher (leaner) A/F ratios, but remain relative-
ly constant with ratios above the stoichio-
metric ratio of about 14.5 to I.1 The be-
havior of gasoline automobile engines before
and after the imposition of pollutant control
measures differs considerably. Depending on
the mode of driving, the average precontrol
engine operates at A/F ratios ranging from
about 11 to a point slightly above the
stoichiometric ratio. During the idling mode,
at low speeds with light load (such as low-
speed cruise), during the full-throttle mode
until speed picks up, and during deceleration,
the A/F ratio is low in precontrol cars and CO
emissions are high. At higher speed cruise and
during moderate acceleration, the reverse is
true. Cars with exhaust controls generally re,
main much closer to stoichiometric A/F ratios
in all modes, and thereby the CO emissions
are kept lower. The relationship between CO
concentration in exhaust and the A/F ratio is
shown in Figure 3-1.
The exhaust flow rate increases with in-
creasing engine power output. During idle the
flow is minimum; during full throttle it is
maximum. At cruise engine conditions (i.e.,
constant engine speed and power output) the
exhaust flow remains constant. It increases
during engine acceleration.
Correlations between total emissions of CO
in pounds per vehicle mile and average route
speed (discussed in greater detail in Chapter
4) show a decrease in emissions with increas-
ing average speed. The greater emissions per
mile during the low-speed conditions (below
20 miles per hour) are due to an increase in
the frequency of the acceleration, decelera-
tion, and idle stages of the driving cycle en-
countered in heavy traffic.
10r
6S
X
O
z
o
z
o
m
a
<
u
^
^J
V
12
13
14 15
AIR-FUEL RATIO
16
17
18
19
Figure 3-1. Effect of air-fuel ratio on exhaust gas carbon monoxide concentrations from
three test engines.1
3-2
-------
3. Stationary Combustion Sources
In stationary combustion systems, the con-
centration of CO is lowest near the stoichio-
metric ratio of air to fuel. At lower than
stoichiometric A/F ratios, high CO concentra-
tions reflect the relatively low oxygen concen-
tration 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. At higher than stoichiometric A/F
ratios, increased CO emissions result from de-
creased flame temperatures and shorter resi-
dence times. These two factors control even
though oxygen concentrations and turbulence
increase. Minimal CO emissions and maximum
thermal efficiency therefore require com-
bustor designs that provide high turbulence,
sufficient residence time, high temperatures,
and near stoichiometric A/F ratios. Com-
bustor design dictates the minimum CO emis-
sion that can be achieved, and operating
practice dictates the actual approach to that
minimum.
C. SUMMARY
Carbon monoxide arises predominantly
from incomplete or inefficient combustion. If
any of the four variables that control this
process are low, CO may be high. These vari-
ables are: (1) oxygen concentration, (2) flame
temperature, (3) gas residence time at high
temperature, and (4) combustion chamber
turbulence. In the internal combustion engine
the air/fuel ratio, corresponding to variable
(1) above, is controlling for CO concentration
in the exhaust, whereas the total volume of
exhaust relates to power output. In stationary
sources, combustor design and operation de-
termine the CO emissions.
D. REFERENCES
1. Hagen, D. F. and G. W. Holiday. The Effects of
Engine Operating and Design Variables on Ex-
haust Emissions (SAE Paper No. 486C). In: Ve-
hicle Emissions, Vol. 6. New York, Society of
Automotive Engineers, Inc., 1964. p. 206-223.
3-3
-------
CHAPTER 4.
ESTIMATION OF CARBON MONOXIDE EMISSIONS
A. INTRODUCTION
The potential for CO emissions exists every-
where man uses his ancient ally, fire. Since
combustion takes such a multitude of forms,
the task of evaluating the relative importance
of different CO sources requires considerable
variety in methods of estimation. Of the num-
erous source categories of CO, fuel combus-
tion in mobile sources utilizing the internal
combustion engine is the principal source
category of CO in the United States. Miscel-
laneous combustion sources, principally forest
fires, and industrial process sources are the
second and third largest categories of CO
emissions. Disposal of solid wastes, either by
open burning or incineration, and stationary
fuel combustion are the fourth and fifth larg-
est categories, respectively.
A more detailed discussion of the informa-
tion presented in this chapter may be found
in AP-65, Control Techniques for Carbon
Monoxide from Stationary Sources, and
AP-66, Control Techniques for Carbon Mon-
oxide, Nitrogen Oxide and Hydrocarbon
Emissions from Mobile Sources,
B. RECENT CARBON MONOXIDE
EMISSION LEVELS
1. National Emission Levels
An estimated 92 x 109 kilograms (102 mil-
lion tons) of CO was emitted in the United
States in 1968 — 50 percent by weight of all
major air pollutant emissions for that year.1
Contributions by source categories to the esti-
mated national emission of CO are presented
in Tables 4-1 and 4-2.
CO emission estimates were derived by the
use of emission factors and activity levels. The
emission factors were developed from source
testing data, material balances, and theoretical
calculations; the activity levels were based on
such quantities as vehicle miles of travel, fuel
consumption, airplane landing and take-off
cycles, and industrial process production.
2. Regional Emission Levels
Emission surveys have been conducted in
various cities in the United States in order to
determine the nature and amount of air pol-
lutants emitted in these communities. Com-
parative emission data from recent emission
inventories of selected metropolitan areas are
presented in Table 4—3 for the years 1967
through 1968. These inventories are based on
a modified rapid survey technique using grid
coordinates. Limitations of the rapid survey
technique are discussed by Ozolins.2 The rela-
tive contributions from different emission
sources to the total CO emissions vary within
each surveyed area. This variability is shown
for 11 selected cities in Figure 4-1. In all
areas, the major source of CO is transporta-
tion, which includes emissions from motor
vehicles, aircraft, trains, and ships.
Table 4—3 includes emission data from
areas constituting 58 percent of the 1968
urban population of the United States. These
emission estimates were obtained by using
specific regional data obtained by government
surveys. In all but two of the 26 cities in the
table, CO emissions are greater than those of
any other pollutant reported.
C. EMISSIONS AND EMISSION FACTORS
BY SOURCE TYPE
1. Mobile Combustion Sources
a. Motor Vehicles
The largest single source of CO (more than
58 percent of the national total) is the ex-
haust of motor vehicles, both gasoline- and
4-1
-------
Table 4-1. CARBON MONOXIDE EMISSION ESTIMATES BY SOURCE CATEGORY-1968*
Source
Transportation
Motor vehicles
Gasoline
Diesel
Aircraft
Vessels
Railroads
Other non-highway use of motor fuels
Fuel combustion in stationary
sources
Coal
Fuel oil
Natural gas
Wood
Industrial processes
Solid waste disposal
Miscellaneous
Man made
Forest fires
Total
CO emissions,
106 tons/yr
63.8
59.2
59.0
0.2
2.4
0.3
0.1
1.8
1.9
0.8
0.1
N
1.0
11.2
7.8
16.9
9.7
7.2
101.6
Percent of total
62.8
58.2
58.0
0.2
2.4
0.3
0.1
1.8
1.9
0.8
0.1
N
1.0
11.0
7.7
16.6
9.5
7.1
100.0
N = Negligible.
aThese emission estimates are subject to revision as more refined information becomes available.
diesel-powered. Other vehicle emissions, such
as hydrocarbons, may come from the fuel
tank, crankcase, or carburetor, as well as from
the exhaust, but of these only the exhaust is a
significant source of CO.3"7
The quantity of emissions from a single
vehicle is not large. They vary in automobiles
by more than an order of magnitude from the
lowest emitters among new vehicles with con-
4-2
trol systems to the highest emitters among un-
controlled vehicles, but are usually in the
range of 1 to 4 percent by volume in the ex-
haust over a complete representative driving
cycle. The national average in 1968 was about
33 grams per kilometer (53 g/mi), but since
1.63 x 10*2 vehicle-kilometers (1015 billion
vehicle-miles) were traveled, the total national
emissions reached the substantial value of 5.4
x 1010 kilograms (5.9 x 107 tons) of CO.
-------
Table 4-2. CARBON MONOXIDE EMISSION ESTIMATES - 1968
Source
Mobile combustion sources
Motor vehicles
Light-duty vehicles - urban
- rural
Heavy-duty vehicles
Class II (6, 000- 10,000
lba) - urban
- rural
Class III (10,000- 19,500
1 ba) - urban
- rural
Class IV (>1 9,500 lba)
- urban
- rural
Diesel
Aircraft
FAA Controlled
Military
Railroad
Vessels
Non highway fuel uses
Fuel combustion in stationary
sources
Coal
Electrical power
Industrial
Domestic and commercial
Fuel oil
Domestic, industrial, and
miscellaneous
Electric power
Wood
Industrial processes
Foundries
Controlled (with afterburners)
Uncontrolled
Petroleum Refineries
Fluid catalytic crackers
Fluid coking
Moving-bed catalytic crackers
Kraft pulp mills
Carbon black
Furnace
Channel
Thermal
Steel mills
Beehive coke ovens
Basic oxygen furnaces
Sintering
Formaldehyde
Emissions,
106 tons/yr
35.6
12.8
1.7
0.9
1.4
0.8
3.0
2.8
0.2
1lD \
1 "3*^ 1
0.1
0.3 \
1.8 /
0.1
0.2C
0.5
0.1
N
1.0
0.2
3.1
2.0
0.2
0.2
2.6
0.30
0.05d
0.01
0.02
0.1
2.4
0.03
Emission factor
Based on method
described in text
Based on LTO cycle -
see text
Distillate fuel oil:
601bCO/103gal.
Distillate fuel oil: 60 Ib CO/103
gal.
gasoline: 2300 Ib CO /I O3 gal.
0.5 Ib CO/ton
3. Olb CO/ton
50.0 Ib CO/ton
84.01bCO/103bbl
1.71bCO/103bbl
45 Ib CO/ton
lOlb CO/ton of charge
250 Ib CO/ton of charge
13.7 Ib CO/bbl of fresh feed
30 Ib CO/bbl of fresh feed
3. 8 Ib CO/bbl of fresh feed
215 Ib CO/ton of product
560 Ib CO/ton of product
47 Ib CO/ton of product
4.5% of exhaust gas by volume
3.2% of exhaust gas by volume
500 ft3/ton
100 Ib CO/ton of product
4-3
-------
TABLE 4-2. (Continued) CARBON MONOXIDE ESTIMATES - 1968
Source
Solid waste combustion
Incineration
Municipal
On site
Open burning
Municipal
Industrial
Commercial, backyard, etc.
Metal conical burners
Miscellaneous combustion
Building fires
Forest fires
Coal banks
Agriculture
Emissions,
1 06 tons/yr
0.01
0.8
1.7
0.9
0.8
3.6
0.2
7.2
1.2
8.3
Emission factor
1 Ib CO/ton
27 Ib CO/ton
85 Ib CO/ton
85 Ib CO/ton
85 Ib CO/ton
260 Ib CO/ton
45 Ib CO/ton
60 Ib CO/ton
50 Ib CO/ton
60 Ib CO/ton
N = Negligible.
aGross vehicle weight.
bUnder3,OOOfeet.
cDoes not include 96,400 tons from coke plants.
"Gross estimate.
The annual CO emission estimates for
motor vehicles presented in Table 4—1 were
derived from a method of analysis that com-
bines actual on-the-road exhaust sampling
data, with simulated driving-cycle data. This
method incorporates emission rates for four
classes of vehicles (one class for passenger cars
plus light-duty trucks, and three classes for
heavy-duty trucks, including diesel trucks).
These emission rates are applied to national
vehicle activity data with consideration of
vehicle operating characteristics, including
urban-rural vehicle speed, vehicle age, and
vehicle deterioration. Three levels of controls
are represented: (1) 1967 and earlier, (2)
1968-69, and (3) 1970 and later. The past and
projected trends in CO emissions from motor
vehicles is depicted in Figure 4—2.
Exhaust emissions from motor vehicles
have been expressed in the literature either in
terms of concentrations in ppm of the con-
taminants emitted from the tailpipe or in
terms of weight in grams or pounds of con-
taminants per vehicle-mile traveled.3'9 The
latter method of expressing emissions is con-
sidered to be more representative and prefer-
able since it is consistent with data on average
traffic volume for major metropolitan areas
(vehicle-miles traveled), and it can be related
directly to engine power demands of the ve-
hicle over various types of routes.9 Exhaust
emissions expressed as ppm can be converted
to pounds per mile if the exhaust volume per
unit time and the vehicle speed are known.
The data for determination of motor ve-
hicle national emissions based on the road-
factor method are derived from recent
studies. These studies of emission data, based
on road tests of a number of vehicles under
average traffic conditions, indicate that the
average speed of a vehicle is a measure that
provides an adequate index of emissions over
a specific route pattern.s-9'10 This param-
eter, called "average route speed," appears
to reflect the engine power demand and con-
sequent pollutant emissions that are associ-
ated with the acceleration, deceleration,
cruise, and idle driving modes imposed by the
-------
Table 4-3. SUMMARY OF TOTAL EMISSIONS FROM METROPOLITAN AREAS
THROUGHOUT UNITED STATES - 1967-1968
Standard metropolitan
statistical area
N.Y. - N.J.a
Chicago"
Los Angeles0
Philadelphiad
San Francisco6
Detroitf
Cleveland^
Washington, D.C.
Boston
Pittsburgh
St. Louisn
Hartford and New Haven1
Seattle and TacomaJ
Houston and Galveston^
Milwaukee^
Minneapolis-St. Paulm
Cincinnati11
Buffalo
Denver0
Kansas City?
Providence0!
Indianapolis
Dayton3"
Louisville5
Birmingham*
Steubenvilleu
Population
15,420,000
7,500,000
7,070,000
5,550,000
4,500,000
4,090,000
3,030,000
2,720,000
2,700,000
2,520,000
2,410,000
2,290,000
2,010,000
2,000,000
,730,000
,660,000
,660,000
,320,000
,230,000
,230,000
1,200,000
1,050,000
880,000
840,000
750,000
370,000
Area, mi^
6,930
4,660
41,000
4,590
7,000
2,680
3,500
2,270
1,280
3,050
4,500
2,650
15,000
7,800
2,630
2,830
2,620
1,470
10,300
3,200
1,000
3,080
2,310
1,390
1,120
1,530
Emissions, 10^ tons/yr
sox
1,590
1,780
168
1,168
157
786
819
247
424
934
662
337
255
144
243
215
428
410
31
125
118
164
108
303
34
638
Particulate
231
586
103
241
77
241
304
35
82
387
176
56
33
156
100
46
123
140
33
60
23
78
94
128
205
155
HC
N.A.
N.A.
1,268
468
788
481
N.A.
310
87
95
326
123
165
292
83
N.A.
55
93
N.A.
233
54
74
64
46
64
N.A.
NOX
N.A.
N.A.
471
406
188
300
N.A.
135
168
267
181
134
74
213
111
N.A.
130
130
N.A.
N.A.
64
69
62
44
26
N.A.
CO
5,297
2,726
4,997
2,691
2,520
1,896
1,384
1,259
921
915
1,643
846
907
1,100
619
960
537
470
616
744
435
757
367
305
253
152
N.A. = not available.,
Includes New York S.M.S.A. less Suffolk County, Jersey City S.M.S.A., Patterson-Clifton-Passaic S.M.S.A.,
and Somerset, Middlesex and Monmouth Counties, NJ. and Fairfield County, Conn.
blncludes Chicago and Gary-Hammond-East Chicago S.M.S.A.'s.
Includes Los Angeles-Long Beach, Oxnard-Ventura, Anaheim-Santa Ana-Garden Grove, San Bernardino-
Riverside-Ontario, and San Diego S.M.S.A.'s.
Includes Philadelphia S.M.S.A., Trenton S.M.S.A. and Wilmington S.M.S.A. less Cecil County.
Includes San Francisco-Oakland S.M.S.A., San Jose S.M.S.A., Vallejo-Napa S.M.S.A. and Sonoma County.
fPlus St. Clair County.
^Includes Cleveland, Lorain-Elyria, Akron, and Canton S.M.S.A.'s.
hPlus Monroe County, 111.
^lus Hampden County, less Tolland County.
JPlus Skagit, Whatcom, Thurston, Mason, Kitsap, Jefferson and Clallam Counties.
kPlus Chambers and Waller Counties.
Includes Milwaukee S.M.S.A., Racine S.M.S.A., Kenosha S.M.S.A., and Walworth County.
mPlus Carver and Scott Counties.
nPlus Butler County.
°Plus Larimer and Weld Counties.
PPlus Leavenworth County, Ky.
^Includes Providence-Pawtucket-Warwick S.M.S.A., Falls River S.M.S.A., New Bedford S.M.S.A., and
Newport County.
rPlus Darke and Sheby Counties.
splus Oldham and Bullitt Counties.
*Less Shelby and Walker Counties.
"Includes Steubenville-Weirton and Wheeling S.M.S.A.'s.
4-5
-------
2.4%
26.8%
1.4%.
PHILADELPHIA
16.3%
1.0%
6.6%
SAN FRANCISCO
19.9%
1.7%
ST. LOUIS
2.2%
1.2%
6.7%
MINNEAPOLIS
CINCINNATI
8.4%
1.3%
BOSTON
2.4%
2.1%
5.1%
CHICAGO
4.0%
1.5%
.7%
DENVER
3.0%
0.4%
NEW YORK
0.5% m 0.5%
LOS ANGELES
[TRANSPORTATION
SOLID WASTE
INDUSTRIAL
STATIONARY
FUEL COMBUSTION
WASHINGTON, D. C.
Figure 4-1. Carbon monoxide emissions by source category for various U.S. metropolitan
areas in 1968.
4-6
-------
UJ '«
0
x „
0 c
Z £ 60
°.o
5 o
Z "~
2 £5°
K o
S «
U !/)
_l I 40
< UJ
K
O
H 30<
—
-
/
1 1
A
/ •
/ \
j \
i i
i i
—
-
v/ -
1950 1960 1970 1980 1990
YEAR
2000
Figure 4-2. Forecast of total carbon monoxide
emissions from motor vehicles.
many driving variables such as route, topog-
raphy, traffic density, climate, and altitude.
Evaluation of auto exhaust data by Rose et
al.9 indicated that an empirical relationship
between speed and CO emission level in
pounds can best be satisfied or expressed by
an inverse power function of the average
route speed:
Y = AX'b
where: Y = weight of CO emitted
X = average route speed
A, b are constants.
From this study, and also the study of
McMichael and Rose,1 ° it has been estab-
lished statistically that average route speed is
related more nearly to weight of emissions per
mile rather than to exhaust concentration.
When CO emissions from 40 randomly se-
lected test vehicles in Cincinnati and Los
Angeles were expressed in ppm and regressed
on vehicle speed, the correlation coefficient
was found to be 0.446 (0.31 to 0.58 at 95
percent confidence). For the same test, when
CO emissions were expressed as pounds of CO
per mile and regressed on vehicle speed, the
correlation coefficient was found to be 0.613
(0.49 to 0.71 at 95 percent confidence). See
Figure 4—3. Further statistical analysis with
individual vehicles showed that most of the
observed variance was due to differences
among vehicles rather than to a poor correla-
tion between CO weight emissions and route
speed (Figure 4—4).
Carbon monoxide emissions are propor-
tionately greater during the low-speed condi-
tions below 20 miles per hour because of an
increase in frequency of the acceleration, de-
celeration, and idle stages of the driving cycle
representative of heavier traffic.9 The same
relationship between mass emissions and
average route speed holds for the low air-to-
fuel (A/F) ratio operation encountered during
high-altitude driving conditions.1 °
The significance of this relationship be-
tween vehicle speed and CO emissions has not
0.60
oo 0.40
z
o
in
to
Q
X
O
z
o
2 0
0.20
0.06
I I I I
CORRELATION COEFFICIENT -
0.613
.10 —
.08-
I I
10 20 30
AVERAGE ROUTE SPEED, mph
Figure 4-3. Effect of average route speed on
carbon monoxide emission by weight.10
4-7
-------
1.0
E
\
-O
Z
o
LLI
Q 0.10
X
o
Z
o
5
O
CO
u
0.01
,r
I
I
10 20 30 60
AVERAGE ROUTE SPEED, mph
Figure 4-4. Carbon monoxide emissions by
individual vehicles, Los Angeles.9
been fully exploited. Since emissions of CO
(and, incidentally, hydrocarbons) are lower
for higher average route speeds, proper com-
munity and highway planning should rec-
ognize that higher speed movement of traffic
within the urban area can effectively reduce
the gross emissions from the exhaust of the
automobile to the lower atmosphere. For ex-
ample, an increase in average urban route
speed from 25 to 35 mph can result in a re-
duction of roughly one-fourth in the mass of
CO emitted to the atmosphere. See Figure
4—3. The implications of such emission con-
trol by means of urban planning are covered
in greater detail in AP-66, Control Techniques
for Carbon Monoxide, Nitrogen Oxide, and
Hydrocarbon Emissions from Mobile Sources.
Gasoline engines produce much more CO
per unit of power output than do diesel en-
gines primarily because of the lower A/F
ratio, and the resulting less complete com-
4-8
bustion by gasoline-powered vehicles.3'7
Carbureted engines, such as are generally
found in passenger vehicles, operate with a
deficiency of combustion air under some con-
ditions; whereas the diesel engine normally
operates with combustion air in substantial
excess of stoichiometric requirements.
b. Aircraft
The contribution from aircraft to the total
National atmospheric CO pollution burden is
at present only slightly more than 2 percent.
This contribution is expected to increase,
however, in both magnitude and in relative
percentage. A projection of the potential rise
in total CO emissions from the civil aircraft
population between 1967 and 1979 has been
estimated to be 59 percent over the base
figure of 0.84 x 109 kilograms (0.93 million
tons) calculated for 1967.11 Although at this
time the contribution of aircraft to total CO
emissions is small, atmospheric concentrations
of CO at and near airports may be creating a
localized problem.
The civil aircraft population is the source
of approximately half of the CO emissions at-
tributed to aircraft; military aircraft contri-
bute the remaining half. Civil aircraft may be
classified as: (1) general aviation aircraft (>
99 percent piston powered) and (2) commer-
cial carriers (> 85 percent turbine powered).
Commercial carriers, while constituting only
about 2 percent of the civil aircraft popula-
tion, nevertheless account for 20 percent of
the activity at civilian aircraft terminals. Civil
aircraft at terminals not controlled by the
Federal Aviation Administration represent a
negligible addition to total aircraft emissions.
In the calculation of aircraft emissions, the
general practice is to include only those emis-
sions below an arbitrarily chosen height of
3000 to 3500 feet. The pollution emitted at
higher altitudes cannot be considered in the
same light as that emitted at or near ground
level. The emission factors for aircraft pre-
sented in this chapter were estimated from
the results of a study11 and report to Con-
gress and were based on actual sampling data.
-------
Emissions at evaluations below 3000 feet
were estimated on the basis of a five-mode
landing-take-off (LTD) cycle, which included
approach, landing, taxiing, takeoff, and climb-
out. Though only about 20 percent of the
total aircraft fuel is consumed during the LTO
cycle, it accounts for approximately 83 per-
cent of the total CO emitted during an entire
trip (LTO cycle plus cruise mode).11
Emission factors were derived and ex-
pressed as weight of CO emitted per unit time
by a particular class of aircraft operating in a
particular mode. Knowledge of the time-
frequency distribution by class and mode
allowed calculation of the figure for total air-
craft CO emissions presented in Tables 4-1
and 4-2.
c. Other Non-Highway Mobile Sources
According to the Bureau of Roads and the
Bureau of Mines, the total non-highway use of
motor fuels, excluding aircraft, amounted to
8.20 billion gallons for 1966.12'14 This total
represents the consumption of gasoline and
diesel fuel by trains, ships, agricultural ma-
chinery, commercial equipment, and con-
struction machinery. Trains and ships also
consumed distillate fuel oil, residual fuel oil,
and coal.
The emissions of CO were calculated using
emission factors of 2,300 pounds of CO per
1000 gallons of gasoline and 60 pounds of CO
per 1000 gallons of the other liquid fuels. The
emission estimates are presented in Tables
4-1 and 4-2.
2. Carbon Monoxide from Combustion
for Power and Heat
The combustion of coal, fuel oil, natural
gas, and wood to produce power and heat also
produces a small, but significant, quantity of
CO when viewed on a national scale. On a
smaller scale, other fuels such as bottled gas
and kerosine are used for miscellaneous heat-
ing purposes. By far the largest percentage of
CO emissions in each fuel category may be
attributed to residential, commercial, institu-
tional, and light industrial burning. This is
brought about by the relatively inefficient
nature of combustion associated with these
facilities.
The following categories were included in
the estimation of the quantity of CO from
coal, gas, and oil combustion presented in
Table 4— 1: electric power utilities, coke
plants, steel and rolling mills, cement mills, oil
companies, other manufacturing and mining
industries, military, residential, commercial,
institutional, and light industrial. Emission
factors are available for all categories but coke
plants.
Coal and wood combustion account for the
majority of CO emissions in the stationary
combustion source category. Approximately
486 million tons of lignite and bituminous
coal and 11.4 million tons of anthracite coal
(excluding trains and ships) were consumed in
the United States in 1966.13 Electric power
utilities and industries are the largest con-
sumers of coal, but account for only about 25
percent of the emissions from this fuel. Total
wood consumption by user category is not
available. Total energy from wood combus-
tion, however, was estimated to be 800 x
1012 Btu for 1966. Assuming 9,000 Btu per
pound of wood, nearly 5.5 x 10^ tons of
wood were consumed resulting in an emission
of approximately 1 million tons of CO as indi-
cated in Table 4—1.
Approximately 568 million barrels of distil-
late fuel oil and 537 million barrels of residual
fuel oil were consumed in stationary fuel
combustion sources in 1966.12 More than 60
percent of the total fuel oil is consumed for
space-heating purposes in residential, com-
mercial, institutional, and light industrial
sources.
Total gas consumption, of which 99 per-
cent consists of natural gas, exceeded 15,000
billion cubic feet in 1966.15 Electrical power
utilities consumed about 17 percent of the
total with residential, commercial, institu-
tional, military, and industrial sources ac-
counting for the remainder.
4-9
-------
3. Industrial Processes Producing
Carbon Monoxide
Industrial processes emit varying quantities
of CO into the atmosphere. The four largest
sources of this pollutant are petroleum re-
fineries, iron foundries, kraft pulp mills, and
sintering plants. Other sources for which emis-
sion estimates were made are steel mills, lamp-
black plants, and formaldehyde manufac-
turers. Emission factors for these processes are
based on analysis of sampling data; however,
the lack of published data from other sources
on production, types of equipment, and con-
trols, as well as emission factors, make it im-
possible to include estimates of emissions for
them. Some other sources of CO include
ammonia and methanol reforming, synthesis
gas manufacture, organic chemical manufac-
ture (acids, esters, ketones, and aldehydes),
reactive metals manufacture, and nonferrous
secondary smelting.
The major source of CO in an iron foundry
is the cupola. A questionnaire survey of the
1,450 foundries located in the United States
indicates that 3.24 million tons of iron was
charged to cupolas in 1966, with approxi-
mately 10 to 20 percent of this production
subject to 90 percent afterburner control.
The major sources of CO in petroleum re-
fining operations are the catalytic cracking
units. The emissions of CO from roughly 75
percent of these units are nearly 100 percent
controlled by waste heat boilers.
The major sources of CO in kraft paper
mills are the lime kilns and the kraft recovery
furnaces. The 23.6 million tons of pulp
produced in 1966 from these sources emitted
CO that was not subject to control.
The sintering of blast furnace feed is
another major source of CO; 1968 production
of both sinter and pellets is estimated to total
108 million tons.
The emissions from these major industrial
sources were calculated as shown in Table
4-2.
4. Solid Waste Combustion
The total annual solid-waste production in
the United States has been estimated to be
4-10
about 357 million tons. About half of this
solid waste is disposed of through incineration
and open burning. This combustion results in
the production of about 8 million tons of CO.
An estimate of the per-capita solid-waste
generation rate was obtained from the results
of a study by the National Center for Urban
and Industrial Health on collected solid
wastes1 6 and from estimates by the National
Air Pollution Control Administration on un-
collected solid wastes. This estimate (10
Ib/day per person), population figures, and in-
formation on the proportions of the various
solid-waste disposal methods allowed estima-
tion of the national CO emissions from this
category.
5. Miscellaneous Combustion
The miscellaneous combustion category in-
cludes emission estimates from both un-
controlled and controlled forest fires, from
agricultural waste burning, from structural
fires, and from coal-refuse bank fires. These
totals, however, do not include the burning of
forest and crop residues.
The United States Forest Service estimates
that over 4,570,000 acres of forest were de-
stroyed by wild ("unprescribed") fires during
1966.17 In addition, there were over 600,000
acres of controlled ("prescribed") burning in
National parks. Prescribed burning by indus-
try and private interest accounted for
2,920,000 acres. An average of 32 tons of
wood per acre was burned in wild fires, and
22 tons per acre, in controlled fires. The total
emission estimates presented in Tables 4-1
and 4-2 were calculated by applying an emis-
sion factor of 60 pounds per ton of burned
material for agricultural open burning. In ad-
dition, 550 million tons of agricultural waste
is generated each year.16 It is estimated that
half of this agricultural waste is burned in
the open. Using an estimated emission factor
of 60 pounds of CO per ton for open burning,
the estimate for this source was calculated.
The National Fire Protection Association
reports that more than a million buildings
were attacked by fire in 1966 with a 20 to 30
-------
percent extent of destruction. The CO emis-
sions from structural fires were estimated
using these assumptions and an average emis-
sion factor for wood burning of 45 pounds
per ton.
The Bureau of Mines estimates that 19 bil-
lion cubic feet of burning coal refuse piles
existed in the United States in 1966, that the
density of these coal piles averages 100
pounds per cubic foot, and that, on the
average, one of these coal banks will burn for
20 years.' 8 With these assumptions, the emis-
sions from this source were estimated using an
emission factor for coal combustion of 50
pounds of CO per ton of coal burned.
D. PROJECTIONS OF CARBON
MONOXIDE EMISSION LEVELS
Two factors must be considered in project-
ing future CO emission levels. The first is the
potential increases caused by population
growth—more motor vehicles and aircraft, ex-
pansion of industry, and the increased use of
fuel combustion for power and heat to be ex-
pected in the coming decades. The second,
and opposing, factor is the application of
more effective control technology. For the
major national CO emitter, motor vehicles, no
further increase in the magnitude of CO emis-
sions would be expected before 2000 because
of present and anticipated (1970) CO control
measures required by existing Federal Stat-
utes. Future trends are depicted in Figure
4-2.
No projections have been made for CO
emissions from stationary sources because of
lack of published data. The national magni-
tude of CO emissions from these sources is
expected to increase, although it is recognized
that changes in fuels, industrial processes, and
methods of solid waste disposal may result in
decreases in CO emissions from specific
sources.
E. SUMMARY
Annual carbon monoxide emissions from
major sources in the United States are esti-
mated to be 92 x 10° kilograms (102 million
tons) for the year 1968. The largest single
source was the gasoline-powered motor ve-
hicle, which accounted for 54 x 10° kilo-
grams (59 million tons), or over 58 percent of
the total. Internal combustion engine sources
used in aircraft, non-highway use, trains,
ships, and diesel-powered motor vehicles ac-
counted for another 5 percent of the total.
Other major sources included fuel combustion
in stationary sources, industrial processes,
solid waste combustion, and forest fires.
Carbon monoxide emission totals were
found to differ among different regions of the
United States, estimates ranged up to about 5
x 10^ kilograms (5 million tons) per year in
New York and Los Angeles. In all but two of
26 cities surveyed, the CO emissions were the
largest component of the total tonnage of pol-
lutants emitted to the atmosphere. The major
source of CO emissions in all of the regions
studied was the motor vehicle.
F. REFERENCES
1, National Air Pollution Control Administration,
Reference Book of Nationwide Emissions. U.S.
DHEW, PHS, CPEHS, NAPCA. Durham, N. C.
2. Ozolins, G. and R. Smith. A Rapid Survey Tech-
nique for Estimating Community Air Pollution
Emissions. National Air Pollution Control Ad-
ministration. Cincinnati, Ohio. PHS Publication
Number 999-AP-29. 1967. 77 p.
3. Elliott, M. A., G. J. Nebel, and F. G. Rounds.
The Composition of Exhaust Gases from Diesel,
Gasoline and Propane Powered Motor Coaches. J.
Air Pollution Control Assoc. 5(2): 103-108,
August 1955.
4. Hagen, D. F. and G. W. Holiday. The Effects of
Engine Operating and Design Variables on Ex-
haust Emissions (SAE Paper No. 486C). In:
Vehicle Emissions, Vol. 6. New York, Society of
Automotive Engineers, Inc., 1964. p. 206-223.
5. Rose, A. H., Jr. Summary Report of Vehicular
Emissions and Their Control. Paper presented at
the St. Louis Section Meeting of the Society of
Automotive Engineers. St. Louis, Mo. January
1969.
6. Caplan, J. D. Causes and Control of Automotive
Emissions. Presented at the Institution of Me-
chanical Engineers. London. April 9, 1963.
7. Motor Vehicle Pollution in California. California
Dept. of Public Health. Los Angeles. January
1967.
8. Chandler, J. M. et al. Engine Variables and Their
Effects on Exhaust Gas Composition. J. Air Pol-
lution Control Assoc. 5(2):65-70, August 1955.
4-11
-------
9. Rose, A. H. et al. Comparison of Auto Exhaust
Emissions in Two Major Cities. J. Air Pollution
Control Assoc. 75:362-366, August 1965.
10. McMichael, W. F. and A. H. Rose, Jr. A Compari-
son of Automotive Emissions in Cities of Low
and High Altitudes. Presented at the Annual
Meeting, Air Pollution Control Association.
Toronto. June 1965.
11. Nature and Control of Aircraft Engine Exhaust
Emissions. Report of the Secretary of Health,
Education, and Welfare to the United States Con-
gress. Pursuant to Public Law 90-148, the Air
Quality Act of 1967. U.S. Dept. of Health, Ed-
ucation, and Welfare. Washington, D.C. U.S.
Government Printing Office. Senate Document
No. 91-9. 91st. Congress. 1st Session. March 4,
1969. 32 p.
12. Shipments of Fuel Oil and Kerosene in 1966.
Mineral Industry Surveys; Fuel Oil Shipments,
Annual. Bureau of Mines. Washington, D.C.
August 9, 1967. 16 p.
13. Production of Bituminous Coal and Lignite.
Weekly Coal Report. Bureau of Mines. Washing-
ton, D.C. Report Number 2609. September 15,
1967.21 p.
14. Highway Statistics 1966. Bureau of Public
Roads. Washington, D.C. 1968. 186 p.
15. 1968 Gas Facts - Statistical Record of the Gas
Utility Industry, 1967 Data. New York, Ameri-
can Gas Association, Inc., 1968.
16. Black, R. J. et. al. An Interim Report: 1968
National Survey of Community Solid Waste
Practices. Bureau of Solid Wastes Management.
Rockville, Md. October 24, 1968. 53 p.
17. 1966 Forest Fire Statistics. U. S. Dept. of Agri-
culture, Forest Service. Washington, D.C.
18. Stahl, R. W. Survey of Burning Coal Mine Refuse
Banks. Bureau of Mines. Washington, D.C. Infor-
mation Circular Number 8209. 1964. 39 p.
4-12
-------
CHAPTER 5.
MEASUREMENT OF CARBON MONOXIDE
CONCENTRATIONS IN AMBIENT AIR
A. INTRODUCTION
Because of the need to measure the wide
range of CO concentrations found in com-
munity air (from less than 1 to about 150
mg/m^), numerous measurement techniques
have been developed. Standardization of CO
in air samples for measurement, and subse-
quent measurement by available aerometric
techniques are discussed in this chapter. Gas
samples may be standardized by volumetric,
gravimetric, and chemical techniques. The
methods available for continuous measure-
ment of CO include: (1) nondispersive in-
frared (NDIR) analysis, (2) electrochemical
analysis, (3) mercury vapor analysis, (4) gas
chromatography, and (5) catalytic and elec-
trolytic analysis. The methods available for
spot or integrated measurements include: (1)
nondispersive infrared analysis, (2) infrared
spectrophotometric analysis, (3) gas chroma-
tographic analysis, and (4) colorimetric an-
alysis.
Several tentative methods for the determi-
nation of CO in ambient air have been pre-
pared for collaborative testing and evaluation
as possible standards by the Intersociety Com-
mittee on Manual of Methods of Air Sampling
and Analysis. Hopefully, one or more of these
methods will qualify as a standard method
against which all instruments and methods
may be calibrated.1
B.
1.
PREPARATION OF CARBON
MONOXIDE GAS STANDARDS
Volumetric Gas Dilution
Techniques
Accurately prepared CO gas standards must
be available for the calibration of methods
and measuring instruments before CO can be
quantified. Volumetric gas dilution is the
technique used most frequently for the prep-
aration of standards. If a large quantity of
standard gas is needed, the dilution may be
made in pressurized tanks.2'3 Care should be
exercised to assure accuracy of the standard
because CO in pressurized tanks may be un-
stable at concentrations of less than 1 milli-
gram per cubic meter (1 ppm).
A known volume of CO is placed in an
evacuated tank of known volume, and the
tank is subsequently filled to a known pres-
sure with CO-free nitrogen or helium. The
concentration of CO in the tank may then be
calculated. Standard samples in 5- to 100-liter
volumes also may be prepared in plastic
bags.4 The diluent gas is metered into an
evacuated plastic bag with a suitable device;
and as it flows into the bag, a measured
volume of pure CO is injected by syringe into
the line connecting the metering device to the
bag. The concentration is calculated from the
total volumes of diluent gas and CO in the
bag.
It is important in these operations to verify
that the diluting gas is free of CO. Some in-
vestigators suggest that pure helium, which is
reliably free of CO, is preferable to nitrogen
as a diluent. A less expensive method is to use
helium periodically as a true "zero" gas to
estimate the CO content in the nitrogen
diluent. A correction factor is then used to
account for the CO content in the nitrogen.
2. Gravimetric Methods for
Standardizing Carbon Monoxide
Gas Mixtures
Gravimetric methods are not used routinely
in air pollution studies to measure CO because
5-1
-------
relatively large samples are needed to quantify
CO concentrations. These methods are useful,
however, for checking CO standards. McCul-
lough et al.5 made use of the reaction:
CO (gas) +HgO (solid, red)(175°'200°,P
Hg(gas) + C02 (gas).
During the passage of the gas sample, the red
mercuric oxide is reduced and loses weight.
This weight loss and the measured volume of
the sample are used to calculate the concen-
tration of CO present in the standard gas mix-
ture.
Salsbury et al.6 used a method in which the
gas containing CO is drawn over Hopcalite at
195°C and the carbon dioxide formed is
absorbed in tubes containing Ascarite. Gas
volumes are determined using a flowmeter and
a stopwatch. From the weight of the CO2
absorbed in the tubes, the CO concentration
is calculated. This method is accurate to
about 2 percent for CO concentrations of
from 25 to 1000 milligrams per cubic meter
(22 to 870 ppm).
Lysyj et al.7 oxidized CO to CO2 with de-
composed silver permanganate (AgMnO^.) as a
catalyst and weighed the CO2 absorbed in an
As,carite tube.
3. Chemical Assay of Carbon
Monoxide Gas Standards
The reduction of iodine pentoxide may be
used to measure CO in standard gas mixtures.
Adams and Simmons8 have given a detailed
discussion of the method. The analysis is
based on the reaction:
5 CO + I2O5 -» 5 CO2 + I2.
When the gas mixture containing CO is passed
over heated I2O5, iodine is liberated. It is
then collected and titrated with standard
sodium thiosulfate.
C. MEASURING CARBON MONOXIDE
IN ATMOSPHERE
1. Continuous Measurement of
Carbon Monoxide
a.
5-2
Definitions of Terms Describing
Instrument Performance
Definitions of some terms commonly used
to describe instrument performance are given
below; in this document these terms will be
used as defined throughout this chapter.
Sensitivity. The smallest change in pollu-
tant concentration that can be detected.
Minimum detectable concentration. The
sensitivity as the pollutant concentration ap-
proaches zero.
Response time. The amount of time taken
by an instrument from the start of a change in
input before the instrument output reaches a
specified percentage of the ultimate change.
(The specified percentage is usually 90 or 95).
The response time is a measure of the mini-
mum averaging time necessary to achieve valid
output data.
Lag time. The time between the start of an
input signal and the observed start of the out-
put response corresponding to that signal. The
lag time is a measure of the delay between
input sample and output data, and is always
less than or equal to the response time.
Accuracy. The degree of agreement of the
true value with the indicated value or values.
True value. The number that is completely
consistent with the (known) value and defini-
tion of the primary standard used.
b. Nondispersive Infrared Analyzers
Nondispersive infrared (NDIR) analyzers
are the most commonly used continuous,
automated devices for determining atmos-
pheric CO and are generally accepted as being
the most reliable reference method for the
calibration of other instruments. An NDIR
analyzer operates on the principle that CO has
a sufficiently characteristic infrared absorp-
tion spectrum that the absorption of infrared
radiation by the CO molecule can be used as a
measure of CO concentration in the presence
of other gases. Although the size, shape, sensi-
tivity, and range of these instruments vary
with manufacturer, 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. The detector senses pressure
changes on either side of a diaphragm sep-
arating portions of gases being irradiated
through the sample cell or the reference cell
of the instrument. These pressure changes are
converted to electrical signals corresponding
to the difference between radiation received
from the sample and reference cells. The
signal is amplified and rectified, and then read
on a meter or recorder calibrated to yield CO
concentration.
Most commercially available instruments
function on the double-beam principle, oper-
ate at atmospheric pressure, and are able to
detect minimum CO concentrations of about
0.6 to 1.2 milligrams per cubic meter (0.5 to
1.0 ppm). The sensitivity of NDIR instru-
ments and the minimum concentrations they
can detect are proportional to the length of
the cells, electronic amplification, and oper-
ating pressures. Measuring ranges usually ex-
tend from 1 to 58 mg/m3 (1 to 50 ppm) CO
or from 1 to 115 mg/m3 (1 to 100 ppm) CO.
Newer NDIR instruments, however, may be
operated at from 1 to 29 mg/m3 (1 to 25
ppm) CO at atmospheric pressure and with
cell path lengths of less than 0.5 meter.
NDIR analyzer response times are deter-
mined by the physical dimensions of the
system, the flow rate of the sample, and the
response time of the meter or recorder. Re-
sponse times may range from less than 1 to 5
minutes.
Carbon dioxide and water vapor interfere
in the determination of CO by NDIR tech-
niques. Filter cells are used to minimize these
interferences. They may be placed in front of
the sample cell or in front of both sample and
reference cells. Filter cells, filled with carbon
dioxide (CO2) and water vapor, absorb radia-
tion at interfering wavelengths so that normal
atmospheric concentrations of CO2 and
water vapor in the sample have minimal effect
on the radiation reaching the detector.9
Optical filters are also used successfully to
limit the infrared wavelength and bandwidth
to a range in which CO2 and water vapor are
transparent and thus invisible to the instru-
ment.
Other techniques may be used to minimize
or prevent CO2 interference. Ascarite-filled
tubes remove CO2 from the entering gas
stream; other systems add nominal quantities
of CO2 (300 to 400 ppm) to the zero and
span gases used to calibrate the NDIR instru-
ment.
Filter cells reduce water vapor interference;
however, they do not adequately cope with
the high absolute humidities frequently en-
countered in atmospheric monitoring. Figure
5-1 shows the effect of water vapor on a
_ 5 10 15 20 25 30
H20 VAPOR PRESSURE, mm Hg
Figure 5-1. Typical nondispersive infrared
analyzer response to water vapor.10
typical NDIR analyzer un compensated for
water vapor interference.1 ° Air streams may
be dried by using dehydrating agents such as
silica gel, anhydrous calcium sulfate, magnes-
ium perchlorate, or combinations of these
media.11'12 Jacobs et al.13 found, however,
anhydrous calcium sulfate to be unsatis-
factory for the removal of water vapor from
the gas stream. Satisfactory results were ob-
tained by saturating the incoming air with
water at a constant temperature, thus elimina-
ting water as a variable. Some commercially
available instrument systems use this techni-
que to eliminate water vapor interference.
Others reduce water vapor interference by pas-
sing the air sample through a refrigerator in
front of the analytical system to condense
moisture from the air. This system, however,
cannot regulate the absolute humidity in the
air stream undergoing analysis when the dew
5-3
-------
point of the sample air is lower than the re-
frigerator temperature (as is the case in cold
weather or with pressurized calibration
gases). It should be realized that most meth-
ods of reducing CO2 and water vapor inter-
ferences also tend to reduce instrument sensi-
tivity or increase instrument response time, or
both.
NDIR systems have several advantages.
They are not sensitive to flow rate, they re-
quire no wet chemicals, they are reasonably
independent of ambient air temperature
changes, they are sensitive over wide concen-
tration ranges, and they have short response
times. Further, NDIR systems may be oper-
ated by nontechnical personnel. 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 manufac-
ture. Such instruments also have automatic
zeroing, spanning, and recalibrating capabil-
ity; they may also be obtained with essential-
ly linear outputs. Features such as these
should be considered when multiple-station
networks are established.
c. Electrochemical Analyzers
(1). Galvanic analyzer. Galvanic cells em-
ployed in the manner described by
Hersch14'15 can be used to measure atmos-
pheric CO continuously. When an air stream
containing CO is passed into a chamber
packed with ^05 and heated to 150°C, the
following reaction takes place:
(150°C)
SCO + I2O5 ^ 5CO2 + 12-
The liberated iodine is absorbed by an electro-
lyte and transferred to the cathode of a
galvanic cell. At the cathode, the iodine is re-
duced, and the resulting current is measured
by a galvanometer. Instruments using this de-
tection system have been used successfully to
measure CO levels in traffic along freeways.1 6
Mercaptans, hydrogen sulfide, hydrogen,
olefins, acetylenes, and water vapor interfere.
5-4
Water may be removed by sampling through a
drying column; hydrogen, hydrogen sulfide,
acetylene, and olefin interferences can be
minimized by sampling through an absorption
tube containing mercuric sulfate (HgSO4) on
silica gel.
(2). Coulometric analyzer. A coulometric
method employing a modified Hersch-type
cell has been used to measure CO in ambient
air on a continuous basis.12 The iodine
pentoxide (1205) reaction with CO liberates
iodine, which is then passed into a Ditte cell,
and the current generated is measured by an
electrometer-recorder combination. Interfer-
ences are the same as those discussed above
for the galvanic analyzer.1 7>1 8
This technique may be used for a minimum
detectable concentration of 1 milligram per
cubic meter (1 ppm) with good reproduci-
bility and accuracy if flow rates and tempera-
tures are well controlled. This method
requires careful column preparation and use
of filters to remove interferences. Its rela-
tively slow response time may be an added
disadvantage in some work.
d. Mercury Vapor Analyzer
A continuous CO analyzer using the reac-
tion of CO with hot mercuric oxide and
photometric determination of the mercury
vapor produced has been developed and
used.11 The reaction involved is:
CO + HgO (s) (210°9 C02 + Hg(g).
Oxygenated hydrocarbons and olefins react
quantitatively and, therefore, present a major
interference; however, these are normally
present in the ambient atmosphere in low
concentrations relative to CO. Free hydrogen
also interferes with the technique, but this
interference is not serious because very little
free hydrogen is present in the air. The effect
of ozone is not reported, but ozone, too, is
normally present in the atmosphere in very
low concentrations relative to CO.
The mercury vapor instrument has a
response time similar to that of the NDIR
-------
analyzer; but because of interferences and
some electronic instability, it does not appear
to be suitable for routine urban atmospheric
monitoring. The instrument is, however, a
useful, portable, continuous analyzer with a
capability for analyzing concentrations of
from 0.029 to 11.5 milligrams of CO per
cubic meter (0.025 to 10.0 ppm). Changes of
0.002 mg/m3 (0.002 ppm) are detectable. For
this reason it has found application in deter-
mining geophysical "background" CO levels
throughout the world.
e. Gas Chromatographic Analyzer
A prototype automated gas chromato-
graphic system has been developed to measure
both CO and methane.19 A gas sampling
valve, a back flush valve, a precolumn, a
molecular sieve column, a catalytic reactor,
and a flame ionization detector comprise the
system. The precolumn prevents CO2, water,
and hydrocarbons other than methane from
reaching the molecular sieve. The catalytic
reactor quantitatively converts CO to meth-
ane, which is then measured by the flame
ionization detector. The system is designed
for semicontinuous operation with the
capability of performing one analysis about
every 5 minutes. It has a linear output for
both CO and methane, and has a wide operat-
ing range suggesting its use in both heavily
polluted areas and relatively clean locations.
Simultaneous CO and methane concentrations
of from 0.1 to 1,000 ppm may be measured
with this instrument. Its semicontinuous
characteristics suggest its use in special sur-
veys and field studies rather than for routine
air monitoring. The fact that the instrument
must be operated by technically trained per-
sonnel may be considered a possible disad-
vantage.
/ Ca taly tic A nalysis
Carbon monoxide may be oxidized catalyt-
ically to CO2 using Hopcalite; the resulting
temperature rise is recorded continuously and
is used to indicate CO concentrations.20'21
These systems are widely used in enclosed
spaces; their applicability for ambient air
monitoring is limited because they function
best at high ambient concentrations.
2. Intermittent Analysis
a. Collection of Spot or In tegra ted Samples
Intermittent samples may be collected in
the field and later analyzed in the laboratory.
A detailed outline of this technique has been
given by Mueller.22 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. Techniques for
analyzing intermittent samples are described
below.
b. Nondispersive Infrared A nalysis
Field NDIR continuous monitoring ana-
lyzers discussed previously can be used for
laboratory analysis of intermittent samples.
NDIR instruments are designed by some
manufacturers primarily for use in the labora-
tory and must be modified for continuous
ambient air monitoring in the field.
c. Infrared Spectrophotometric Analysis
Carbon monoxide may be measured by its
infrared absorption at 4.6 microns. Other
gases may absorb at 4.6 microns, but they can
be differentiated from CO by examining the
complete spectrum from 2 to 15 microns. The
sensitivity and range of the technique depends
on the sophistication of the instrument used.
A minimum detectable concentration of 2.9
milligrams per cubic meter (2.5 ppm) CO has
been obtained by instruments using scale
expansion and a 1-meter path-length cell.23 It
can be expected that a similar infrared
spectrophotometer equipped with a 10-meter
cell and ordinate scale expansion would have
a 0.3-milligram-per-cubic-meter (0.3 ppm) CO
detection capability. Water vapor and CO2
must be removed from the sample before the
infrared scan can be made; in most applica-
tions magnesium perchlorate and Ascarite
5-5
-------
are used to remove interfering substances. The
technique is specific and accurate, but re-
quires expensive, nonportable equipment.
d. Gas Chromatographic Analysis
After reduction of CO over a reduced
nickel catalyst, a gas chromatograph equipped
with a flame ionization detector, discussed
earlier, becomes a satisfactory tool for deter-
mining low levels of CO.10'1*'24'26 One
mole of CO produces 1 mole of methane.
Since methane may be detected at concen-
trations of about 0.01 ppm, it is possible to
detect such a concentration of CO.27 The
technique does not suffer from interferences
because the measurement is made on a meth-
ane peak derived from a separated CO peak.
Operating temperatures and other parameters
must be controlled, however, before reliable
results can be obtained.
e. Colorimetric Analysis
(1). Colored silver sol method. Carbon
monoxide reacts in an alkaline solution with
the silver salt of p-sulfamoylbenzoate to form
a colored silver sol. Concentrations of from
12 to 23,000 milligrams per cubic meter (10
to 20,000 ppm) CO may be measured by this
method.28'32 The procedure has been modi-
fied to determine CO concentrations in incin-
erator effluents.17 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 sul-
fate on silica gel. Carbon monoxide concen-
trations of from 6 to 20,700 milligrams per
cubic meter (5 to 18,000 ppm) may be
measured with an accuracy of 90 to 100 per-
cent of the true value.
(2). National Bureau of Standards colori-
metric indicating gel. A National Bureau of
Standards (NBS) colorimetric indicating gel
(incorporating palladium and molybdenum
salts) has been devised to measure CO in the
laboratory and in the field.33-34 The labora-
tory method involves colorimetric comparison
with freshly prepared indicating gels exposed
to known concentrations to CO. The method
has an accuracy range of from 5 to 10 percent
of the amount of CO involved, and the
minimum detectable concentration is 0.1
milligram per cubic meter (0.1 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.
(3). Length-of-stain indicator tube. An in-
dicator tube method using potassium pallado-
sulfite is a commonly used manual meth-
od.35 Carbon monoxide reacts with the con-
tents of the tube and produces a discolora-
tion. The length of discoloration is an expo-
nential function of the CO concentration.
This method and other indicator tube manual
methods are estimated to be accurate to with-
in ± 25 percent of the amount present, par-
ticularly at CO concentrations of about 115
milligrams per cubic meter (100 ppm). Such
indicator tube manual methods have been
used frequently in air pollution studies.
Ramsey3 6 used the technique to measure CO
at traffic intersections, and Brice and
Roesler37 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 physiochemical
monitoring 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.
D. SUMMARY
Because CO levels exist over such a wide
concentration range, the use of a variety of
chemical and physical procedures may be
required to evaluate atmospheric concentra-
tions fully and accurately. The accuracy of
any aerometric method used can be no better
than the standards used to calibrate the
instrument used. When pure CO and CO-free
nitrogen are available, volumetric gas dilution
techniques are satisfactory ways to prepare
standard gases. Gas mixtures of doubtful or
5-6
-------
unknown concentrations of CO may be
assayed by the gravimetric and chemical
(iodine pentoxide) standardization methods,
which are time-consuming, but accurate.
The continuous measurement of atmos-
pheric CO can be accomplished by using a
variety of techniques. The most commonly
used device is the nondispersive infrared
(NDIR) analyzer, which is reasonably sensi-
tive, but subject to a number of interferences.
These interferences may be removed or mini-
mized by proper treatment of the air stream.
New NDIR analyzers have the capability of
measuring CO in the range of from 1 to 29
milligrams per cubic meter (1 to 25 ppm), and
they may be equipped with automatic zero-
ing, spanning, and calibrating equipment; also,
they are linear in output. All NDIR systems
have the advantages of being insensitive to
flow rates, requiring no wet chemicals, and
being reasonably independent of ambient air
temperature changes if the instrument is prop-
erly thermostatted. The NDIR analyzer is
generally accepted as being the most reliable
reference method for the calibration of other
instruments.
Continuous CO monitoring instruments
based on galvanic and coulometric principles
have not been used extensively in field opera-
tions. They are flow- and temperature-depend-
ent, and require the use of filters to remove
multiple interferences.
The mercury vapor analyzer, which
depends on the liberation of mercury vapor.
when CO is passed over hot mercuric oxide,
has been used as a portable, continuous moni-
toring analyzer with a special capability for
measuring low CO concentrations (0.29 milli-
gram per cubic meter, or 0.25 ppm). The
instrument does not appear to be suitable for
routine CO monitoring of urban atmospheres.
The automated gas chromatographic sys-
tem is semicontinuous in operation, but has
the advantage of measuring both CO and
methane. Concentrations of from 0.1 to
1,150 milligrams per cubic meter (0.1 to 1000
ppm) may be determined, and instrument
output for both gases is linear over the range
mentioned. Instruments of this kind may be
available soon, and it appears this technique
will be useful for measuring CO in heavily
polluted areas as well as at remote, relatively
clean locations.
CO monitoring systems based on catalytic
conversion principles are used widely in
enclosed spaces, but their applicability for
ambient air monitoring is limited.
Colorimetric (colored silver sols) methods
are not recommended for monitoring ambient
air. The approach may be useful, however, for
measuring CO in stack effluents. Colorimetric
techniques and length-of-stain discoloration
methods are recommended for use only when
the above-mentioned physiochemical 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.
E. REFERENCES
1. Analytical Methods of the Intersociety Commit-
tee on Methods for Ambient Air Sampling and
Analysis. Health Lab. Sci., 7:1, in press, 1970.
2. Feldstein, M. Methods for the Determination of
Carbon Monoxide. In: Progress in Chemical
Toxicology, Stolman, A. (ed.), Vol, 3, New York,
Academic Press, 1967. p. 99-119.
3. Kuley, C. J. Gas Chromatographic Analysis of Cj
to C4 Hydrocarbons in the Parts Per Million
Range in Air and Vaporized Liquid Oxygen.
Anal. Chem. 55(10): 1472-1475, September
1963.
4. Schuette, F. J. Plastic Bags for Collection of Gas
Samples. Atmos. Environ. 7(4):515-519, July
1967.
5. McCullough, J. D., R. A. Crane, and A. O. Beck-
man. Determination of CO in Air by Use of Red
Mercuric Oxide. Anal. Chem. 79:999-1002,
December 1947.
6. Salsburg, J. M., J. W. Cole, and J. H. Yoe. Deter-
mination of Carbon Monoxide—A Microgravi-
metric Method. Anal. Chem. 79:66-68, January
1947.
7. Lysyj, I., J. E. Zarembo, and A. Hanley. Rapid
Method for Determination of Small Amounts of
5-7
-------
Carbon Monoxide in Gas Mixtures. Anal. Chem.
31:902-904, May 1959.
8. Adams, E. G. and N. T. Simmons. The Deter-
mination of Carbon Monoxide by Means of
Iodine Pentoxide. J. Appl. Chem. (London).
KSuppl. 0:20-40, 1951.
9. Information supplied by State of California.
Dept. of Public Health. August 1968.
10. Moore, H. A Critical Evaluation of the Analysis
of Carbon Monoxide with Nondispersive Infrared
(NDIR). Presented at the 9th Conference on
Methods in Air Pollution and Industrial Hygiene
Studies. Pasadena. February 7-9, 1968.
11. Robbins, R. C., K. M. Borg, and E. Robinson.
Carbon Monoxide in the Atmosphere. J. Air
Pollution Control Assoc. 75:106-110, February
1968.
12. Dubois, L., A. Zdrojewski, and J. R. Monkman.
The Analysis of Carbon Monozide in Urban Air
at the PPM Level, and the Normal Carbon Mon-
oxide Value. J. Air Pollution Control Assoc.
16:135-139, March 1966.
13. Jacobs, M. B., M. M. Braverman, and S. Hoch-
heiser. Continuous Determination of Carbon
Monoxide and Hydrocarbons in Air by a Modi-
fied Infrared Analyzer. J. Air Pollution Control
Assoc. 9(2): 110-114, August 1959.
14. Hersch, P. Galvanic Analysis. In: Advances in
Analytical Chemistry and Instrumentation,
Reilley, C. A. (ed.), Vol 3. New York, Inter-
science Publishers, 1964. p. 183-249.
15. Hersch, P. Process for Measuring the Carbon
Monoxide Content of a Gas Stream (Beckman
Instruments, Inc., U.S. Patent No. 3, 258, 411).
Official Gazette U.S. Patent Office. 827(4):
1276-1277, June 1966.
16. Haagen-Smit, A. J. Carbon Monoxide Levels in
City Driving. Arch. Environ. Health. 72:548-551,
May 1966.
17. Levaggi, D. A. and M. Feldstein. The Colorimet-
ric Determination of Low Concentrations of
Carbon Monoxide. Amer. Ind. Hyg. Assoc. J.
25:64-66, January-February 1964.
18. Feldstein, M. The Colorimetric Determination of
Blood and Breath Carbon Monoxide. J. Forensic
SciJ0:35-42, January 1965.
19. Stevens, R. K., A. E. O'Keefe, and G. C. Ortman.
A Gas Chromatographic Approach to the Semi-
Continuous Monitoring of Atmospheric Carbon
Monoxide and Methane. Presented at the 156th
National Meeting of the American Chemical
Society. Atlantic City. September 1968.
20. Linderholm. H. and T. Sjostrand. Determination
of Carbon Monoxide in Small Gas Volumes. Acta
Physiol. Scand. (Stockholm). J 7(2-3): 240-250,
September 26, 1956.
5-8
21. Lukaci, J. and J. Chriastel. Determination of
Carbon Monoxide in Air. Anal. Abstr. 6:751,
February 1959.
22. Mueller, P. K. Detection and Analysis of Atmos-
pheric Pollutants. Presented at the Engineering
Extension Course of Combustion Generated Air
Pollution. University of California. Berkeley.
June 1965.
23. Kemmner, G., G. Nonnenmacher, and W. Wehl-
ing. Analytical Application of Infrared Spectros-
copy with Gratings: Quantitative Analysis of
Gas Tracings [Analytische Anwendung der
Infrarot-Spektroskopie mit Cittern: Quantitative
Analyse von Gasspuren]. Fresenius' Z. Anal.
Chem. 222(2): 149-161, October 13, 1966.
24. Porter, K. and D. H. Volman. Flame lonization
Detection of Carbon Monixide for Gas Chromat-
ographic Analysis. Anal. Chem. 34(1): 748-749,
June 1962.
25. Altshuller, A. P., I. R. Cohen, and T. C. Purcell.
Photooxidation of Propionaldehyde at Low
Partial Pressures of Aldehyde. Can. J. Chem.
44(24):2973-2979, December 15, 1966.
26. Altshuller, A. P. and I. R. Cohen. Atmospheric
Photooxidation of the Ethylene-Nirtic Oxide
System. Int. J. Air Water Pollution.
8(11/12):611-632, December 1964.
27. Recommended Methods in Air Pollution Meas-
urements. California Dept. of Public Health.
Berkeley. 1967.
28. Ciuhandu, G. New Method for the Determination
of Carbon Monoxide in Air. Acad. Rep. Populare
Romine, Baza Cercetari Stiint. Timisoara, Studii
Cercetari Stiint., Ser. I (2):133-142, 1955.
29. Ciuhandu, G. Photometric Determination of
Carbon Monoxide in Air [Photometrische
Bestimmung von Kohlenmonoxyd in der Luft]
Fresnius' Z. Anal. Chem. 155(5):321-327, March
21,1957.
30. Ciuhandu, G. Micromethod for the Photometric
Determination of Carbon Monoxide in Air
[Mikromethode fur die photometrische Kohlen-
monoxydbestimmung in der Luft]. Fresenius' Z.
Anal. Chem. 7
-------
34. Shepherd, M. Rapid Determination of Small 36. Ramsey, J. Concentration of Carbon Monoxide
Amounts of Carbon Monoxide. Anal. Chem. at Traffic Intersections in Dayton, Ohio. Arch.
79:77-81, February 1947. Environ. Health 7J(l):44-46, July 1966.
35. Silverman, L. and G. R. Gardner. Potassium 37. Brice, R. M. and J. F. Roesler. The Exposure to
Pallado Sulfite Method for Carbon Monoxide Carbon Monoxide of Occupants of Vehicles
Detection. Amer. Ind. Hyg. Assoc. J. Moving in Heavy Traffic. J. Air Pollution Control
26(2):97-105, March-April 1965. Assoc. 76:597-600, November 1966.
5-9
-------
CHAPTER 6.
ATMOSPHERIC CARBON MONOXIDE
CONCENTRATIONS
A. INTRODUCTION
The concentration of CO in urban com-
munities varies widely with time and location.
Continuous monitoring for CO has been con-
ducted at stations operated by the National
Air Pollution Control Administration's Con-
tinuous Air Monitoring Program (CAMP), the
State of California, and Los Angeles County.
These efforts and special studies have made it
possible to discern some patterns in CO con-
centration variations.
Statistical analysis techniques have led to
the development of methods for analyzing CO
concentration data. From CO monitoring
information for a given location, the fre-
quency of occurrence of a specific CO con-
centration can be estimated. Further, theo-
retical diffusion models may clarify CO
patterns and help in predictions.
B. TEMPORAL VARIATIONS IN CARBON
MONOXIDE CONCENTRATIONS
1. Diurnal Patterns
Community CO levels follow a regular
diurnal pattern of variation dependent pri-
marily on human activity.1"5 Ambient CO
concentrations generally correlate well with
traffic volume; the highest correlations and
levels are associated with measurements taken
where vehicular traffic is heaviest.
While the exact shape and magnitude of the
diurnal CO curve for a community is depend-
ent to a large extent on meteorologic factors,
two peaks corresponding with the morning
and evening traffic "rush" hours are usually
detectable. See Figures 6—1 and 6—2. Carbon
monoxide levels in most cities reach their
initial daily maximum between 7:00 and 9:00
a.m., coincident with heavy morning auto-
mobile traffic. Another peak is reached in the
late afternoon and early evening hours.1 -2.4.5
Although a late afternoon rise is evident at all
monitoring sites depicted in Figures 6—1 and
6—2, a distinct evening rush-hour peak is not
evident from the Los Angeles data. This situa-
tion probably resulted from the greater wind
speed in Los Angeles in the afternoon, usually
about twice the wind speed in the morning.6
An exception to these general observations
may be found in "downtown" New York
City, where there is a rapid rise in the morn-
ing corresponding to the morning rush hour
traffic, then a constant plateau that lasts until
afternoon when a slower rise begins and
builds to a peak in late afternoon. See Figure
6—3. The shape of the traffic curve seen in
this figure is indicative of saturation levels of
traffic.7
The diurnal pattern within a community,
being directly related to traffic volume, shows
little variation with day of the week except
for weekends and holidays. The weekday con-
centrations are higher than those recorded on
Saturdays, which are higher than those
recorded on Sundays and holidays.2'4'6
Colucci and Begeman, sampling at a variety of
sites in Detroit, New York, and Los Angeles,
found that, in general, the average CO con-
centration on Saturdays and Sundays was
about 20 percent less than that on weekdays.6
Changes in traffic volume resulting from
changes in human activities were found to be
responsible for these variations. For example,
only at the freeway sites sampled in New
York and Los Angeles did the weekend
average equal or exceed the weekday average.
The diurnal variations of CO concentrations
6-1
-------
z
LU
(J
o
u
z
<
LU
5
14
12
£ 10
A LODGE-FORD FREEWAY INTERCHANGE
• GRAND CIRCUS PARK (COMMERCIAL AREA)
• GM TECHNICAL CENTER, WARREN (RESIDENTIAL AREA)
I 1 I I I I I I I I I I I I I I I I 1 I M I .
12
10 12
10 12
-p.m.
HOUR OF DAY
Figure 6-1. Diurnal variation of carbon monoxide levels on weekdays in Detroit.
on weekdays, Saturdays, and Sundays are
shown for the Chicago CAMP station in
Figure 6—4.
The variation of atmospheric levels of CO
with traffic density was studied by Brief,
Jones, and Yoder at six locations in a North-
eastern metropolitan city of the United
States.3 Based on 30 data points, these inves-
tigators found that CO concentrations showed
a linear correlation with traffic density. The
CO levels were correspondingly lower on
Sundays where the average traffic flow was
reduced by one-third to one-half the overall
weekday station average. Figure 6—5 depicts
the regression line found by these investi-
gators along with the corresponding 95 per-
cent confidence limits for the regression of
atmospheric CO concentration on traffic den-
sity. The extent to which the correlations and
confidence intervals can be generalized in
other cities varies with such factors as meteor-
ology, type of traffic flow, and the influence
of other sources.3 Under conditions (not
experienced during these tests) of high wind
6-2
and vertical turbulence, which promote maxi-
mum dilution, the slope of the correlation
curve could be lessened so that even under
conditions of high traffic density, the levels of
CO might be below the lower confidence
limits. On the other hand, in an area with
predominantly stagnant weather conditions,
the slope of the correlation curve might be
greater than that shown in Figure 6—5.
In their studies in Detroit, New York, and
Los Angeles, Colucci and Begeman found cor-
relation coefficients between CO concentra-
tions and traffic counts ranged from 0.75 to
0.95.6 Similar analyses have been conducted
by others.7-9
The intimate relationship between urban
CO concentrations and traffic conditions
represents a means of practical CO emission
control beyond the specific engineering con-
trols on individual vehicles. As was indicated
in Chapter 4, an increase in average auto-
mobile speeds in urban driving reduces CO
emissions. It should be possible to capitalize
on this fact in city planning by designing to
-------
E
Q.
a
o
H
<
UJ
u
z
o
u
<
UJ
16
14
12
10
• PICO BOULEVARD (COMMERCIAL
AREA)
A HARBOR - SANTA MONICA
FREEWAY INTERCHANGE
• SANTA MONICA (RESIDENTIAL
AREA)
12
10
12
10
12
-p.m.
HOUR OF DAY
Figure 6-2. Diurnal variation of carbon monoxide levels on week days in Los Angeles.
increase speed and continuity of traffic
through central urban areas.
2. Seasonal Patterns
Community atmospheric CO levels reveal
seasonal patterns, which result primarily from
changes in meteorologic parameters. CAMP
data for the years 1964 through 1967 indicate
that CO concentrations are generally highest
in the fall, followed by the summer, spring,
and winter, respectively.10 The tendency
toward increased atmospheric stability and
low wind speeds in the two former seasons
contribute a substantial part to the occur-
rence of high CO concentrations.
3. Annual Variations
The data available for studying differences
by year and trends of CO concentrations are
shown in Tables 6-1 through 6-3. Calcula-
tions from continuous measurements at 46
sampling sites (located mainly in California)
indicate that no essential change in annual
average concentrations occured from year to
year. To be sure, there were average annual
changes of 1 milligram per cubic meter (1
ppm) up or down, but there does not appear
to be any consistent upward or downward
trend in annual average CO concentrations.
It has been noted, however, that for some
California stations associated with marked
population increases, significant increases in
CO concentrations were observed during the
first few years of sampling.
C. EFFECT OF METEOROLOGICAL
FACTORS
The rate of emission and dispersion deter-
mine the concentration of a pollutant at a
given location. Both macro- and micro-
meteorological factors play a role in the rate
of dispersion of CO emissions. For dispersion
over short distances, microscale factors are
most important,1 '8 but over extended dis-
tances, macroscale factors dominate. The
6-3
-------
4,000
HOUR OF DAY
Figure 6-3. Hourly average carbon monoxide concentration and traffic count in mid-town
Manhattan.
MONDAY-
FRIDAY / \SATURDAY
SUNDAY
I I I I I I I I I I I I I I I I I I I I II I
-H*-
-p.m.
HOUR OF DAY
Figure 6-4. Diurnal variation of carbon
monoxide levels on weekdays, Saturdays,
and Sundays in Chicago, 1962-1964.4
fundamental meteorological factors involved
in dispersion are wind speed, wind direction,
turbulence, and atmospheric stability. The
largest single source of CO is the automobile.
95 PERCENT CONFIDENCE
INTERVAL
^_ 20 40 60
< TRAFFIC DENSITY, vehicles/min
Figure 6-5. Correlation of carbon monoxide
concentration and traffic density.3
Logically, the greatest emissions are expected
to be found on city streets when traffic vol-
ume is high. On city streets where people are
close to sources, the micrometeorological
factors become critical in determining expo-
sures.
6-4
-------
Because automobiles usually are moving
and create their own rather small, but intense,
field of mechanical turbulence, the diffusion
resulting therefrom is important in the deter-
mination of neaby CO concentrations. This is
particularly true when the wind speed is low
(mean wind speed of < 1.3 m/sec or 3
mi/hr).8'11 When there are high wind speeds,
the air flowing over and around buildings adds
turbulence and mixing to that generated by
vehicles. Higher wind speeds, therefore,
increase turbulence and dilution, and there-
by generally lower pollutant concentrations.
During prolonged periods of air stagnation,
which do occur in most urban communities
periodically, poor or inadequate diffusion,
contributes to the buildup of atmospheric
levels of CO and other air pollutants. In the
Fall of 1964, during unusually prolonged and
severe inversions, CO concentrations in Los
Angeles and in Sacramento, California, ex-
ceeded 35 mg/m3 (30 ppm) for 8 hours.1 2 In
the results -of sampling done in London from
October 1956 to October 1957, Lawther et
al. reported a peak CO reading of 270 mg/m3
(235 ppm) measured on a traffic island and a
level of 415 mg/m3 (360 ppm) CO measured
on a calm day at another street-level loca-
tion.13 In 1967, of 15,216 samples from 317
locations in Paris, 235 exceeded 115 mg/m3
(100 ppm) CO. Of these, 11 were equal to or
greater than 345 mg/m3 (300 ppm), 21 were
between 230 and 345 mg/m3 (200 and 300
ppm), and 203 were between 115 and 230
mg/m3 (100 and 200 ppm).14
Because smog is indicative of air stagnation
conditions, a comparison of CO levels on
smoggy and nonsmoggy days is of interest.
Based on sampling in a moving vehicle (with
the intake level about 5 feet above the street)
Castrop15 et al. reported that the mean CO
concentrations at street level were 11.1
mg/m3 (9.7 ppm) CO for nonsmoggy days
and 45.3 mg/m3 (39.4 ppm) for smoggy days
(defined visually). The highest concentration
detected, 135 mg/m3 (160 ppm), occurred
during a smog period.
A similar analysis of stationary CO meas-
urements in a Log Angeles commercial area
showed that the average CO concentration on
21 smoggy days (defined by a 1-hour oxidant
concentration greater than or equal to 0.15
ppm) was 13.2 mg/m3 (11.5 ppm) versus 6.9
mg/m3 (6 ppm) recorded on 16 smogless
days.6
The concentration of CO in the vicinity of
a city street is the product of emissions not
only on that street but also from streets
upwind. Accordingly, the "background"
concentration from more distant sources
depends for the most part on the number of
streets upwind acting as CO sources and the
macrometeorological factors mentioned pre-
viously.
D. OBSERVED URBAN CARBON
MONOXIDE CONCENTRATIONS
1. Sources of Data
Continuous, automatically recorded CO
data are available for selected cities in the
United States from metropolitan monitoring
stations of the Continuous Air Monitoring
Program (CAMP). See Tables 6-1 and 6-4.
Similar data are also available from the State
of California for 23 communities (Table 6—2)
and 28 local sites in Los Angeles County
(Table 6—3). Because all of these stations use
similar recording equipment and techniques,
some basis for comparison of CO data exists.
2. Techniques of Data Analysis
a. Introduction
The collection of air quality data is of little
value unless these data are properly analyzed.
For this reason, the method of analysis to be
applied should be clearly defined before
sampling is begun. In fact, the data acquisi-
tion process itself should be determined by
techniques of analysis available. Careful exam-
ination may show that a proposed sampling
scheme may be unsatisfactory for acquiring
data for the desired purpose or may even
provide entirely irrelevant information.
The purpose' of the following discussion of
data analysis techniques is threefold: (1) to
indicate those data parameters frequently
6-5
-------
0\
Table 6-1. CARBON MONOXIDE CONCENTRATION AT CAMP SITES, BY AVERAGING TIME AND
FREQUENCY, 1962 THROUGH 1967
(ppm)
City and
averaging
time
Chicago
S min
1 hr
8hr
1 day
1 mo
lyr
Cincinnati
S min
1 hr
8hr
1 day
1 mo
1 yr
Denver
S min
1 hr
8hr
1 day
1 mo
lyr
Los Angeles
S min
1 hr
8hr
1 day
1 mo
1 yr
Philadelphia
S min
1 hr
8hr
1 day
1 mo
1 yr
1962-1967
Annl
max
81
54
39
33
19
14
43
27
18
14
8
5
114
61
37
28
12
8
72
46
32
26
15
11
83
48
31
24
12
8
Geo
mean
13.0
13.2
13.4
13.5
13.9
14.1
4.6
4.8
4.9
4.9
5.1
5.3
6.4
6.7
6.9
7.1
7.5
7.9
9.5
9.7
9.9
10.0
10.3
10.6
6.7
6.9
7.1
7.2
7.6
7.9
SGD
1.51
1.44
1.38
1.34
1.21
1.00
1.66
1.57
1.48
1.44
1.26
1.00
1.93
1.79
1.66
1.60
1.35
1.00
1.58
1.50
1.43
1.39
1.24
1.00
1.77
1.66
1.56
1.50
1.30
1.00
Maxima
Max
78
59
44
33
21
17
50
34
21
17
11
6
73
55
30
20
12
8
81
47
28
23
14
11
67
54
36
25
14
8
Min
43
28
20
17
7
12
26
20
12
9
5
4
63
40
27
16
10
7
70
35
27
22
13
9
43
37
23
14
9
6
Maximum for year
62
43
28
20
17
7
81
43
28
22
14
11
51
47
36
23
63
50
36
22
19
10
70
35
28
22
13
9
52
47
35
25
14
64
64
46
35
27
17
12
26
22
19
17
11
6
75
47
27
23
14
11
43
37
27
21
13
7
65
61
44
37
32
21
17
50
34
21
16
5
4
70
40
27
16
10
7
67
54
26
19
11
6
66
78
59
44
33
18
13
32
20
12
9
7
5
73
55
29
20
12
8
47
43
34
20
10
7
67
63
56
33
23
11
47
27
17
13
8
5
63
43
30
20
10
8
44
42
23
14
9
6
%
data
avail
53
54
55
55
60
50
72
73
74
75
77
100
73
73
74
76
81
100
79
79
81
82
89
100
58
58
59
60
61
67
% of time concentration is exceeded:
0.001
69
45
69
81
65
0.01
58
54
31
27
58
49
50
43
48
45
0.1
45
41
35
21
19
18
44
40
29
36
34
27
35
33
27
1
34
31
27
25
15
15
14
13
26
24
18
16
25
25
21
19
21
21
19
18
10
22
22
21
20
18
9
9
8
8
7
14
14
12
11
10
16
16
15
15
13
13
12
12
11
10
30
16
16
16
15
15
6
6
6
6
5
9
9
9
9
8
12
12
12
12
12
9
9
8
8
8
50
11
12
12
12
11
12
4
5
5
5
4
5
7
7
7
7
7
7
10
10
10
11
11
11
7
7
7
7
7
7
70
8
8
8
8
9
3
3
4
4
4
5
5
6
6
7
9
9
9
9
9
5
5
5
5
6
90
4
4
5
5
7
2
2
2
3
3
2
2
3
4
6
7
7
8
8
9
3
3
3
4
5
-------
St. Louis
5 min
1 hr
8hr
1 day
1 mo
1 yr
San Francisco
5 min
1 hr
8hr
1 day
1 mo
1 yr
Washington
5 min
1 hr
8hr
1 day
1 mo
1 yr
54
32
21
17
9
6
39
25
17
14
7
5
93
46
26
19
7
4
5.3
5.5
5.6
5.7
5.9
6.1
4.7
4.8
4.9
5.0
5.1
5.3
3.3
3.5
3.7
3.8
4.2
4.4
1.69
1.59
1.50
1.45
1.27
1.00
.62
.53
.46
.41
.25
.00
2.13
.95
.80
.72
.42
.00
68
29
18
17
9
6
40
38
18
14
7
5
49
41
34
23
10
7
45
25
14
11
8
6
38
22
14
10
6
5
29
25
17
11
5
3
30
25
19
14
7
38
38
18
14
6
44
41
34
23
10
7
45
25
18
17
9
6
40
22
14
10
7
5
29
28
18
13
6
6
53
27
18
15
9
6
49
32
17
11
6
4
68
29
18
12
8
6
47
38
22
15
5
3
60
27
14
11
8
6
37
32
23
15
7
5
86
86
88
89
94
100
67
68
68
69
67
SO
70
70
71
71
75
83
55
38
42
27
27
20
35
31
23
17
20
18
13
28
22
19
17
14
12
14
13
11
9
30
17
16
14
11
11
10
9
8
9
8
8
7
6
9
8
8
8
7
7
7
7
7
7
6
6
6
6
6
6
5
5
6
5
5
5
6
6
6
6
5
5
5
5
5
5
4
4
4
4
4
4
4
4
4
5
5
4
4
4
4
5
3
3
3
3
4
2
2
3
3
5
2
2
3
3
4
2
2
2
2
3
Table 6-2. CARBON MONOXIDE CONCENTRATION BY AVERAGING TIME AND FREQUENCY,
1963 THROUGH 1967, IN CALIFORNIA
(ppm)
Location and
averaging time
Anaheim
1 hr
8hr
1 day
1 mo
1 yr
Bakersfield
1 hr
8hr
1 day
1 mo
1 yr
Calculated
Annl
max
36
23
18
9
6
24
14
10
4
3
oeo
mean
5.4
5.6
5.6
5.9
6.1
2.2
2.3
2.3
2.5
2.6
SGD
1.64
1.54
1.49
1.30
1.00
1.87
1.73
1.66
1.39
1.00
Measured
maxima
Max
35
23
19
10
7
23
15
11
4
3
Min
18
13
11
6
5
12
8
5
3
2
Maximum for year
63
18
13
11
6
5
12
8
5
3
64
26
20
12
7
6
17
8
5
3
2
65
26
18
13
8
7
19
11
7
4
2
66
35
23
17
8
7
23
15
11
4
3
67
35
23
19
10
7
22
12
7
4
2
%
data
avail
94
94
96
98
100
81
81
81
84
79
% of time concentration is exceeded:
0.01
12
19
0.1
25
22
15
11
1
15
14
13
10
8
6
10
9
9
9
8
4
4
4
3
30
7
7
7
7
3
3
3
3
50
6
6
6
6
6
2
2
2
2
2
70
5
5
5
6
1
2
2
2
90
3
4
4
5
1
1
1
1
-------
OO
Table 6-2 (continued). CARBON MONOXIDE CONCENTRATION BY AVERAGING TIME AND FREQUENCY,
1963 THROUGH 1967, IN CALIFORNIA
(ppm)
Location and
averaging time
Fresno
1 hr
8 hr
1 day
1 mo
1 yr
La Habra
1 hr
8hr
1 day
1 mo
1 yr
Oakland
1 hr
8hr
1 day
1 mo
1 yr
Port Chicago
1 hr
8hr
1 day
1 mo
lyr
Redlands
1 hr
8hr
1 day
1 mo
1 yr
Redwood City
1 hr
8hr
1 day
1 mo
1 yr
Annl
max
41
19
13
4
2
31
23
19
12
9
30
16
12
5
3
8
5
3
1
1
28
19
15
8
5
15
10
9
5
4
Calculated
Geo
mean
1.2
1.4
1.4
1.7
1.9
8.4
8.5
8.5
8.7
8.9
2.1
2.2
2.3
2.5
2.7
0.7
0.8
0.8
0.8
0.9
4.7
4.8
4.9
5.1
5.2
3.3
3.3
3.3
3.4
3.5
SGD
2.50
2.23
2.09
1.61
1.00
1.41
1.35
1.32
1.20
1.00
2.01
1.84
1.75
1.44
1.00
1.87
1.73
1.66
1.39
1.00
1.60
1.51
1.46
1.28
1.00
.48
.41
.37
.23
.00
Measured
Maxima
Max
35
18
9
5
2
26
20
15
9
27
16
11
5
4
8
4
3
2
1
21
15
13
6
15
9
7
4
3
Min
18
13
5
3
2
26
20
15
9
20
12
9
4
3
7
4
3
2
1
21
15
13
6
15
9
7
4
3
Maximum for year
63
18
13
5
3
27
12
9
4
3
64
27
15
8
3
2
26
14
10
5
3
65
29
18
9
5
2
26
16
10
5
4
66
35
15
7
4
2
25
12
11
5
3
7
4
3
2
1
67
26
16
7
3
2
26
20
15
9
20
12
9
4
3
8
4
3
2
1
21
15
13
6
15
9
7
4
3
%
data
avail
79
79
79
84
79
5
7
7
7
0
89
91
91
94
100
36
36
36
36
41
0
0
0
2
0
14
14
14
14
19
% of time concentration is exceeded:
0.01
27
25
25
7
20
13
0.1
21
15
24
18
18
12
5
4
20
14
11
9
1
12
10
6
19
16
14
11
10
9
4
3
3
18
14
10
8
7
6
10
4
4
4
3
13
12
11
9
6
6
5
4
2
2
2
2
11
11
7
0
5
5
5
4
30
2
2
2
3
10
10
9
9
3
4
4
4
1
2
1
1
6
6
6
0
4
4
4
3
50
2
2
2
2
2
8
9
9
9
9
2
3
3
3
3
1
1
1
1
1
5
5
5
0
0
3
3
3
3
3
70
1
1
1
2
7
7
7
7
2
2
2
2
1
1
1
1
4
4
4
0
3
3
3
3
90
1
1
1
1
4
4
5
0
1
1
1
2
1
1
1
1
2
3
4
0
2
2
2
3
-------
Richmond
1 hr
8hr
1 day
1 mo
1 yr
Riverside
1 hr
8hr
1 day
1 mo
1 yr
Sacramento
1 hr
8hr
1 day
1 mo
1 yr
Salinas
1 hr
8hr
1 day
1 mo
1 yr
San Bernardino
1 hr
8hr
1 day
1 mo
1 yr
San Diego
1 hr
8hr
1 day
1 mo
1 yr
San Francisco, Mission St
1 hr
8hr
1 day
1 mo
lyr
26
15
11
4
3
26
17
13
7
4
70
31
21
6
3
10
7
5
3
2
30
21
17
10
7
48
23
16
5
3
34
19
14
6
4
2.1
2.2
2.3
2.5
2.6
3.9
4.0
4.0
4.2
4.4
1.8
2.0
2.1
2.5
2.9
1.6
1.6
1.6
1.7
1.7
6.5
6.6
6.7
6.9
7.0
1.9
2.1
2.2
2.5
2.8
2.9
3.0
3.1
3.3
3.5
1.92
1.77
1.69
1.41
1.00
1.65
1.55
1.49
1.30
1.00
2.60
2.31
2.16
1.65
1.00
1.63
1.53
1.48
1.29
1.00
1.48
1.41
1.37
1.23
1.00
2.32
2.09
1.97
1.55
1.00
1.91
1.76
1.68
1.40
1.00
25
15
7
4
3
74
19
18
8
5
55
39
17
6
3
10
5
3
2
1
35
22
16
10
8
45
23
14
8
4
38
21
12
6
4
13
9
5
3
3
15
10
8
4
3
36
24
12
4
2
6
4
2
1
1
20
15
11
6
4
26
16
10
3
2
27
14
10
5
3
17
10
8
4
3
36
24
12
3
2
20
18
13
6
4
33
17
12
5
4
15
10
8
5
3
51
30
14
5
3
24
15
11
6
5
38
23
14
8
4
24
16
14
6
4
44
31
15
6
3
35
22
15
10
7
45
20
10
6
3
27
14
10
5
4
13
9
5
3
17
15
12
6
5
51
28
13
5
2
6
4
2
1
30
19
16
10
8
37
22
12
3
2
27
15
12
5
3
25
15
7
4
3
74
19
18
8
5
55
39
17
5
3
10
5
3
2
1
33
21
16
10
8
26
16
11
5
2
38
21
11
6
3
22
22
22
24
19
77
77
77
89
100
96
96
96
98
100
22
22
22
22
19
86
86
86
94
100
81
81
81
84
100
55
55
57
57
60
21
22
50
9
30
34
34
16
11
18
16
35
28
7
5
22
19
26
20
21
15
10
8
7
13
12
11
16
13
11
4
4
3
16
15
13
15
12
10
12
10
9
5
5
4
4
8
8
7
6
5
5
4
4
2
2
2
2
10
10
10
9
6
6
6
5
6
6
6
5
3
3
3
3
5
5
5
5
3
3
3
3
2
2
2
2
8
8
8
8
3
3
3
3
4
4
4
4
2
2
2
3
3
4
4
4
4
3
2
2
2
2
2
1
1
1
1
1
6
6
7
6
5
2
2
2
3
2
3
3
3
3
3
1
2
2
2
2
3
3
3
1
1
2
2
1
1
1
1
5
5
5
6
1
1
2
2
2
2
3
3
-------
ON
o
Table 6-2 (continued). CARBON MONOXIDE CONCENTRATION BY AVERAGING TIME AND FREQUENCY,
1963 THROUGH 1967, IN CALIFORNIA
(ppm)
Location and
averaging time
San Francisco, Union Square
1 hr
8hr
1 day
1 mo
1 yr
San Jose
1 hr
8 hr
1 day
1 mo
1 yr
San Rafael
1 hr
8hr
1 day
1 mo
1 yr
Santa Ana Airport
1 hr
8hr
1 day
1 mo
1 yr
Santa Barbara
1 hr
8hr
1 day
1 mo
1 yr
Santa Cruz
1 hr
8 hr
1 day
1 mo
1 yr
Calculated
Annl
max
23
16
13
7
S
30
17
13
6
4
24
14
10
4
3
14
12
11
8
6
39
20
14
5
3
4
3
2
1
1
Geo
mean
4.9
5.0
5.0
5.2
5.3
2.9
3.0
3.1
3.3
3.5
2.2
2.3
2.3
2.5
2.6
6.3
6.3
6.3
6.4
6.4
2.0
2.1
2.2
2.5
2.7
0.8
0.8
0.8
0.9
0.9
SGD
1.50
1.43
1.39
1.24
1.00
1.83
1.70
1.63
1.37
1.00
1.87
1.73
1.66
1.39
1.00
1.23
1.20
1.18
1.12
1.00
2.17
1.98
1.87
1.50
1.00
1.53
1.46
1.41
1.2S
1.00
Measured
Maxima
Max
22
17
14
6
5
29
19
13
7
5
17
7
5
3
15
11
10
7
31
19
9
5
3
4
3
2
2
1
Min
16
13
9
6
5
19
14
7
3
3
17
7
5
3
15
11
10
7
26
12
8
5
3
4
3
2
1
1
Maximum for year
63
18
17
14
6
19
14
7
3
64
22
13
9
6
5
27
19
13
6
4
26
12
9
5
3
65
20
16
9
6
20
14
12
7
S
31
15
8
5
3
66
20
14
10
S
3
28
19
9
5
4
3
2
2
67
29
IS
10
5
3
17
7
5
3
15
11
10
7
4
3
2
1
1
%
data
avail
29
29
29
31
19
79
81
81
84
79
2
2
2
2
0
7
7
7
7
0
46
48
48
48
41
22
22
22
24
19
% of time concentration is exceeded:
0.01
20
25
15
14
20
4
0.1
17
13
19
15
15
7
12
10
22
IS
3
3
1
13
11
9
13
11
10
12
6
5
10
9
9
14
11
8
3
3
2
10
8
8
7
6
7
7
6
5
6
5
4
3
8
8
8
7
S
5
5
4
2
2
2
1
30
6
6
6
5
4
4
4
4
3
4
4
3
7
7
7
7
3
3
3
4
1
1
1
1
50
5
5
5
S
5
3
3
3
3
3
2
3
3
3
3
6
6
6
6
6
2
3
3
3
3
1
1
1
1
1
70
3
4
4
4
2
2
2
3
2
2
3
3
6
6
6
6
2
2
2
2
1
1
1
1
90
2
2
3
4
1
1
2
2
1
2
2
0
5
(5
5
0
1
2
2
2
1
1
1
1
-------
Stockton
1 hr
8hr
1 day
1 mo
lyr
Upland APCD
I hr
8hr
1 day
1 mo
1 yr
Ventura
1 hr
8hr
1 day
1 mo
lyr
24
13
9
3
2
28
17
13
6
4
14
8
6
3
2
1.3
1.4
1.5
1.7
1.8
3.0
3.1
3.1
3.3
3.5
1.5
1.5
1.6
* 1.7
1.8
2.13
1.94
1.84
1.49
1.00
1.80
1.67
1.60
1.36
1.00
1.80
1.67
1.60
1.36
1.00
35
19
13
4
2
28
12
8
5
3
13
6
4
3
2
15
7
4
2
1
26
12
8
5
3
12
6
4
2
2
16
8
5
2
23
14
7
3
2
12
6
4
3
2
21
11
6
3
2
13
6
4
3
2
15
7
4
2
1
26
12
8
5
12
6
4
2
35
19
13
4
2
28
12
8
5
3
86
86
86
91
79
22
22
22
24
19
48
48
48
50
41
22
26
12
14
11
18
12
9
6
8
7
5
12
10
8
5
4
4
3
3
3
2
6
6
5
5
3
3
3
3
2
2
2
2
4
4
4
4
2
2
2
2
1
1
1
1
2
3
3
3
3
3
2
2
2
2
2
1
1
1
1
2
3
3
3
2
2
2
2
0
0
1
1
1
2
2
2
1
1
1
2
Table 6-3. CARBON MONOXIDE CONCENTRATION BY AVERAGING TIME AND FREQUENCY,
1956 THROUGH 1967, IN LOS ANGELES COUNTY
(ppm)
Location and
averaging time
Avalon Village
1 hr
8hr
1 day
1 mo
lyr
Azusa, 803 Loren
1 hr
8hr
1 day
1 mo
lyr
Azusa, 827 N Azusa
1 hr
8 hr
1 day
1 mo
1 yr
Calculated
Annl
max
40
28
24
13
10
23
18
16
11
9
18
13
11
7
5
Geo
mean
9.0
9.1
9.2
9.5
9.7
8.8
8.8
8.9
9.0
9.1
5.1
5.1
5.2
S.3
5.3
SGD
1.48
1.41
1.37
1.23
1.00
1.28
1.25
1.22
1.14
1.00
1.39
1.34
1.30
1.19
1.00
Measured
maxima
Max
37
29
23
14
11
27
23
20
12
11
17
13
9
6
5
Min
28
24
14
11
9
11
8
7
5
4
16
12
8
6
5
Maximum for year
56
16
13
8
6
5
57
11
8
7
5
4
17
12
9
6
58
28
24
14
11
9
18
12
8
5
4
59
37
27
18
13
10
27
22
15
10
9
60
35
29
23
14
11
18
16
15
10
8
61
36
27
21
14
11
22
20
17
12
9
62
32
28
19
13
10
24
18
15
11
10
63
27
23
20
11
9
64
25
17
15
10
8
65
20
16
16
11
9
66
19
18
14
12
9
67
21
18
16
12
11
%
data
avail
35
36
36
37
42
81
82
83
85
92
9
9
9
10
8
% of time concentration is exceeded:
0.01
34
23
16
0.1
30
27
19
18
14
12
1
23
22
18
15
15
14
11
10
8
10
15
14
13
13
12
12
12
11
7
7
7
6
30
11
11
11
11
10
10
10
10
6
6
6
5
50
9
9
10
10
10
8
9
9
9
9
5
5
5
5
5
70
8
9
9
9
7
7
7
8
4
4
4
4
90
7
7
8
8
4
4
4
4
3
3
3
4
-------
to
Table 6-3 (continued). CARBON MONOXIDE CONCENTRATION BY AVERAGING TIME AND FREQUENCY,
1956 THROUGH 1967, IN LOS ANGELES COUNTY
(ppm)
Location and
averaging time
Burbank, 1 508 Burbank
1 hr
8hr
1 day
1 mo
1 yr
Burbank, 228 W Palm
1 hr
8hr
1 day
1 mo
1 yr
Calculated
Annl
max
69
40
30
13
8
60
40
33
18
12
Downey, Ranch Los Amigos
1 hr
8hr
1 day
1 mo
1 yr
El Monte, 2720 Peck
1 hr
8hr
1 day
1 mo
1 yr
El Segundo, 301 Coast
1 hr
8hr
1 day
1 mo
1 yr
Florence, Roosevelt Park
1 hr
8hr
1 day
1 mo
1 yr
40
28
24
13
10
36
21
16
7
4
18
13
11
7
5
45
30
24
13
9
Geo
mean SGD
6.5 1.85
6.8 1.72
7.0 1.65
7.5 1.38
7.9 1.00
11.2 1.55
11.4 1.47
11.5 1.42
12.0 1.26
12.3 1.00
9.0 1.48
9.1 1.41
9.2 1.37
9.5 1.23
9.7 1.00
3.7 1.81
3.8 1.68
3.9 1.61
4.2 1.36
4.4 1.00
5-1 1.39
S.I 1-34
5.2 1.30
5.3 1.19
5.3 1.00
7.9 1.57
8.1 1.49
8.2 1.44
8.5 1.27
8.8 1.00
Measured
maxima
Max
56
47
26
16
11
68
50
29
21
IS
40
27
21
13
11
29
20
15
8
S
16
13
10
7
6
43
31
25
13
10
Min
41
31
18
12
5
30
25
18
9
12
35
24
17
13
9
27
18
12
7
4
13
11
9
7
6
32
20
13
10
7
Maximum for year
56
41
33
18
12
5
27
18
15
8
5
57
43
35
22
13
7
29
20
12
7
4
13
11
9
7
58
42
31
21
13
8
16
13
10
7
6
59
43
32
20
14
9
35
25
17
13
9
60
51
40
26
15
11
37
27
18
13
11
32
20
13
10
61
56
47
26
16
9
30
25
18
9
35
24
20
13
11
42
26
19
12
7
62
60
50
23
14
12
40
27
21
13
43
31
25
13
10
63
68
50
29
17
14
64
54
42
28
21
13
65
40
33
27
17
14
66
39
31
24
19
IS
67
42
31
25
17
12
%
data
avail
43
44
44
47
50
48
48
49
50
50
26
26
26
26
25
12
12
12
13
17
8
8
8
9
8
15
1 5
15
17
17
% of time concentration is exceeded:
0.01
53
54
35
28
16
42
0.1
44
37
43
37
30
25
23
17
14
12
32
27
1
29
26
21
29
27
24
23
20
17
15
13
11
11
10
9
23
19
17
10
15
14
13
12
18
18
17
16
15
14
13
13
8
8
8
7
8
8
8
7
13
13
12
11
30
9
9
9
9
14
14
IS
14
11
11
11
11
5
6
5
5
6
6
6
6
10
10
10
10
50
7
7
7
7
8
13
13
13
13
13
10
10
10
10
9
4
4
5
4
4
6
6
6
6
6
8
9
9
9
7
70
5
5
6
6
11
11
12
12
9
9
9
10
3
4
4
4
5
5
5
6
7
7
7
9
90
3
3
4
4
9
9
10
10
7
7
8
9
2
2
3
3
4
4
4
4
i
-------
Hollywood Freeway
Ihr
8hr
1 day
1 mo
1 yr
Inglewood, 5037 W Imperl
1 hr
8hr
1 day
1 mo
1 yr
Lennox, 4380 Lennox
1 hr
8hr
1 day
1 mo
1 yr
L A, Plrshing Square
1 hr
8hr
1 day
1 mo
1 yr
L A, 434 S San Pedro
1 hr
8hr
1 day
1 mo
lyr
L A, USC Medical Center
1 hr
8hr
1 day
1 mo
1 yr
North Long Beach
1 hr
1 hr
1 day
1 mo
1 yr
S3
37
30
17
12
57
41
34
19
14
66
44
36
19
13
62
38
29
14
9
49
33
26
14
10
40
29
25
15
12
38
29
24
15
12
11.4
11.6
11.7
12.1
12.3
13.1
13.3
13.4
13.8
14.1
11.9
12.2
12.3
12.8
13.1
7.5
7.8
7.9
8.4
8.7
8.7
8.9
9.0
9.4
9.6
10.9
11.0
11.1
11.4
11.5
11.0
11.1
11.2
11.4
11.6
1.49
1.42
1.38
1.23
1.00
1.47
1.40
1.36
1.22
1.00
1.56
1.48
1.43
1.26
1.00
1.73
1.62
1.56
1.33
1.00
.57
.49
.44
.27
.00
1.40
1.35
1.31
1.19
1.00
.18
.33
.30
.19
.00
50
38
26
18
15
48
40
29
20
15
56
47
35
21
15
58
32
24
14
9
60
32
26
16
13
40
29
22
18
13
37
28
24
18
14
42
33
21
14
11
31
24
17
13
12
42
31
21
13
8
44
27
18
11
8
37
21
14
9
6
32
25
19
13
11
25
20
17
13
12
42
31
21
13
8
44
31
18
11
38
21
14
9
6
48
40
34
21
15
54
32
21
13
8
41
23
14
10
8
56
47
35
21
58
27
20
11
9
47
26
18
11
8
52
32
24
14
55
30
22
14
50
27
21
13
11
57
28
23
13
10
31
24
17
13
63
32
26
14
11
32
28
22
14
11
25
20
17
13
48
35
21
14
11
48
39
27
17
12
42
31
21
15
11
38
29
35
28
23
14
12
45
33
22
47
40
29
20
15
47
26
22
14
11
38
29
22
17
13
37
28
24
17
14
42
33
24
18
15
47
34
26
20
37
28
22
16
13
40
28
22
18
13
34
27
23
18
14
50
36
26
18
14
38
27
20
14
10
35
25
20
15
12
33
26
22
16
13
50
38
26
18
14
40
26
21
12
10
.
32
26
19
13
12
33
26
22
15
12
33
34
34
35
42
17
17
18
18
17
18
19
19
20
17
20
21
21
21
17
86
87
88
91
92
47
47
48
49
50
40
41
41
42
42
48
48
55
52
47
37
34
39
35
43
36
47
40
41
31
35
27
31
26
30
26
29
26
22
33
29
25
35
32
27
27
23
18
25
22
19
24
22
20
25
23
21
19
18
18
17
21
20
20
19
21
20
20
19
14
13
13
11
15
15
14
13
16
16
16
IS
17
17
16
15
14
14
15
14
16
16
16
15
15
15
16
16
10
10
10
9
11
12
12
11
13
13
13
13
13
14
14
13
12
12
13
13
12
13
14
14
13
12
12
12
12
12
8
8
8
8
8
8
9
10
10
10
10
12
12
12
12
12
12
12
12
12
12
10
10
11
11
11
12
12
13
8
8
8
9
6
7
7
7
8
8
8
9
10
11
11
11
11
11
11
11
-------
Table 6-3 (continued). CARBON MONOXIDE CONCENTRATION BY AVERAGING TIME AND FREQUENCY.
1956 THROUGH 1967, IN LOS ANGELES COUNTY
(ppm)
Location and
averaging time
Pasadena, Memorial Park
1 hr
8hr
1 day
1 mo
1 yr
Pasadena, 862 Villa
1 hr
8 hr
1 day
1 mo
1 yr
Pomona, 924 N Garey
1 hr
8hr
1 day
1 mo
1 yr
Lennox, 11408 Lacienga
1 hr
8 hr
1 day
1 mo
1 yr
Reseda, 18330Gault
1 hr
8hr
1 day
1 mo
1 yr
Reseda, 19630 Sherman
1 hr
8hr
1 day
1 mo
1 yr
Calculated
Annl
max
41
28
23
12
9
46
32
26
15
11
26
21
19
14
12
61
43
37
22
16
53
37
30
17
12
25
17
14
7
5
Geo
mean
8.0
8.2
8.3
8.6
8.8
9.7
9.9
10.0
10.3
10.6
11.7
11.7
11.8
11.9
11.9
14.9
15.1
15.2
15.6
15.9
11.4
11.6
11.7
12.1
12.3
4.8
4.9
5.0
5.1
5.3
SGD
.13
.46
.41
.25
.00
1.30
1.13
1.09
1.24
1.00
1.23
1.20
1.18
l.ll
1.00
1.44
1.38
1.34
1.21
1.30
1.49
1.42
1.38
1.23
1.00
1.53
1.46
1.41
1.25
1.00
Measured
maxima
Max
40
27
17
11
10
48
34
25
18
13
30
22
16
13
12
59
42
35
26
19
44
36
24
17
14
20
15
10
7
5
Min
27
19
15
9
7
36
26
19
11
10
23
18
16
13
12
51
34
29
17
12
43
34
22
14
11
20
15
10
7
5
Maximum for year
56
27
19
15
9
7
20
15
10
7
5
57
40
27
16
ie
9
58
34
20
17
11
10
40
31
20
12
59
48
34
22
14
12
60
40
30
23
18
12
61
38
29
25
15
11
62
37
26
20
14
11
63
37
32
25
17
13
64
40
30
24
11
10
65
41
33
22
13
11
25
22
16
13
57
39
32
25
19
43
34
22
14
13
66
38
29
19
13
11
30
18
16
13
12
59
42
35
26
16
44
35
24
14
11
67
36
26
20
13
11
23
19
16
13
12
51
34
29
17
12
44
35
24
17
14
%
data
avail
21
22
22
22
25
70
71
72
73
75
20
20
20
20
17
23
23
23
24
25
22
22
23
22
25
6
6
6
6
8
% of time concentration is exceeded:
0.01
40
40
24
55
43
20
0.1
30
21
34
29
22
18
46
39
39
34
18
14
1
20
17
14
26
23
20
18
17
15
36
33
30
28
26
22
13
12
10
10
13
12
11
10
17
16
15
13
14
14
14
13
23
23
22
22
17
17
16
15
8
8
7
6
30
10
10
10
9
12
12
12
12
13
13
13
12
18
18
18
17
14
14
14
14
6
6
6
5
50
8
8
8
9
7
11
11
11
11
11
12
12
12
12
12
15
15
15
15
12
12
12
12
12
11
5
5
5
5
5
70
6
7
7
7
9
10
10
10
11
11
11
12
11
12
12
13
10
11
11
11
4
4
4
5
90
4
5
6
6
7
8
8
9
10
11
11
11
9
10
10
10
9
9
9
10
3
3
3
4
-------
Rivera, 8841 E Slauson
1 hr
8hr
1 day
1 mo
1 yr
Torrance, 1657 Gramercy
1 hr
8hr
1 day
1 yr
1 yr
Vernon, 5201 Santa Fe
1 hr
8hr
1 day
1 mo
lyr
West L A, 844 S La Brea
1 hr
8hr
1 day
1 mo
1 yr
West L A, 4409 W Pico
1 hr
8hr
1 day
1 mo
1 yr
West L A, 2351 Westwood
1 hr
8hr
1 day
1 mo
1 yr
38
24
19
9
6
34
22
18
9
6
42
25
19
8
5
64
40
31
15
10
63
37
28
11
7
50
35
29
16
11
5.4
5.5
5.6
5.9
6.1
5.5
5.6
5.7
5.9
6.1
4.4
4.6
4.7
5.0
5.3
8.3
8.6
8.8
9.2
9.6
5.8
6.0
6.2
6.7
7.0
10.5
10.7
10.8
11.2
11.4
1.67
1.57
1.51
1.31
1.00
1.62
1.52
1.47
1.29
1.00
1.30
1.67
1.60
1.36
1.00
1.70
1.69
1.63
1.32
1.00
1.87
1.13
1.66
1.39
1.00
.50
.43
.39
.24
.00
40
23
18
9
7
34
23
16
10
7.
40
24
19
11
6
61
41
28
16
13
48
35
22
12
8
52
41
25
16
13
23
18
9
6
5
27
18
13
7
5
26
17
12
7
5
34
22
14
9
7
47
31
18
10
7
11
10
20
12
10
33
18
9
6
5
31
18
13
7
5
26
17
12
7
5
48
35
18
10
8
31
19
12
8
6
27
20
14
9
7
31
23
19
11
6
34
22
14
9
47
31
22
12
7
40
23
18
9
7
34
23
16
10
40
19
15
8
6
55
37
21
10
7
23
19
11
6
38
24
17
8
58
33
25
14
9
61
41
28
15
10
58
36
25
14
11
48
37
25
16
13
11
10
48
34
25
15
12
45
29
21
13
11
38
28
22
16
13
52
41
24
16
13
45
32
20
12
10
24
24
24
26
25
18
18
19
19
17
25
26
26
27
25
40
40
40
42
42
14
14
14
15
17
40
40
41
42
42
33
31
35
55
48
47
26
19
24
19
27
21
43
36
40
31
37
32
18
16
12
18
15
13
18
16
14
28
25
,22
26
21
16
26
23
20
10
9
8
8
11
10
10
9
10
9
9
8
15
15
14
14
13
12
12
10
17
16
16
14
7
6
7
6
7
8
8
7
6
7
7
6
11
11
11
11
8
8
9
8
13
13
13
13
5
5
6
5
5
6
6
6
6
5
5
5
5
6
5
9
9
9
9
9
6
7
7
7
7
11
11
12
12
11
4
4
5
5
5
5
5
5
4
4
4
5
7
8
8
8
5
6
6
6
10
10
10
11
3
3
3
4
3
4
4
4
3
3
3
4
5
6
6
7
4
4
5
5
8
8
9
10
NOTE: The Los Angeles County Air Pollution Control District estimates that its reported concentration of carbon monoxide prior to April, 1968 at all locations in Los Angeles
County are from 1 to 4 ppm high because of water vapor interference; the actual amount in this range is dependent on the absolute humidity at the time of measurement.
-------
O-v
OS
Table 6-4. CARBON MONOXIDE CONCENTRATION BY AVERAGING TIME AND FREQUENCY,
FROM DECEMBER 1, 1961, TO DECEMBER 1, 1967, CHICAGO CAMP STATION
(ppm)
Averaging
time
5 min
10 min
1 5 min
30 min
1 hr
2 hr
4hr
8 hr
12 hr
1 day
2 day
4 day
7 day
14 day
1 mo
2 mo
3 mo
6 mo
1 yr
Annl
aiith
mean
12
12
12
12
12
12
12
12
12
12
12
12
12
12
12
13
12
12
14
Max
78
75
69
63
59
52
51
44
39
33
30
27
24
23
21
21
20
19
17
Min
0
0
0
0
0
0
0
0
0
0
2
3
3
5
6
7
7
8
12
%
data
avail
53
54
54
54
54
53
54
55
55
55
52
54
56
59
60
58
63
58
50
% of time concentration is exceeded:
0.001
69
0.01
58
57
56
55
54
0.1
45
43
42
41
41
38
36
35
1
34
33
32
32
31
30
29
27
26
25
24
10
22
22
22
22
22
22
21
21
21
20
20
19
19
19
18
20
18
18
18
18
18
18
18
18
18
18
17
17
17
17
16
17
15
14
30
16
16
16
16
16
16
16
16
15
15
15
15
15
15
15
14
14
12
40
13
14
14
14
14
14
14
14
14
13
14
13
13
14
13
13
13
12
50
11
12
12
12
12
12
12
12
12
12
12
11
11
11
11
11
11
10
12
60
10
10
10
10
10
10
10
10
10
10
10
10
10
10
10
11
11
9
70
8
8
8
8
8
8
8
8
8
8
9
9
9
9
9
9
9
9
80
6
6
6
6
6
6
6
7
7
7
7
8
8
8
7
8
8
8
90
4
4
4
4
4
4
4
5
5
5
6
6
6
7
7
99
0
0
0
0
1
1
1
;
1
2
3
99.9
0
0
0
0
0
0
0
0
99.99
0
0
0
0
0
99.999
0
-------
used to describe aerometric measurements;
(2) to suggest a means of organizing the data
in order to arrive at the aforementioned
parameters; and (3) to present an air quality
model that makes use of these parameters and
statistical considerations to extract as much
information as possible from the data at hand.
b. Averaging Time
The air quality of an area is estimated by
analysis of the pollutant concentrations taken
at specific locations over a selected period of
time. Each recorded measurement of concen-
tration is indicative both of the absolute
magnitude of the actual concentration and of
the response time of the instrument. Because
of the response time of the instrument, any
single recorded concentration is of necessity
an average concentration over the time inter-
val of the measurement.
Reported CO measurements are based on
either spot or integrated measurements taken
over a variety of sampling time periods. It is
necessary to arrive at a uniform averaging
time because of two basic considerations:
1. The need to compare concentrations
measured at different sampling sites.
2. The need to select an averaging time
meaningful to the effects produced by
the pollutant.
The minimum averaging time is an inflex-
ible parameter of the particular instrument
used, but the resulting data may be reported
on the basis of any averaging time equal to
or greater than this minimum value. For
example, while the nondispersive infrared CO
analyzer (NDIR), used in the CAMP network,
senses and measures on a continuous basis, it
only records an instantaneous measurement
once every 5 minutes. The 12 consecutive
5-minute measurements within an hour may
then be averaged to give the 1-hour averaging
time value.
An averaging time of 8 hours is frequently
used for the presentation of CO concentra-
tions. At low atmospheric CO concentrations,
such as those found in community air, from 4
to 12 hours is required for the carboxyhemo-
globin levels in the human body to reach equi-
librium with the average concentration of CO
being inspired. Because of the slow absorption
and desorption of CO at these low levels by
man, short-term concentrations are of less in-
terest than this 8-hour average-value.
c. Frequency Distribution
Use of a frequency distribution is a com-
mon method of reducing a set of data of con-
sistent averaging time. The advantage in using
such a technique is that it automatically
attaches an estimate of the probability of
occurrence to any single measurement. This
feature is important in assessing the severity
of pollution. Moreover, certain frequency
distributions have been well studied and lend
themselves to statistical analysis. The fre-
quency distribution of the available data can
then be used to determine whether one of
these common distributions may be fitted,
thereby facilitating the extraction of statis-
tical parameters of the data.
Most .samples of atmospheric pollution
concentrations have been found to exhibit a
log-normal frequency distribution. Simply
stated, this implies that the logarithms of the
concentrations have a gaussian (normal) distri-
bution; therefore, the wealth of statistical
techniques used with normally distributed
data may be applied as well to the logarithms
of aerometric data.
One such technique is the use of proba-
bility graph paper to graphically depict a
distribution under consideration. When the
cumulative frequency distribution of a collec-
tion of air quality measurements is plotted on
log-versus-normal-probability paper, the re-
sulting curve can usually be approximated by
a straight line. The concentration at the 50
percent mark, representing the arithmetic
median value, is termed the geometric mean.
Theoretically, half of the time measured con-
centrations will be below this value and half
of the time they will be above it.
For a log-normal distribution, the geo-
metric mean is a measure of central tendency.
Similarly, the 84.13 percentile value divided
by the 50.00 percent value (geometric mean)
6-17
-------
is termed the standard geometric deviation
and is a measure of the dispersion of the data.
Knowing these two values permits determina-
tion of the entire distribution.
The arithmetic mean of log-normally-
distributed air-quality measurements is always
larger than the geometric mean. The arithme-
tic mean, m, may be calculated16 from the
geometric mean, Mg, and standard geometric
deviation (ag), by means of the following
equation:
log m = log Mg + 1.151 (logag)2
All of the CAMP data for the periods 1962
through 1967 inclusive have been analyzed to
give concentration as a function of averaging
time and frequency. Examples of the types of
summaries that may be extracted from these
data are shown in Tables 6-1 and 6-4, and
Figure 6-6.
Table 6—4 shows a summary of 5-minute
CO concentrations measured continuously for
6 years in Chicago. As indicated in the table,
the 8-hour-averaging-time concentrations of
CO from 5-minute values measured at the
CAMP site in Chicago from December 1,
1961, to December 1, 1967, had an arithme-
tic mean of 14 mg/m3 (12 ppm), a maxi-
mum of 51 mg/m3 (44 ppm), and a minimum
of 0 mg/m3 (0 ppm). Data were available for
55 percent of all the 8-hour periods. The
8-hour-averaging-time measured concentra-
tions exceeded 24 mg/m3 (21 ppm) for 10
percent of all the 8-hour periods for which
values were available and exceeded 14 mg/m3
(12 ppm) half of the time (50 percentile).
Table 6—1, prepared by using a similar
analysis, presents comparable data for the
entire CAMP network.
It is evident by proceeding down the per-
centile columns in Table 6—4 or by reference
second
i
10,000
i.ooo
AVERAGING TIME,
minute hour day
5 1015 30 I 2 4 8 12 1 2 4
month
2361
year
3
o
LU
O
z
o
o
0 1
0.01
T
1 T
T
T~
T~T
200.3
79.7
53.6
38.5 32.5
19.0
14.1
EXPECTED ANNUAL MAXIMUM CONCENTRATION, ppm
O O O OO
GEOMETRIC MEAN FOR 1-hour AVERAGE IS 13.2 PP"
STANDARD GEOMETRIC DEVIATION IS 1.44
54 percent OF HOURS HAVE DATA AVAILABLE"
0.0001 0.001 0.01 0.1 1 10
AVERAGING TIME, hours
100
1,000
10,000
Figure 6-6. Concentration versus averaging time and frequency for carbon monoxide from
December 1, 1961, to December 1, 1967, Chicago CAMP station.
6-18
-------
to Figure 6-6 that the magnitude of concen-
trations greater than the geometric mean tend
to decrease with an increase in averaging time
whereas the magnitude of concentrations less
than the geometric mean tend to increase
with an increase in averaging time. Similarly,
the geometric mean concentration for any
averaging time tends to remain relatively con-
stant. These trends are inherent in the averag-
ing process and result in a decrease in the
dispersion of the concentration values as the
time over which these concentrations are
averaged increases. As would be expected, this
decrease in dispersion is reflected in a de-
crease of standard geometric deviation with
increasing averaging time.
d. An Air Quality Model
Certain trends become apparent when the
frequency of occurrence of various CO con-
centrations and their variability with averag-
ing time are examined. In an extensive anal-
ysis of urban pollution data, Larsen17 has
found that:
1. Concentrations are approximately log-
normally distributed for CO and other
pollutants in all cities for all averaging
times.
2. The median concentration (50th per-
centile) is proportional to the averag-
ing time raised to an exponent.
These two factors greatly simplify the anal-
ysis of aerometric data. The former implies a
common form of distribution of concentra-
tions, independent of geographic location and
amenable to statistical analysis. Such a distri-
bution plots as a straight line on a log-versus-
probability scale; therefore the distribution
may be defined by relatively few points. The
latter factor implies that once the distribution
of concentrations for one averaging time is
known, distributions for other averaging times
may then be calculated.
These characteristics of the measurement
data have been used to build a statistical
model expressing air pollutant concentration
as a function of averaging time and frequency.
The accuracy of this model in depicting the
expected air quality of a region depends on
certain characteristics of the sampling data
input; the larger the sample and the closer the
sample data to meeting the two conditions
cited above, the more accurately will the
model simulate reality. (Because of the strong
dependence of this model on the assumption
of log normality and the ease with which a
data set may be checked for exhibition of a
log-normal distribution, i.e., the use of the log-
versus-normal-probability paper, it is wise to
check any data set against this assumption.
before applying the model.)
Two values of air quality, the 1-hour-aver-
aging-time concentration that is exceeded 0.1
percent of the time and the 1 -hour-averaging-
time concentration that is exceeded 30 per-
cent of the time, are used to produce a model
that best depicts the most polluted half of the
air samples, which are of greatest interest.
One-hour averaging times are used because the
model is general for gaseous air pollutants and
the response times for some air-sampling
instruments (such as those for nitrogen
oxides) may be as long as a half hour (thus
causing errors in concentration measurements
averaged over less than 1 hour). Another rea-
son is that more data averaged over 1 hour are
available than for any other averaging period.
3. Eight-hour 0.1 Percentile Averages
In the CO data to follow, the concentra-
tions listed are those that were exceeded at a
particular sampling site 0.1 percent of the
time. There are 1095 discrete 8-hour periods
contained in a year; therefore, the 0.1 per-
centile value approximates the 8-hour-aver-
aging-time concentration likely to be ex-
ceeded an average of once a year. This value
then represents an estimate of the highest
8-hour exposure to which an individual would
be subjected in a particular community annu-
ally. The sampling year was chosen to begin at
midnight on December 1.
a. CAMP Observations
Figure 6—7 depicts the 0.1 percentile
8-hour-averaging-time CO concentrations
recorded at CAMP sites throughout the
Nation. These stations, which use similar
measurement techniques, are located in the
6-19
-------
Figure 6-7. Eight-hour-averaging-time carbon
monoxide concentrations (ppm) exceeded 0.1
percent of the time at CAMP sites, 1962
through 1967.
central business area from 10 to 100 feet
from the edge of the street, depending on
local considerations. The values depicted in
Figure 6-7 range from 15 mg/m3 (13 ppm)
in San Francisco to 40 mg/m3 (35 ppm) in
Chicago and are, on the average, 3.4 times the
median (geometric mean) concentrations
recorded at these sites.
Maximum air pollutant concentrations
within a community (including CO) may vary
markedly from year to year. The maximum
measured in one year in a particular commun-
ity may be twice the maximum measured in
another year. This is the case, for instance in
Chicago, Cincinnati, and Washington (Table
6-1), where the maximum 8-hour concentra-
tion measured in each of these cities in the
most polluted year is about twice the maxi-
mum concentration measured in the cleanest
year. The developed statistical model has been
used to calculate the maximum concentration
predicted to occur on the average of once a
year, i.e., the calculated annual maximum
8-hour concentration. For any averaging time,
although observed year-to-year mean and
peak CO values may vary markedly within
any community, the calculated annual
maximum value remains constant.
b. California Observations
Continuous air monitoring networks have
been operated by the State of California and
by the County of Los Angeles for a number
of years. The localized patterns of CO concen-
tration that have been observed and measured
on a continuous basis in these two networks
reveal the CO variability from time to time
and place to place. Using an analysis similar to
that used for the CAMP data in Table 6-1,
comparable information is presented for the
State of California in Table 6-2. The values
for 8-hour-averaging time CO concentrations
that are exceeded 0.1 percent of the time at
various California sites are plotted in Figure
6-8.
• BAKERSFIELD
"•SANTA BARBARA
Figure 6-8. Eight-hour-averaging-time carbon
monoxide concentrations (ppm) exceeded 0.1
percent of the time at various California
sites, 1963 through 1967.
Similar data from the Los Angeles Area are
given in Table 6—3 and shown in Figure 6-9.
The concentration range displayed in Figure
6-9 is from 12 to 46 mg/m3 (10 to 40 ppm).
As noted at the end of Table 6—3, Los
Angeles County estimates that water vapor
contributed up 5 mg/m3 (4 ppm) of their
measured carbon monoxide concentrations.
This water vapor interference is a function of
6-20
-------
'-I
\
LOS ANGELES COUNTY
\
\
\
»
SAN FERNANDO
\ \VALLEY
35
25 20
30
18
/
15
/
18./
.r
,34 BURBANK
I 37* «37
HOLLYWOOD,
36 ST HfS
OWNTOWN
21 li? /
« ^jj""^VJ
I* DISNEYLAND \
/
v»; LONG BEACH
SAN BERNARDINO
19
« REDLANDS
414
/
~y
RIVERSIDE
Figure 6-9. Eight-hour-averaging-time carbon monoxide concentrations (ppm) exceeded 0.1
percent of the time in Los Angeles area, 1956 through 1967.
the absolute humidity, as was discussed in
Chapter 5. Considering the humidity range in
the Los Angeles area, it would be expected,
on the basis of the curve shown in Figure
5—1, that water vapor interference would be
on the order of up to 12 mg/m^ (10 ppm)
rather than the- stated 1 to 5 mg/m^ (1 to 4
ppm.) This later expectation cannot be
checked, however, with any degree of cer-
tainty because the water vapor interference
study depicted in Figure 5—1 was not deter-
mined with Los Angeles County instruments.
Nevertheless, it is important to recognize that
water vapor was affecting the reported CO
values for Los Angeles County prior to April,
1968. Since that time, the instruments have
been modified to eliminate this interference.
4. Special Carbon Monoxide Exposure
Situations
a. Variations with Type of Vehicle Traffic
Larsen and Burke18 have recently ana-
lyzed, using the frequency distribution de-
scribed earlier, aerometric CO data from a
variety of sampling locations in many cities.
These studies included data from various
cities of the continuous air monitoring net-
works, commuter traffic surveys, and special
studies. The data were treated so as to calcu-
late on a uniform basis the maximum 8-hour
averaging time concentrations to be expected
annually. This was done for values measured
in the following situations:
1. Vehicles in downtown traffic.
6-21
-------
E
a.
o
H
LLJ
(J
o
u
X
o
o
cfl
u
200
100
80
60
40
20
10
8
w r\ •
IN VEHICLES IN DOWNTOWN TRAFFIC U
IN VEHICLES TRAVELING EXPRESSWAYS Q
AND ARTERIAL ROUTES O
IN RESIDENTIAL-COMMERCIAL AREAS O
IN MIXED INDUSTRIAL AREAS
IN COMMERCIAL AREAS
— •— IN RESIDENTIAL AREAS
10
20
30
40 50 60
70
80
90
95
98
PERCENT OF SAMPLING SITES WHERE STATED CONCENTRATION IS EXPECTED TO BE
EXCEEDED ONCE A YEAR
Figure 6-10. Maximum annual 8-hour-averaging-time concentrations of carbon monoxide
expected at various types of sites.
2. Vehicles on expressways or arterial
routes.
3. Residential-commercial areas.
4. Mixed industrial areas.
5. Commercial areas.
6. Residential areas.
The results are shown in Figure 6—10.
Studies of the first two types of exposure
have been conducted.19"34 The average citi-
zen is not often subject to the first two types
of exposure for 8 hours. Nevertheless, cab
drivers, bus drivers, delivery truck drivers, and
some policemen are so exposed. A number of
epidemiological studies on occupationally ex-
posed groups are discussed in Chapter 9.
Figure 6-10 shows that, if the most pol-
luted 5 percent of the off-street central urban
6-22
areas represented by the commercial classifi-
cation were selected, then the maximum
8-hour annual concentration would approxi-
mate 36 mg/m3 (40 ppm). The CO concentra-
tions expected inside the passenger compart-
ment of motor vehicles on city streets in
heavy traffic at the most polluted 5 percent
of the locations would be almost 3 times this
level, or 132 mg/m3 (115 ppm). In vehicles
travelling on expressways or arterial routes,
the value would be 85 mg/m3 (75 ppm), and
in residential or suburban areas the value
would be about 26 mg/m3 (23 ppm). The CO
concentrations in downtown traffic appear to
be about 5 times those found in residential
areas. Similar findings reported by Colucci
and Begeman are illustrated in Figures 6-1
and 6—2.
-------
b. Car Passenger Exposure to Carbon
Monoxide
Each working day a sizeable segment of the
population spends considerable time driving
in traffic of varying density. During that time
most vehicle occupants are exposed to higher
concentrations of CO than they would other-
wise encounter.
The results of a study of driver exposure to
CO for 20- to 30-minute periods over various
driving routes are given in Table 6—5.4>21
The results indicate that exposure levels vary
with vehicular route. Average CO concentra-
tions were highest on center city routes,
somewhat lower on arterial routes, and lowest
on expressway routes.
c. Severe Carbon Monoxide Exposure
Locations
While significant concentrations of CO,
which affect large subgroups of the popula-
tion, occur on city streets, even higher con-
centrations, often exceeding 100 mg/m3 (84
ppm), have been reported in underground
garages, tunnels, and loading platforms.25-28
A survey was conducted recently by the
National Air Pollution Control Administra-
tion at the Chicago Post Office in the Air
Rights Building, which is built over a four-
lane vehicle expressway. Preliminary results
indicate that CO concentrations ranged from
17 to 89 mg/m3 (15 to 77 ppm) at the east
loading platform of the building, with an
average concentration of 47 mg/m3 (41 ppm).
The west loading platform showed CO levels
that ranged from 9 to 75 mg/m3 (8 to 65
ppm), with an average of 28 mg/m3 (24
ppm). Other locations and rooms showed
lower CO concentrations.2 9
Chovin2 8 has recorded average CO levels of
170 mg/m3 (150 ppm) between 7:30 and
8:00 a.m. and 210 mg/m3 (180 ppm) be-
tween 7:30 and 8:00 p.m. in the air of a Paris
police garage. Trompeo30 et al. measured the
CO levels in 12 underground garages in Rome.
The average CO level based on 132 readings
was 113 mg/m3 (98 ppm), ranging from a
minimum of 12 mg/m3 (10 ppm) to a maxi-
mum of 350 mg/m3 (300 ppm). Forty-two
percent of the readings showed CO levels of >
115 mg/m3 (100 ppm).
Waller25 et al. reported on CO concentra-
tions in the Blackwell and Rotherhithe
Tunnels in London during periods of high
traffic volume. The mean CO concentrations
during the morning and evening "rush" hours
were slightly more than 115 mg/m3 (100
ppm). While the usual sampling periods were
short, one of the sampling periods in the
Rotherhithe Tunnel exceeded 1.75 hours.
This study indicated that peak CO levels
reached 600 mg/m3 (500 ppm) at midnight
on a Sunday; other peaks were 500 mg/m3
(450 ppm) on a Friday evening and 390 mg/m3
(340 ppm) on a Saturday evening. (The fans
in these tunnels were shut off during the
night, thereby reducing ventilation.) Wilkins
reported earlier that CO concentrations in the
Blackwell Tunnel ranged from 170 to 680
mg/m3 (150 to 590 ppm) in September 1954.
Other air samples taken in this tunnel be-
tween June and December 1955 showed CO
levels ranging from 270 to 540 mg/m3 (235
to 470 ppm) CO during the morning rush
hours.3 1
d. Indoor Levels of Carbon Monoxide
Carbon monoxide found inside buildings
may be attributable to internal sources such
as space heating units and cooking stoves as
well as sources outside the building.35
In 1969 NAPCA supported a preliminary
study of the contribution of both outdoor
and indoor sources to levels of CO in single-
family homes.36 Figure 6—11 shows that the
major source of CO in the house with gas-
burning devices was inside the house,
although between 8 and 10 p.m. on Friday an
outdoor source was dominant. Figure 6—12,
which probably represents an extreme situa-
tion, indicates the presence of a strong CO
source in the house. Further investigation
showed that a leaky hand-fired coal-burning
furnace was the offender.
6-23
-------
Table 6-5. IN-TRAFFIC 20- TO 30-MINUTE CARBON MONOXIDE EXPOSURES FOR VARIOUS DRIVING ROUTES
City
Atlanta
Baltimore
Chicago
Chicago
Cincinnati
Cincinnati
Denver
Detroit
Houston
Louisville
Los Angeles
Minneapolis-
St. Paul
Minneapolis
St. Paul
New York
New York
Philadelphia
Phoenix
St. Louis
Washington
All
Date
May 11-17, 1966
April 8-15, 1966
May 2S-June 8, 1966
Feb 27-Mar 17, 1967
Aug 2, 16, 17, 1966
June 1967
Sept 19-30, 1966
June 13, -July 14, 1966
Dec 5, 1966-Jan 29, 1967
Mar 1-4, 1966
Oct-Nov 3, 1966
Aug 29 -Sept 9, 1966
Aug 29-Sept 9, 1966
Aug 29-Sept 9, 1966
April 21 -May 5, 1966
May 1-31, 1967
June 1-16, 1967
Nov 9-18, 1966
Feb 6-17, 1967
April 5-27, 1967
Mar 1966-June 1967
Center city routes
No.
runs
7
14
17
10
8
6
10
16
14
10
17
15
13
48
30
20
12
19
34
320
Average CO concentrations, ppm
Min.
13
15
24
19
17
12
21
15
16
16
27
20
21
14
9
18
27
15
8
8
Avg.,
all
runs
21
24
32
34
29
20
34
25
38
23
40
30
35
32
27
29
38
28
26
30
90th
percentile
27
34
40
50
48
32
49
35
60
33
59
44
58
44
39
37
53
45
42
44a
Max.
27
38
55
53
50
32
54
36
70
33
60
45
65
58
42
38
54
50
63
70
Arterial routes
No.
runs
9
25
51
28
25
11
41
51
23
14
15
59
Average CO concentrations, ppm
Min.
21
6
7
1
3
9
11
14
5
4
24
10
Avg.,
all
runs
30
17
16
16
17
15
32
25
15
16
38
23
90th
percentile
38
29
21
27
26
19
47
33
28
26
58
36
Max.
40
33
31
41
32
19
61
41
33
31
60
41
No arterial runs made
No arterial runs made
40
26
38
17
473
9
13
8
10
1
22
27
17
20
22
35
37
23
29
33a
38
43
34
30
61
Expressway routes
No.
runs
10
18
31
35
7
24
24
48
31
14
87
Average CO concentrations, ppm
Min.
12
2
13
3
3
7
10
11
2
2
9
Avg.,
all
runs
23
9
24
20
10
15
21
25
16
8
29
90th
percentile
33
19
34
31
15
24
33
33
33
15
47
Max.
35
21
37
35
15
34
38
54
39
21
62
No expressway runs
31
17
20
39
37
35
508
8
5
8
12
2
2
2
23
21
17
23
10
12
18
36
38
28
34
17
26
29a
45
39
38
50
22
33
62
aEstimated.
-------
e 3
X
O
z
o
CO
K
<
U
/:r-
//I-
••* « I •
• I I • ».
• I I • •
'. ' • \ '
I I • •
\ '•
• •
INDOORS, KITCHEN
OUTDOORS
"V ^ > —
12
-p.m.
FRIDAY
12
-U-
12
SATURDAY
HOUR OF DAY
4 8
p.m.
12
-*U-
12
SUNDAY
Figure 6-11. Hourly average CO levels inside and outside gas-heated house with gas-
burning kitchen stove.36
e. Projected Future Trends
A number of studies and calculations of fu-
ture CO emissions and concentrations from
urban traffic data have been made; other stud-
ies are in progress. Ott3 2 et al. calculated pres-
ent and future CO emissions and ambient CO
concentrations in Washington, D.C., using
1964 and projected 1985 traffic volumes and
emission factors with a meteorological diffu-
sion model. They found that: (1) with no
emission control, the total CO emitted in
Washington will approximately double in a
nonuniform manner; the smallest increases
will occur downtown and the greatest increas-
es in the outskirts; (2) the principal effect of
such nonuniformity, also apparent in Chicago,
is to increase the area of the city exposed to
high emission densities, leading to consequent
increases in the area over which higher con-
centrations occur; (3) without control, the
mean annual CO concentrations at four select-
ed sites in Washington would range from 2.5
to 12.6 mg/m3 (2.2 to 11.0 ppm) in 1985,
representing increases of from 44 to 69 per-
cent over the 1964 values.
A corollary to finding No. 2 above is ap-
parent. If the area of a city subjected to high
pollutant concentrations is increased, the pop-
ulace in some downwind parts of that area
will be exposed to high concentrations for
longer periods of time than previously, be-
cause cleaner air has to come from farther
away. The probability of exceeding a given
8-hour-average CO concentration is, therefore,
increased; or, conversely, the 0.1 percentile
level in Larsen's model1 7 will be higher.
Taking the increase presented in No. 3
above to be about 50 percent implies that if
maximum urban concentrations approxi-
mated 45 mg/m3 (40 ppm) in 1965, and if
CO from motor vehicles were not controlled,
concentrations of about 70 mg/m3 (60 ppm)
would be expected in 1985. In-vehicle con-
centrations of at least twice this, or 140
mg/m3 (120 ppm), would be expected.
6-25
-------
UJ
O
X
o
o
CO
o:
<
u
60
50
40
30
20
10
INDOORS, LIVING ROOM
OUTDOORS
12
-p.m.
12 4 8 12 4 8 12
>l< a.m. ^4-< p.m. ^l<
12
MONDAY
TUESDAY
HOUR OF DAY
-a.m.-
WEDNESDAY
Figure 6-12. Hourly average CO levels inside and outside house heated with hand-
fired coal-burning furnace.^
E. METEOROLOGICAL DIFFUSION
MODELS
Emissions data provide a general idea of the
presence of certain pollutants in a given area
and may be thought of as showing the poten-
tial for exceeding an atmospheric concentra-
tion. Whether this potential is realized de-
pends strongly on meteorological factors.
These factors have, consequently, been sub-
jected to much study. Simple meteorological
indices, such as the number and persistence of
low-level inversions per year, give some indica-
tion of the frequency with which unfavorable
meteorological conditions occur in a particu-
lar region. In recent years much effort has
gone into the development of relatively com-
plex models that permit a quantitative estima-
tion of the effect of weather on the dispersion
of the pollutant.32-34-37-39
6-26
Georgii et al.40 studied CO concentrations
in Frankfurt/Main. The summarized results
are:
1. The temporal pattern of CO emission
in streets is determined by traffic
density.
2. In cities, CO concentration distribu-
tions, both lateral and vertical, are
largely dependent on wind speed and
direction relative to building configu-
ration.
3. Highest concentrations are measured
during periods of rush hour traffic
that occur during periods of minimal
atmospheric dilution.
4. Wind flow above rooftop level is effec-
tive at street level only at speeds great-
er than 2 meters per second (4.5
mi/hr); at wind speeds greater than 5
-------
meters per second (11 mi/hr) at roof
height a complete mixing of the street
air takes place.
5. The effect of wind direction is that
higher CO concentrations are pro-
duced on the leeward sides of build-
ings.
The mathematical-meteorological model is
a useful tool with which to examine the at-
mospheric impact of the various sources of
CO. Although much information may be ob-
tained from such a model, the user should be
aware of the nature and limitations inherent
in the particular model he has chosen for use.
For example, the relative frequency of occur-
rence and averaging time of predicted concen-
trations along with limitations imposed by
terrain are integral parts of every model. Such
features must be evaluated before application.
The input to all diffusion models consists
of emission and meteorological parameters.
Normally, the former category includes pol-
lutant emission rates and source heights, and
the latter includes wind velocities and those
parameters that determine atmospheric dis-
persion. The output from these models is
usually in the form of a pollutant concentra-
tion at specified locations. The gaussian dif-
fusion equation is the most widely accepted
of its type and forms the basis of most mod-
els. Turner has described this equation and its
use.4 *
The modelling of CO emission and disper-
sion is complicated by the fact that the chief
source of CO, the motor vehicle, is a multiple
source and is mobile, rather than a source at a
fixed point. However, the use of CO in diffu-
sion models also simplifies some aspects of
the modelling effort. Since automotive-
generated CO is usually of primary concern,
source height may be considered as constant
at ground level. Also, no consideration of
effective residence time, i.e., removal rate of
CO, is required because of the assumed stabili-
ty of this pollutant in an urban environment.
By incorporating into a model assumptions
about the way traffic flows and distributes
the CO over particular routes or throughout
the city, it is possible to apply a simulation
approach to this pollutant.
These models are usually used to estimate
concentrations for one source-receptor pair at
a time. In order to estimate the air quality at
a chosen location, it is necessary to perform a
large number of these individual calculations
and sum the results. Additionally, the air
quality of a region is determined by examin-
ing the concentrations predicted for many in-
dividual points. Because of the magnitude of
the number of calculations to be performed,
electronic data processing is almost always
needed.
In order to evaluate the accuracy of a given
model, the general practice has been to com-
pare measured concentrations at a particular
receptor location with those predicted by the
model. The model usually then is "calibrated"
with respect to these measured concentra-
tions. For CO, diffusion models usually pre-
dict concentrations of 0.5 to 0.1 of those
measured at the monitoring station.32' 42-48
This difference is attributed to the effect of
street traffic near the station, which is not
allowed for in these models. In addition,
although not nearly as important, some part
of the concentrations measured in urban areas
may be contributed by nonautomotive
sources or by meteorological transport of pol-
lutants from other cities. This factor also is not
recognized in these models. These variables,
therefore, must be accounted for in the appli-
cation of such models.
In using atmospheric diffusion models,
meteorologists have been called on mostly to
provide estimates of seasonal or annual mean
CO concentration distributions over urban
areas, where spatial scales of 1 to 100 kilo-
meters (0.6 to 62 miles) are of primary inter-
est. For these applications, the CO emission
inventories available as input to the diffusion
model permit only a relatively large-scale or
gross treatment of the data. The local effects
connected with travel distances of less than 1
kilometer are determined predominantly by
aerodynamic or micrometeorological mech-
anisms, rather than atmospheric diffusion and
transport or macrometeorological mecha-
nisms.
6-27
-------
F. SUMMARY
Diurnal, weekly, and seasonal patterns of
CO concentrations correspond to man's pat-
tern of activities and to meteorological fac-
tors. Since urban CO concentrations generally
correlate with the community traffic volume,
there are usually two peaks in concentration
corresponding to the morning and evening
rush hours. Peak concentrations are higher on
weekdays than on weekends and holidays be-
cause of the greater weekday rush-hour traffic
volume. Distinct seasonal patterns are due
primarily to both traffic and meteorological
variables; the mean concentration of CO is
generally higher in autumn and summer than
in spring and winter.
Both macro- and micrometeorological fac-
tors affect the rate of dispersion of ambient
CO. The former is a predominant factor in
areawide dispersion; the latter, in local disper-
sion. Atmospheric stability and wind speed
are important macrometeorological factors;
mechanical turbulence produced by auto-
mobiles and airflow around buildings is an im-
portant micrometeorological factor.
Because of physiological considerations,
the averaging time of most interest for CO is 8
hours. A statistical model has been developed
to convert CO aerometric data based on var-
ious averaging times to data based on a uni-
form 8-hour-averaging time. Based on prob-
ability theory, the 0.1 percentile 8-hour-
averaging time CO concentration approxi-
mately represents the worst 8-hour period to
be expected in a year. An analysis of air moni-
toring data indicates that 0.1 percentile
8-hour-averaging-time urban CO concentra-
tions vary from approximately 12 to 46
mg/m3 (10 to 40 ppm). Analyses of CAMP
data suggest that these 0.1 percentile values
averaged about 3 times the corresponding
median annual CO values.
A statistical analysis of CO aerometric data
from 30 technical papers was made. The data
were reviewed in order to calculate, on a uni-
form basis, the maximum 8-hour averaging
time concentrations expected annually. From
these calculations, it is estimated that, for the
most polluted 5 percent of the urban sites,
the maximum annual 8-hour average in
commercial areas would approximate 46
mg/m3 (40 ppm), in motor vehicles in down-
town traffic it would approximate 132
mg/m3 (115 ppm), and in vehicles on express-
ways or arterial routes the value would be
about 85 mg/m3 (75 ppm). The CO concen-
trations in heavy traffic in city streets were
almost 3 times the CO levels found in the
central urban areas, and 5 times the CO levels
found in residential areas.
Concentrations exceeding 100 mg/m3 (87
ppm) have been measured in underground
garages, in tunnels, and in buildings con-
structed over highways.
Using emission and meteorological data,
diffusion models are capable of estimating CO
concentrations at a particular receptor point,
thus enabling the evaluation of community air
quality under a variety of conditions.
G. REFERENCES
1. Dickinson, J. E. Air Quality of Los Angeles
County. Air Pollution Control District, Los
Angeles. Technical Progress Report, Vol. II.
February 1966.
2. Continuous Air Monitoring Program, Washing-
ton, D.C. 1962-1963. Division of Air Pollution.
Cincinnati, Ohio. PHS Publication Number
999-AP-23. 1966. 215 p.
3. Brief, R. S., A. R. Jones, and J. D. Yoder. Lead,
Carbon Monoxide, and Traffic, a Correlation
Study. J. Air Pollution Control Assoc.
70(5):384-388, October 1960.
4. The Automobile and Air Pollution: A Program
for Progress. Part II. Subpanel Reports to the
Panel on Electrically Powered Vehicles. U.S.
Dept. of Commerce. Washington, D.C. U.S. Gov-
ernment Printing Office. December 1967. 160 p.
5. Hamming, W. J., R. D. MacPhee, and J. R.
Taylor. Contaminant Concentrations in the
Atmosphere in Los Angeles County. J. Air Pollu-
tion Control Assoc. 70(1):7-16, February 1960.
6. Colucci, J. M. and C. R. Begeman. Carbon Mon-
oxide in Detroit, New York, and Los Angeles
Air. Environ. Sci. Technol. 3:41-47, January
1969.
7. Johnson, K. L., L. H. Dworetzky, and A. N.
Heller. Carbon Monoxide and Air Pollution from
Automobile Emissions in New York City. Sci-
ence. 7<50(3823):67-68, April 5, 1968.
8. McCormick, R. A. and C. Xintaras. Variation of
Carbon Monoxide Concentrations as Related to
6-28
-------
Sampling Interval, Traffic, and Meteorological
Factors. J. Appl. Meteorol. 1(2):237-243, June
1962.
9. Clayton, G. D., W. A. Cook, and W. G. Fredrick.
A Study of the Relationship of Street Level Car-
bon Monoxide Concentrations to Traffic Acci-
dents. Amer. Ind. Hyg. Assoc. J. 27:46-54, Feb-
ruary 1960.
10. Continuous Air Monitoring Projects - 1962-1967
Summary of Monthly Means and Maximums.
National Air Pollution Control Administration.
Washington, D.C. Publication Number APTD
69-1. April 1969.
11. Georgii, H. W. and E. Weber. Investigations of
Carbon Monoxide Emissions in a Large City. Int.
J. Air Water Pollution. 6:179-195, May-August
1962.
12. Tebbens, B. D. Gaseous Pollutants in the Air. In:
Air Pollution, Stern, A. C. (ed.), Vol. 1, 2d ed.
New York, Academic Press, 1968. p.28-33.
13. Lawther, P. J., B. T. Commins, and M. Hender-
son. Carbon Monoxide in Town Air. An Interim
Report. Ann. Occup. Hyg. 5:241-248, October-
December 1962.
"14. Chovin, P. Etudes de Pollution Atmospherique a
Paris et dans les Departments Peripheriques en
1967, Laboratoire Centrale. Paris. June 1968.
15. Castrop, V. J., J. F. Stephens, and F. A. Patty. A
Comparison of Carbon Monoxide Concentrations
Detroit and Los Angeles. Amer. Ind. Hyg. Assoc.
Quart. 76(3):225-229, September 1955.
16. Hatch, T. and S. P. Choate. Statistical Descrip-
tion of the Size Properties of Non-Uniform Par-
ticulate Substances. J. Franklin Inst.
207:369-387, 1929.
17. Larsen, R. I. A New Mathematical Model of Air
Pollutant Concentration, Averaging Time and
Frequency. J. Air Pollution Control Assoc.
79:24-30, January 1969.
18. Larsen, R. I. and H. W. Burke. Ambient Carbon
Monoxide Exposures. Presented at the 62nd
Annual Meeting of the Air Pollution Control
Association. New York. June 1969.
19. Haagen-Smit, A. J. Carbon Monoxide Levels in
City Driving. Clean Air Quarterly 8(4):8-9,
December 1964. Also in: Arch. Environ. Health
72(5):548-551,May 1966.
20. Brice, R. M. and J. F. Roesler. The Exposure to
Carbon Monoxide of Occupants of Vehicles Mov-
ing in Heavy Traffic. J. Air Pollution Control
Assoc. 76(11):597-600, November 1966.
21. Lynn, D. A. et al. Present and Future Commuter
Exposures to Carbon Monozide. Presented at the
60th Annual Meeting of the Air Pollution Con-
trol Association. Cleveland. June 11-16, 1967. p.
67-75, 188.
22. Georgii, H. W. The Concentration of Carbon '
Monoxide Measured at Different Altitudes Simul- '_
taneously in City Streets [Die Vertikalverteilung -,'
des Kohlenmonoxid in Grossstadtstrassen in
Abhangigkeit von den Meteorologischen Bedin-
gungen] In: Proceedings of International Clean
Air Congress Part I, October 4-7, 1966. Lon-
don, National Society for Clean Air, 1966. p.
209-210.
23. Ramsey, J. M. Concentrations of Carbon Mon-
oxide at Traffic Intersections in Dayton, Ohio.
Arch. Environ. Health. 75(l):44-46, July 1966.
24. Waller, R. E., B. T. Commins, and P. J. Lawther.
Air Pollution in a City Street. Brit. J. Ind. Med.
22(2): 128-138, April 1965.
25. Waller, R. E., B. T. Commins, and P. J. Lawther.
Air Pollution in Road Tunnels. Brit. J. Ind. Med.
7
-------
36. Yocum, J. E., Cote, W. A., and Clink, W. L. Sum-
mary Report of a Study of Indoor-Outdoor Air
Pollutant Relationships to the National Air Pollu-
tion Control Administration, Travelers Research
Corporation, Hartford, Connecticut.
37. Clarke, J. R. A Simple Diffusion Model for Cal-
culating Point Concentrations from Multiple
Sources. J. Air Pollution Control Assoc.
74:347-352, September 1964.
38. Miller, M. E. and G. C. Holzworth. An Atmos-
pheric Diffusion Model for Metropolitan Areas.
J. Air Pollution Control Assoc. 77:46-50, Janu-
ary 1967.
39. Ott, W. and R. Fankhauser. Models for Calculat-
ing Carbon Monoxide Concentrations on Streets.
National Air Pollution Control Administration,
Durham, N.C. Unpublished report. 1967.
40. Georgii, H. W., E. Busch, and E. Weber. Investi-
gation of the Temporal and Spatial Distribution
of the Emission Concentration of Carbon Mon-
oxide in Frankfurt/Main. University of Frank-
furt/Main. Institute for Meteorology and Geo-
physics. Germany. May 1967.
41. Turner, D. B. Workbook of Atmospheric Disper-
sion Estimates. National Center for Air Pollution
Control. Cincinnati, Ohio. PHS Publication Num-
ber 999-AP-26. 1967. 84 p.
42. Martin, D. O. and J. A. Tikvart. A General
Atmospheric Diffusion Model for Estimating the
Effects on Air Quality of One or More Sources.
Presented at 61st Annual Meeting, Air Pollution
Control Association. St. Paul, Minn. June 1968.
43. Report for Consultation on the Air Quality Con-
trol Region for the New Jersey-New York-Con-
necticut Interstate Area. National Air Pollution
Control Administration. Washington, D.C.
August 30, 1968. 95 p.
44. Report for Consultation on the Metropolitan
Chicago Interstate Air Quality Control Region
(Indiana-Illinois). National Air Pollution Control
Administration. Washington, D.C. September
1968. 85 p.
45. Report for Consultation on the Metropolitan
Philadelphia Interstate Air Quality Control
Region (Pennsylvania-New Jersey-Delaware),
U.S. Dept. of Health, Education, and Welfare,
Public Health Service. October 1968. 74 p.
46. Report for Consultation on the Metropolitan Los
Angeles Air Quality Control Region. National Air
Pollution Control Administration. Washington,
D.C. November 1968. 79 p.
47. Report for Consultation on the Washington, D.C.
National Capital Interstate Air Quality Control
Region. National Air Pollution Control Adminis-
tration. Raleigh, N.C. July 1968. 77 p.
48. Report for Consultation on the Metropolitan
Denver Air Quality Control Region. National Air
Pollution Control Adminstration. Washington,
D.C.October 1968. 80 p.
6-30
-------
CHAPTER?.
EFFECTS OF CARBON MONOXIDE ON
PLANTS AND CERTAIN MICROORGANISMS
A. GENERAL DISCUSSION
Plants are relatively insensitive to carbon
monoxide (CO) at the lower levels of concen-
trations that have been found to be toxic for
animals. Much of the early research on the
effects of CO on plants was motivated by the
assumption that the phytotoxicant in smoke
and illuminating gas was CO and the knowl-
edge that plants may be sensitive to some air
pollutants at concentrations that do not
affect animals. Knight and Crocker1 were the
first to demonstrate that ethylene was the
effective contaminant in smoke and illuminat-
ing gases and that CO had little or no effect
on plants. Much of the early literature re-
ferred to studies with impure or undeter-
mined sources of CO. Carr,2 who reviewed
the literature up to 1961, concluded that CO
was not particularly toxic to plants. Although
injury from CO and ethylene was similar,
5,000 times more CO than ethylene was
required to cause injury.
Most of the work on effects of CO on
plants was done in the 1920's and 1930's at
Boyce Thompson Institute, where Zimmer-
man, Hitchcock, and Crocker3 >4 exposed over
100 species to experimental concentrations
ranging from 115 to 575,000 mg/m3 (100 to
500,000 ppm). The plants were exposed to
CO under bell jars or in Wardian cases, with
apparently no regulation of concentration
after introduction of the gas into the
chamber. Exposure time ranged from 7 to 23
days. Concentrations of 115 mg/m3 (100
ppm) caused "practically" no growth retarda-
tion, suggesting that concentrations of CO
needed to affect plant growth were consider-
ably higher than those normally encountered
in ambient air.
The experiments at Boyce Thompson Insti-
tute showed that plant species varied widely
in their susceptibility to CO and in symptom
expression. The most important detrimental
responses were: (1) epinasty (downward curl)
and hyponasty (upward curl) of leaf stem; (2)
increased rate of aging of leaves and stimula-
tion of abscission of leaves, flower buds, and
fruits; (3) overgrowth of lenticular tissue; (4)
retardation of stem growth; (5) reduction of
leaf size; (6) initiation of adventitious roots
from young stem or leaf tissue; and (7)
modification of the natural response to grav-
ity, causing the roots to grow upward out of
the soil.
Several researchers reported alterations of
plant characteristics by exposure to CO. At a
concentration of 11,500 mg/m3 (10,000
ppm) "feminization" of plants occurred.5'7
Female sex expression is promoted in relation
to male by early formation of pistillate
flowers and an increase in their numbers. The
effects on flower formation, leaf epinasty,
abnormal stem growth, and adventitious root
formation suggest substantial elevation in
auxin content in CO treated plants. Dubro-
vina8 reported that seeds pretreated with CO
before planting produced plants with in-
creased leaf size. Amoore9 described a reduc-
tion in adenosine triphosphate production
during a 4-hour exposure to 460,000 mg/m3
(400,000 ppm) of CO plus an oxygen and
nitrogen mixture.
The effects of CO on microorganisms are
focused primarily on inhibition of nitrogen
fixation. Nitrogen fixation by microorganisms
7-1
-------
is of great importance to the life of higher-
type plants. Lind and Wilson10 showed that
fixation of free nitrogen by Azotobacter
vinelandii, a free-living nitrogen-fixing bacte-
rium, was inhibited when cultures were ex-
posed to 2,300 mg/m3 (2,000 ppm) CO for 35
hours. Uptake of combined forms of nitrogen
such as ammonium nitrate, ammonium phos-
phate, sodium nitrate, and urea were unaf-
fected by CO levels as high as 5,750 mg/m3
(5,000 ppm) during the same exposure time.
The same authors, using the same bacteria but
employing microrespiration techniques, found
some inhibition of combined nitrogen uptake
at 6,900 mg/m3 (6,000 ppm) for 4 hours.1 *
Lind and Wilson12 exposed red clover
plants inoculated with Phizobium trifolii for 1
month to 0, 58, 115, 230, 345, 575, and
1,150 mg/m3 (0, 50, 100, 200, 300, 500, and
1,000 ppm) of CO in separate treatments. At
0 and 58 mg/m3 (0 and 50 ppm) CO, no
inhibition of nitrogen fixation was detected,
but at 115 mg/m3 (100 ppm) a 20 percent
reduction in total nitrogen production oc-
curred. At 575 mg/m3 (500 ppm) inhibition
of nitrogen fixation was essentially complete.
By comparison non-inoculated plants sup-
plied with nitrogen in the form of ammonium
nitrate showed no effects of CO at concentra-
tions of 1,150 mg/m3 (1,000 ppm). Parallel
experiments reported in the same paper
showed similar results when rate of nitrogen
fixation, rather than total nitrogen, was con-
sidered.
B. SUMMARY
Carbon monoxide has not been shown to
produce detrimental effects on the higher-
type plant life at concentrations below 115
mg/m3 (100 ppm) during exposures for 1 to 3
weeks. Nitrogen fixation by free-living bac-
teria was inhibited at exposures of 2,300
mg/m3 (2,000 ppm) CO for 35 hours. Nitro-
gen fixation by efficient nitrogen-fixing bac-
teria in clover roots was also inhibited by 115
mg/m3 (100 ppm) CO when exposed for 1
month.
Ambient CO levels rarely reach 115 mg/rn3
(100 ppm) even for very short periods of
7-2
time. In view of this and the foregoing
information concerning CO effects, a signifi-
cant impact on vegetation and associated
microorganisms seems improbable.
It should be pointed out that no informa-
tion is available on CO concentrations in soils.
Most higher plants grow with their roots in
the soil, and nitrogen-fixing organisms as soil
dwellers would be vulnerable to soil-borne
CO. Hundreds of species of both flora and
fauna, whose activities are important to soil
development and to plant growth, may also
be affected.
C.. REFERENCES
1. Knight, L. I. and W. Crocker. Toxicity of Smoke.
Botan. Gaz. 55:337-371, May 1913.
2. Carr, D. J. Chemical Influences of the Environ-
ment. In: Encyclopedia of Plant Physiology,
Ruhland, W. (ed.). Vol. 16. Berlin, Springer-
Verlag, 1961. p. 773-775.
3. Zimmerman, P. W., W. Crocker, and A. E.
Hitchcock. The Effect of Carbon Monoxide on
Plants. Contrib. Boyce Thompson Inst.
5(2): 195-211, April-June 1933.
4. Zimmerman, P. W., W. Crocker, and A. E.
Hitchcock. Initiation and Stimulation of Roots
from Exposure of Plants to Carbon Monoxide
Gas. Contrib. Boyce Thompson Inst. 5(1):1-17,
January-March 1933.
5. Minina, E. G. and L. G. Tylkina. Physiological
Study of the Effect of Gases Upon Sex Determi-
nation in Plants. Dokl. Akad. Nauk SSSR.
55(2): 169-172, January 11, 1947.
6. Heslop-Harrison, J. and Y. Heslop-Harrison.
Studies on Flowering-Plant Growth and Organo-
genesis II. The Modification of Sex Expression
in Cannabis sativa by Carbon Monoxide. Proc.
Roy, Soc. Edinburgh B. 66:424-434, 1956-1957.
7. Heslop-Harrison, J. and Y. Heslop-Harrison. The
Effect of Carbon Monoxide on Sexuality in
Mercurialis Ambigua L. fils. New Phytologist.
56(3):352-355, November 1957.
8. Dubrovina, A. V. Presowing Carbon Monoxide
Fumigation Treatment of Cucumber Seeds.
Fiziol. Rast. (USSR). 5(1): 16-23, 1958.
9. Amoore, J. E. Non-identical Mechanisms of
Mitotic Arrest by Respiratory Inhibitors in Pea
Root Tips and Sea Urchin Eggs. J. Cell Biol.
M(3):555-567, September 1963.
10. Lind, C. J. and P. W. Wilson. Carbon Monoxide
Inhibition of Nitrogen Fixation by Azotobacter.
Arch. Biochem. 7(l):59-72, October 1942.
-------
11. Wilson, P. W. and C. J. Lind. Carbon Monoxide oxide as an Inhibitor for Nitrogen Fixation by
Inhibition of Azotobacter in Microrespiration Red Clover. J. Amer. Chem. Soc. 55:3511-3514,
Experiments. J. Bact. 45:219-232, March 1943. December 1941.
12. Lind, C. J. and P. W. Wilson. Mechanism of
Biological Nitrogen Fixation. VIII. Carbon Mon-
7-3
-------
CHAPTER 8.
TOXICOLOGICAL APPRAISAL OF CARBON MONOXIDE
A. INTRODUCTION
There is extensive documentation of the
fact that high concentrations of carbon mon-
oxide (CO) can cause many physiological and
pathological changes and ultimately death.
The effects of exposure to levels of CO of less
than 115 mg/m^ (100 ppm) are not so well
documented. The purpose of this chapter is to
evaluate the data on experimental exposure of
animals and humans to CO, emphasizing both
the acute and long-term effects of low CO
concentrations. A recent review1 provides
additional information on most of the studies
discussed in this chapter, particularly with
regard to areas for future research.
The principal toxic properties of CO are
based on its reactions with hemoproteins. The
most important of these reactions is the
reversible combination of CO with hemo-
globin (Hb) to form carboxyhemoglobin
(COHb). In addition to varying exposures to
exogenous CO, the body is steadily exposed
to a small amount of endogenous CO formed
as a by-product in the course of heme cata-
bolism; in normal humans, this amounts to
about 0.4 milliliter of CO per hour. The
presence of this relatively small amount of CO
results in a "normal" or "background" level
of COHb in the bloodstream of about 0.5 per-
cent.
Both oxygen and CO react with hemo-
globin in a very similar manner, and their
transport depends on their reaction with the
iron atom of the heme prosthetic group. The
affinity of hemoglobin for CO is more than
200 times greater than that for oxygen.
Heme is an iron complex of protoporphy-
rin. The iron, in the ferrous form, combines
reversibly with ligands in a ratio of 1:1. There
are four heme units in the hemoglobin
molecule and, hence, four molecules of
oxygen or CO may be utilized in the forma-
tion of saturated oxyhemoglobin (O2Hb) or
carboxyhemoglobin (COHb). Hemoglobin
may also be present in a reduced form, which
is the predominant source of the darker color
of venous blood. When the iron is in the
oxidized form, the molecule becomes
methemoglobin, which is inactive in the trans-
port of oxygen or CO.
The dissociation curves of O2Hb and COHb
are sigmoid in shape. The sigmoid character of
the dissociation curves implies that the affin-
ity of the binding sites changes as a result of
the presence of the ligand on the other sites;
i.e., there are interactions between the various
binding sites. These are commonly called the
heme-heme interactions or allosteric effects.
Since one hemoglobin molecule contains four
heme units, the binding of oxygen or CO to
these units may be associated with conforma-
tional changes that reflect these interactions
in the protein molecule.
Carbon monoxide is potentially capable of
reacting with other hemoproteins in vivo. In
vitro it will combine with myoglobin (Mb) to
from carboxymyoglobin (COMb) and may
also interfere with certain enzyme systems.
The biologic significance of these reactions
will be discussed in Section G of this chapter.
B. THEORETICAL CONSIDERATIONS
When air containing a certain concentration
of CO is inhaled for several hours, a state of
equilibrium with respect to this gas is reached
in which the partial pressure of CO (PCQ) in
the pulmonary capillary blood is virtually
8-1
-------
equal to that in the alveolar and ambient air.
The equilibrium of the reaction:
CO + Hb ^ COHb
depends on the partial pressure of CO and on
that of oxygen (?O2) because the two gases
compete for the same reactive sites on the
hemoglobin molecule. The relationship is de-
scribed by the Haldane equation:
[COHb] =
[02Hb]
PCO
PQ2
where [COHb] and [O2Hb] are the concen-
trations of COHb and O2Hb (usually ex-
pressed as percent saturation), and M is the
relative affinity constant. At physiologic pH
and temperature, the value of M is about 210,
although values of up to 245 have been
reported.2 This means that the affinity of
hemoglobin for CO is about 210 times that
for oxygen, or that equal amounts of COHb
and O2Hb exist in equilibrium with gas
mixtures containing 210 oxygen molecules
for every CO molecule.
Although a number of theories and models
have been proposed to explain the sigmoid
shape of the oxygen dissociation curve (a plot
of the partial pressure of oxygen against the
percent of hemoglobin present as O2Hb),
none has adequately explained all of the vari-
ous features and kinetics of the reaction of
hemoglobin with ligands. At present, the
Adair model3 seems the most acceptable, al-
though it is likely to be oversimplified since
some aspects of the equilibrium and kinetics
of hemoglobin cannot be accommodated
within its framework. This model describes
the reactions of hemoglobin in terms of four
individual equilibrium and kinetic constants
corresponding to the four hemes contained in
the molecule. The scheme is usually written as
follows:
Hb4
Hb4Xi;K! = —
Hb4X2
Hb4X3
X^ Hb4X2; K2 = —
k'-j I,1-
,<- _
[-*• Hb4X3; K3 -
k3 k3
k4 k4
X^ Hb4X4; K4 = —
k4 k4
where Hb4 is the hemoglobin tetramer; X is
the activity of the ligand; and K, k, and k' are
the equilibrium constant, the combination
velocity constant, and the dissociation veloc-
ity constant, respectively. From experimental
data gathered so far, the sigmoid shape of the
curve appears to be due to a very large value
of K4, which exceeded those of Kj, K2, and
K3-4
Consideration of the toxicity of CO must
include not only the displacement of oxygen
from hemoglobin in arterial blood, but also
the interference with oxygen release at the
tissue level. The latter effect can be under-
stood by a study of the O2Hb dissociation
curve as described by Roughton and Darling5
(Figure 8-1). The presence of COHb causes a
100
-60% COHb
40% COHb
20% COHb
0 % COH b
100 120
PARTIAL PRESSURE OF OXYGEN
Hg
Figure 8-1. Oxyhemoglobin dissociation
curves of human blood containing varying
amounts of carboxyhemoglobin, calculated
from observed 02 dissociation curve of
CO-free blood (pH - 7.4, T = 37 °C, P
40 mm Hg). 5
CO
8-2
-------
shift of the C^Hb dissociation curve to the
left for the remaining hemoglobin (not bound
to CO), which implies that for a given oxygen
saturation there is a lower partial pressure of
oxygen. The shift of the C^Hb dissociation
curve is best understood if the most accessible
binding sites are considered to be those that
first pick up and discharge CO or oxygen. Es-
sentially, the bottom part of the S-shaped
hemoglobin dissociation curve is inactivated
-by CO; therefore only the top part reacts with
oxygen. This top part, then, is reexpanded to
fit between vertical and horizontal axes with
altered scales for O2Hb and PQ2, respectively.
Since the increased affinity of hemoglobin
for CO implies that some of the accessible
sites are occupied by CO while the hemo-
globin molecule circulates through the body
several times, it would also mean that some of
the sites that would convey labile oxygen are
actually conveying nonlabile CO. The PQO °f
mixed venous blood (40 mm Hg) occurs at a
steep part of the curve, and the effect of a
shift to the left on release of oxygen at the
tissue level may be considerable. This shift im-
plies that in the presence of COHb there ex-
ists an impairment of oxygen unloading at the
tissue level and thus a decreased circulatory
efficiency, as estimated by oxygen delivery.
At rest, there is a close correlation between
the PQ2 °f mixed venous blood and the PQ2
of the tissues; hence, a lowering of the mixed
venous Pc»2 following CO inhalation reflects a
similar decrease in the tissue PQ2- Klausen6 et
al., using eight healthy male students as sub-
jects, have estimated a 15 to 20 percent
lowering of the tissue PQ2 a* re§t in response
to the presence of an average of 15 percent
COHb.
The effect of CO on the O2Hb dissociation
curve has been demonstrated experimentally
in vitro with solutions of human hemoglob-
in.3 The leftward shift of the oxygen dissocia-
tion curve has also been demonstrated by
Lilienthal7 et al. in vivo; the data given in
their paper have been recalculated (Table 8-1)
and are shown graphically in Figure 8-2. More
recently, Mulhausen8 et al. have shown, that
the average P(>2 corresponding to 50 percent
saturation, dropped from 26.7 to 23.2
mm Hg in eight subjects who were intermit-
tently exposed to CO and had an average of
15 percent COHb at the end of the 7-day ex-
posure period.
In these theoretical considerations, the im-
pairment of oxygen delivery to the tissues is
only implied from the O2Hb dissociation
curve. Recently, however, Baumberger9 et al.
created an experimental model to study the
oxygen delivery rate (ODR) of human blood
in vitro. They found that the ODR increased
with a decrease in percent saturation of hemo-
globin and that there were significant differ-
ences in the ODR between individuals.
Whether the ODR responds to small amounts
of COHb at a fixed saturation of hemoglobin
in vivo remains to be determined.
C. MEASUREMENT OF CARBOXYHE-
MOGLOBIN IN BLOOD
Several methods exist for the determina-
tion of blood COHb levels, but for the pur-
pose of this document only the measurement
of levels of less than 10 percent is consid-
ered. Of prime importance in this concentra-
tion range are the accuracy and reproduca-
bility of the determinations. Other aspects to
be considered are the volume of blood re-
quired for accurate determinations and the
sensitivity of the method to small variations
in COHb. The available methods fall into
three categories: nondestructive, destructive,
and equilibrium methods.
1. Nondestructive Methods
The nondestructive methods are mainly
spectrophotometric. Two such methods have
been published recently, and both rely on the
differences in the absorption between O2Hb
and COHb at given wave lengths. The ad-
vantages of these methods are: (1) a very
small amount of blood is required, (2)
separate determinations of hemoglobin con-
centrations -do not have to be made, and (3)
the methods are extremely simple and quick.
The first method is that of Amenta.10 The
blood samples are added to dilute solutions of
ammonium hydroxide and absorbances are
8-3
-------
00
Table 8-1. BLOOD AND GAS STUDIES (AVERAGES OF TWO MEASUREMENTS TAKEN 30 MINUTES
APART) AFTER ADMINISTRATION OF CARBON MONOXIDE AND AIR UNTIL
ATTAINMENT OF CARBOXYHEMOGLOBIN EQUILIBRIUM7
Subject
1
(Light smoker)
2
(Heavy smoker)
3
(Nonsmoker)
No. on
Fig. 8-2
1
2
3
4
5
6
PaO2,
mm Hg
57.5
56.0
40.0
67.5
63.5
54.0
PaO2 + MpCO,3'0
mm Hg
62.7
60.9
48.7
89.1
74.3
59.7
Arterial
O2Hb,
%sat.
88.9
88.1
80.7
97.1
96.2
89.1
Arterial
COHb,
% sat.
7.5
7.3
15.0
23.7
14.1
8.6
Arterial
02Hb+COHb,
%sat.
89.8
88.9
83.5
97.8
96.7
90.0
O2Hb
COHb+O2Hb+Hb
83.4
82.9
72.3
81.0
83.3
82.7
O2Hb + COHb
1 nn -v
COHb + O2Hb + Hb
90.4
89.7
85.2
96.2
97.6
90.8
aPaO2 + Mf>CO = adjusted O2 tension.
= 210 =
[021
Po x [COHb]
P0 x [02Hb]
-------
O
O
£
u
CD
0.
o
o
en
o
_O
X
o
(J
+
_Q
X
tN
O
-Q
X
-Q
*T"
O
(J
-4-
n
X
CM
O
Z
CO
O
_l
O
o
UJ
X
o
Q±
2CO
<0
mo
OS
-JLLI
OX
100
90
80
70
so
LUO
XCQ
x<
ou
50
20% COHb
(ADJUSTED BY
ADDITION OF
Mp CO)
OXYHEMOGLOBIN
OXYHEMOGLOBIN AND
CARBOXYHEMOGLOBIN —
NUMBERS IN PARENTHESES REFER TO
SUBJECTS LISTED IN TABLE 8-1.
20
30
40 50 60 70
ARTERIAL OXYGEN TENSION, mm Hg
80
90
100
Figure 8-2. Effect of CO administration on arterial oxygen tension, compared with 02
dissociation curves in Figure 8-1, based on data in Table 8-1.
determined at 575, 560, and 498 millimicrons
). The ratio obtained,
p =A575-A560 ,
A498
is compared with the ratios obtained with
standard solutions of C^Hb and COHb. The
percent of COHb is calculated from the equa-
tion
Percent COHb = lOOx
RQ2-RX
RQ2'RCO
where RQ2> RCO> a"d RX are the ratios ob-
tained, respectively, from 100 percent O2Hb,
100 percent COHb, and the unknown COHb
solution. The relationship between RCQ and
COHb concentration is linear. Since wave-
length 498 mju is an isosbestic point, i.e., the
extinction coefficients of COHb and O2Hb
are the same, the absorbance at this wave-
length can also be used to determine the total
hemoglobin.
Tuddenham and Hitchcock undertook to
evaluate this method, but found it somewhat
unsatisfactory because of the inconsistent shift
induced by the varying concentrations of
COHb, particularly at low levels, prevented
the construction of an acceptable calibration
curve.1 * The reproducibility of the isosbestic
point for the determination of hemoglobin
concentration, however, appeared to be satis-
factory, with an accuracy to ± 0.39 percent
hemoglobin.
The second method is that of Commins and
Lawther.1 2 In this method, the absorption of
COHb is directly compared to that of 100
percent O2Hb. The method as described in
8-5
-------
the literature is unsatisfactory for the follow-
ing reasons: (1) the use of fingerprick blood is
unsuitable because the varying amounts of tis-
sue fluid contained in the different samples
may lead to inaccuracies due to variations in
the true volume of blood and interferences in
the adsorption peaks and (2) the method of
preparing standard solutions of 100 percent
COHb and 100 percent C^Hb involves bub-
bling CO or oxygen into the solutions. This
produces an excess of dissolved gases; hence,
when solutions containing less than 100 per-
cent COHb were prepared, they were inac-
curate. To overcome the above difficulties,
mixed venous blood samples have been used
and are equilibrated in separating funnels with
either CO (as described by Amenta) or air. By
mixing calculated proportions of the two
solutions, an acceptable calibration curve has
been prepared. From the calibration curve, it
appears that the method as described is sensi-
tive to detect a minimum of 2 percent COHb.
When mixed venous blood from heavy
smokers and nonsmokers was assayed for
COHb, small amounts of unsaturated hemo-
globin in the sample caused substantial inter-
ference between wavelengths 416 and 410
rriM. When ©2 was bubbled through the non-
smoker's blood sample, the interference dis-
appeared, showing that the hemoglobin had
become saturated. Interference caused by the
saturated hemoglobin corresponded to about
10 percent COHb at 420 mju and about 20
percent at 439 mju. It must be concluded that
the spectrophotometric methods for the de-
termination of COHb are not suitable to
measure low levels and can only be used for
clinical diagnoses.
2. Destructive Methods
The destructive methods involve, for the
most part, the liberation of blood gases with
either total destruction of the hemoglobin or
its transformation into a compound without
any activity with respect to CO. The gases
freed from the blood are then examined by
various methods, and the CO present in them
is assayed. The disadvantages of these meth-
ods are: (1) larger amounts of blood are re-
8-6
quired than for spectrophotometric methods,
(2) separate determinations of hemoglobin
concentrations must be made, and (3) the
methods are fairly tedious. The released CO
may be measured utilizing (1) detector tubes,
(2) the reaction of CO with palladium
chloride, (3) manometric and volumetric
methods, (4) infrared spectrophotometry, and
(5) gas-phase chromatography.
a. Carbon Monoxide Detector Tubes
Carbon monoxide detector tubes have been
used to assay CO in gases extracted from
blood. Views on the reliability of this method
are varied, although it reportedly has an ac-
curacy ranging from 2 to 20 percent when
compared to the manometric method.13 The
method only gives an estimate of the CO con-
tent of blood and is not suitable for accurate
determinations.
b. Reduction of Palladium Chloride
by the Micro diffusion Technique
The apparatus used for this is the Conway
microdiffusion apparatus. The blood gases are
liberated, and the released CO reduces the pal-
ladium chloride to metallic palladium. The ex-
cess palladium chloride is usually assayed by
volumetric analysis or colorimetry.14 The
method is said to be sensitive to 1 percent
COHb (standard deviation of approximately
±0.03 ml/100 ml). The disadvantage is that
the method is tedious and requires a skilled
chemist to perform it.
c. Manometric and Volumetric Methods
Manometric methods include the tech-
niques of Van Slyke15 (SD ± 0.05 ml/100 ml)
and Horvath and Roughton16 (SD ± 0.03
ml/100 ml). The volumetric methods that
have been successfully used are the syringe
capillary method of Scholander and Rough-
ton17 (SD + 0.03 to 0.05) and the Van
Slyke syringe technique of Roughton and
Root18 (SD ± 0.007 ml/100 ml). These meth-
ods are accurate and considered adequate, al-
though they are time-consuming, technically
difficult, and require large volumes of blood.
There is some doubt, however, as to the sensi-
tivity of the methods at COHb levels below 5
percent.
-------
d. Spectrophotometric Determination of
Released CO by NDIR (Nondispersive
Infrared) Method
This method calls for costly equipment, al-
though it provides the most accurate results.
Methods based on this technique have been
published by Coburn19 et al. (SD ± 0.006
ml/100 ml in the range of 0.1 to 1.0 ml/100
ml) and by Schuette.20 Care must be taken to
maintain the correct pH range and to prevent
warming the blood prior to extracting the CO;
otherwise, inaccurate results are obtained. A
small amount of mercury is required to pre-
vent CO formation from hemoglobin break-
down. An advantage of this method is that
measurement of CO by the NDIR method is
virtually specific (for a discussion on interfer-
ences, see Chapter 6, Section C.l.b on meas-
urement of atmospheric CO by NDIR) and is
considerably more sensitive than the other
methods described.
e. Gas-phase Chromatography
Hackney et al.21 have successfully used
this method whereby the CO is released from
blood in the Van Slyke apparatus, diluted,
and then flushed through a gas chro-
matograph. The characteristics of the chroma-
tography system are described in detail in the
original paper. The sensitivity of the method
is about 20 parts per million ± 1 percent with
a 25-cubic-centimeter gas-sample size.
The destructive methods described provide
data for only the concentration of CO in
blood; to obtain the percent COHb present,
separate determinations of hemoglobin must
be made.
3. Equilibrium Methods - Analysis of
Expired Air
This type of analysis cannot be categorized
as destructive or nondestructive. Its success
depends on the consideration that the lung,
during breath-holding, is thought to be
analogous to a closed vessel in which blood
COHb equilibrates with the lung gas. Sjo-
strand,22 Jones23 et al., and more recently
Ringold24 et al. have shown that COHb may
be estimated from expired air after breath-
8-7
holding for 20 seconds. The subject is asked
to exhale deeply, to take a deep inspiration,
and hold his breath for 20 seconds; at the end
of that time, the subject is asked to expire
through a side arm tube. The first 150 to 250
milliliters of gas is allowed to escape, and the
remaining gas expired from the lung is col-
lected into a polyvinyl bag with a simple
push-pull valve. Several studies have produced
graphs correlating expired air CO with blood
COHb; this is treated further in Section D of
this chapter.
The method as published appears to be
suitable for studying the relationship of
COHb to occupational and ambient air pollu-
tion exposures where large populations need
to be studied. Recent studies have shown,
however, that the CO content of expired air
in smokers does not always correlate well
with blood COHb. Thus, further studies are
required to demonstrate the validity of this
method.
4. Discussion
The most accurate methods for determina-
tion of COHb are generally those that liberate
and measure the CO bound to hemoglobin.
The CO should be determined by the NDIR
method, and the hemoglobin must be deter-
mined separately.
D. UPTAKE OF CARBON MONOXIDE
BY HUMANS
References to the uptake of CO by human
blood2 s'35 are numerous; however, Forbes et
al. in 1945 produced the first extensive study
on the rate of uptake of CO by normal
men.30 Approximately 100 observations were
made on seven presumedly healthy male
adults exposed to from 115 to 23,000 mg/irP
(100 to 20,000 ppm) CO for periods of up
to 5 hours. Exposures to the lower concentra-
tions were conducted in a chamber; those to
the higher concentrations required the sub-
ject to inhale through a mouthpiece. Not all
of the subjects were exposed to each concen-
tration for each exposure time. Four grades of
activity were used: (1) rest (subject lying
upon a bed); (2) light activity (walking about
-------
chamber, taking blood samples, and reading
instruments); (3) light work (riding a bicycle
ergometer at 2,220 foot-pound per minute,
activity equal to walking on the level); and (4)
heavy work (riding a bicycle ergometer at
4,440 foot-pounds per minute, activity equal
to a slow jog trot). Blood COHb was deter-
mined by the Scholander and Roughton31
method. (Reservations pertaining to this
method of analysis have been discussed in
Section C of this chapter.) Although no in-
formation concerning the smoking habits of
the subjects is given in Forbes' paper, the
stated preexposure COHb values of 0 to 5 per-
cent suggest that some of the subjects were
probably smokers.
Nearly half of the observations were made
on subjects engaging in light activity. Average
results for the whole range of activities and
inspired CO (0 to 23,000 mg/m3) are given in
Figure 8-3. Figure 8-3 also indicates the per-
cent COHb increase that would be expected
for the various concentrations of CO at equili-
brium. Although no individual data are given
in the figure, it should be noted that out of
41 observations, 18 were off the curves by
only 1 percent COHb or less, 9 were off by 2
percent, 9 by 3 percent, 3 by 4 percent, and 2
by 5 percent. These individual variations are
believed to be due to variation in the ratio of
tidal volume to the dead space of the lung and
also to the diffusion constant of the lung
The data in Figure 8—3 show that the up-
take of CO by the blood increases with (1)
the concentration of CO, (2) the length of
exposure, and (3) the ventilation rate. The
rate of uptake, as estimated by the linearity
of COHb with time, appears to be constant up
to values of approximately one-third of the
equilibrium level of COHb for a given concen-
tration. For example, it is demonstrated in
Figure 8-3 that exposure to 575 mg/m3 (500
ppm or 0.05 percent) CO for 10, 20, 40, and
80 minutes during light work results in
respective increases of COHb of approxi-
mately 4, 8, 12, and 22 percent. For this con-
centration of CO, the equilibrium value of
COHb was calculated to be about 39 percent.
These calculations are consistent with data on
the rate of uptake of CO published by Pace3 2
et al. and the more recent studies by Bosaeus
and Friberg.33
In Forbes' studies, when CO was adminis-
tered in 98 percent oxygen instead of in air,
the rate of CO uptake decreased. This effect
t =00
24.6%
REST, PULSE 70
LIGHT ACTIVITY,
PULSE 80
LIGHT WORK,
PULSE 110
HARD WORK,
PULSE 135
Figure 8-3. Uptake of CO at various concentrations and rates of ventilation. 30
-------
was more pronounced in experiments in
which subjects had undergone hard work
rather than remaining at rest. For reasons un-
known, some subjects were found to hyper-
ventilate in response to the 98 percent oxygen,
and their apparent rate of uptake under these
conditions was not the same as when the CO
was in air. When a correction was made to
take into account the increased ventilation,
uptake at rest was reduced 23 percent and
during hard work 38 percent. Exposure of
four subjects to 3,450 to 4,600 mg/m3 (3,000
to 4,000 ppm) CO for 6 minutes at an atmos-
pheric pressure of 410 mm Hg, simulating an
altitude of 16,000 feet, produced no altera-
tion in the rate of uptake of CO when a cor-
rection was made for hyperventilation due to
anoxia.3 ° These experiments will be discussed
more fully in Section H of this chapter.
One study made of exposure of humans to
low concentrations of CO (less than 115
mg/m3, or 100 ppm) was reported recently
by Smith.34 Ten healthy men were exposed
to 35 ± 3 mg/m3 (30 ± 3 ppm) of CO for
periods of up to 24 hours. Seven of the sub-
jects were non-smokers, and the other three
were asked to refrain from smoking for at
least 12 hours prior to the experiment. Blood
CO was determined by the Scholander and
Roughton method,3 * and hemoglobin deter-
minations were made with a Hellige
hemometer. The subjects were divided into
two groups. Six subjects exposed throughout
the entire 24-hour period had blood samples
taken at 4, 8, 12, 16, 20, and 24 hours. Four
subjects exposed for only 4 hours had blood
samples taken after 0, 0.5, 1.0, 1.5, 2.0, and 4
hours of exposure. All subjects were able to
rest or engage in light activity at will. The
individual data are given in Table 8-2.
The average data for the nonsmokers are
shown in Figure 8-4. It appears that ex-
posure to 35 mg/m3 of CO produces a blood
level of about 5 percent COHb at equilibium.
Figure 8-4 indicates that 60 percent of the
equilibrium concentration was reached within
the first 2 hours, 80 percent within 4 hours,
and the remaining 20 percent slowly over the
next 8 hours. Exposure to 35 mg/m3 (30
ppm) of CO for 4 hours made no contribution
to the blood COHb level of subject 7, a
smoker. Although the preexposure COHb
levels of the two remaining smokers (subjects
1 and 6) were above those of the nonsmokers,
their values after 8 hours of exposure were
within the same range as those of the non-
smokers.
A relatively simple formula for estimating
the increase in equilibrium value of COHb
above background after continuous exposure
to CO concentrations of less than 115 mg/m3
Table 8-2. PERCENT CARBOXYHEMOGLOBIN IN BLOOD OF SUBJECTS EXPOSED TO
35 mg/m3 (30 ppm) CO34
Subject
1
2
3
4
5
6
7
8
9
10
Smoking
habits
None
None
Cigarettes
None
None
Cigarettes
Cigarettes
None
None
None
Time from beginning of exposure, hr
0
1.4
1.0
2.4
0.7
1.2
3.2
5.8
0.0
0.9
1.0
0.5
5.3
1.0
1.3
2.0
1.0
5.3
2.5
3.8
2.5
1.5
5.8
3.0
3.4
2.5
2.0
4.8
4.5
3.4
3.5
4.0
4.3
3.5
3.0
4.5
8.0
2.8a
6.0
5.0
3.5
3.0
3.9a
12.0
5.6
5.0
5.0
5.5
5.0
4.6
16.0
4.2
5.0
5.0
5.0
4.2
4.6
20.0
4.7
5.0
4.0
4.5
5.0
5.7
24.0
4.7
4.5
5.0
4.5
5.5
5.2
aThese samples were taken at 9.5 hr.
8-9
-------
CO
o
o
o
X
o
CO
a:
u
6.0
5.0
4.0
3.0
2.0
1.0
0
I
•
12
16
20
24
TIME, hours
Figure 8-4. Average values of percent
carboxyhemoglobin in seven nonsmokers
exposed to 35 mg/m3 (30 ppm) CO. 34
(100 ppm) has recently been included in a
review3 6 of the effects of CO:
(COHb) in percent = 0.16 x (CO) in ppm
Assuming a background COHb level of 0.5
percent, this formula can be expressed to esti-
mate the equilibrium value of COHb attained
after continuous exposure:
(COHb) in percent =
[0.16 x (CO) in ppm] +0.5.
Tlois affer an exposure to 35 mg/m3 (30
ppm) CO, the predicted equilibrium value of
COHb would be 5.3 percent, which is quite
close to Smith's results. Similarly, it can be
anticipated from this formula that exposure
to 23 mg/m3 (20 ppm) CO for about 8 or
more hours should result in a blood COHb
concentration of about 3.7 percent; after ex-
posure to 12 mg/m3 (10 ppm) CO for about 8
or more hours, a blood COHb level of 2.1
percent would be predicted.
Experimental data are available to estimate
the blood COHb levels anticipated after ex-
posures to CO for periods of time less than
would be necessary to attain equilibrium.35
Peterson and Stewart have recently studied
young human volunteers exposed to CO at
concentrations s of < 1, 29, 58, 115, 575, and
1,150 mg/m3 (< 1, 25, 50, 100, 500, and
1000 ppm) for periods of 30 minutes to 24
hours. Blood COHb was measured periodical-
8-10
ly during the experiment by both a direct de-
termination in a CO-Oximeter and by meas-
uring the CO liberated from the COHb using a
gas chromatograph equipped with a helium
ionization detector. The following relation-
ship was derived to describe the absorption of
CO by these subjects:
Log % COHb = 0.85753 Log CO
+ 0.62995 Log t-2.29519
where CO is measured in ppm and t is the
duration of exposure in minutes. Figure 8-5
is based on this relationship and permits the
estimation of COHb levels of sedentary
humans if the concentration and exposure
time are known.
E. EFFECT OF CARBON MONOXIDE ON
THE CENTRAL NERVOUS SYSTEM
1. Animal Data
a. Morphological Changes
Changes in the morphology of the brain
and central nervous system have been ob-
served in dogs exposed to high concentrations
of CO over extended periods.
Lewey and Drabkin exposed six dogs to
115 mg/m3 (100 ppm) CO for 5-3/4 hours
a day, 6 days a week, for 11 weeks.37 The
COHb level reached each day was about 20
percent. During the exposure, no changes
were observed in the electroencephalogram
(EEG) or in the function of the peripheral
nerves. The dogs showed a consistent disturb-
ance of postural and position reflexes and of
gait. After exposure, morphologic examina-
tions of the nervous system showed that all
animals had some indication of cortical dam-
age. No such findings were observed in the
five control animals. There were also histologic
changes in the white matter of the cerebral
hemospheres, the globus pallidus, and the
brain stem. These changes tended to follow
the course of the blood vessels. A seventh
dog, which had had its posterior coronary
artery ligated 1 year prior to exposure,
showed the most severe cerebral changes as
well as severe cardiac changes, although he was
-------
E
a
a.
«
Z
o
QL
I-
Z
LLI
U
Z
o
U
o
U
1 t\J\J\J
900
800
700
600
500
400
300
250
200
150
100
90
80
70
60
50
40
30
25
20
15
1 n
— I M XJ I I '-
^ X x —
^w ^w *».
— X N \ —
— x x x. —
- \ sx \
^w ^ X
— x x x% -v —
>X \ X \ /*%
~^x X X. x
— 'x, ss X, -^
— ""*"• X x —
X NSNX _
"•- SVH Vrx
s >
II IX M
1.15O
1,035
920
805
690
575
460
345
288
230
173
1 15
104
92
81
69
58
46
35
29
23
17
11
0.10 0.20 0.30 0.40 0.60 0.80 1.0 2.0
EXPOSURE, hours
3.0 4.0
6.0 8.0 10.0
CO
E
O)
E
z"
O
U
z
o
U
o
U
Figure 8-5. Concentration and duration of continuous CO exposure required to produce blood
COHb concentrations of 1.25, 2.0, 2.5, 5.0, 7.5, and 10 percent in healthy male subjects en-
gaging in sedentary activity. 35
exposed for only 18 days. Although it cannot
be determined whether the observed changes
are attributable to acute or chronic CO ex-
posure, these results suggest that inadequate
cardiac function may predispose to cerebral
anoxia and increase the risk of brain damage
from CO poisoning.
In dogs that were continuously or intermit-
tently exposed to 115 or 58 mg/m3 (100 or
50 ppm) of CO for 6 weeks, Lindenberg et
al.38 observed that the brain showed no areas
of necrosis or demyelination. There was a
mobilization of glia, which suggests that a
disease process was under way, and also a dila-
tation of the lateral ventricles. These investi-
gators felt that brain changes were secondary
to myocardial changes.
b. Behavioral Changes
Carbon monoxide has been found to in-
duce behavioral changes in trained, unanes-
thetized, unrestrained rats.39'40 Some studies
report alterations in simple learned perform-
ance in the rat. The animal usually performs
8-11
-------
in a box that contains a lever that the rat has
been taught to press. For reinforcement, the
food-deprived animal receives a food pellet
for some of its presses on this lever. Rats can
learn to make long pauses between responses,
and the ability with which the animal presses
the lever has also been shown to be influenced
by various drugs.
In one series of experiments conducted by
Beard and Wertheim,39 a differential rein-
forcement of low rate of response (DRL)
schedule was used. During certain periods, the
animal had to refrain from pressing the lever
for more than a predetermined fixed time in
order for the next lever press to be reinforced.
Mean data for six rats exposed to CO are
shown in Figure 8-6. Exposure to CO never
exceeded 48 minutes, and all experimental
sessions, including control periods, lasted
approximately 2 hours. Carbon monoxide de-
creased the response rate on this schedule.
Figure 8-6 gives the time of onset of a per-
formance decrement large enough to fall at
least 2 standard deviations below the rate
measured during normal atmospheric condi-
tions. The number to the right of each curve
gives the minimum delay required of the
animal for a response to be reinforced. For
instance, perceptible effects were observed
after exposure to 115 mg/m3 (100 ppm) for
11 minutes when the minimum delay required
was 30 seconds. It took 30 minutes of ex-
posure to 115 mg/m3 to produce the same
relative decrement in rate when the minimum
delay was only 15 seconds.
I-
z
LU
s
LU
u
LU
Q
LU
(J
O
LL.
o:
LU
Q.
13
Q
Z
6
u
o
LU
100
250 500
CARBON MONOXIDE, ppm
I
i
115
290 575
CARBON MONOXIDE, mg/m3
865
2 seconds
5 seconds
10 seconds
15 seconds
20 seconds
30 seconds
750 1.000
1,150
Figure 8-6. Effect of CO on mean DRL response rate in rats.39
8-12
-------
Xintaras et al. have established that altered
electrical activity in the cerebral cortex in rats
can be observed after exposure to CO concen-
trations below those required to produce an
impairment of performance.40 Six adult rats
were fitted with implanted electrodes, one in
the visual cortex and one in the superior col-
liculus. The stimulus used to detect changes in
these areas was a flashing light lasting 10
microseconds with a frequency of two flashes
per second. A Skinner-type apparatus was
used to monitor behavioral responses and was
adjusted to reward each depression of the
lever. When the rate of lever depression had
stabilized, the flashes of light were initiated.
Following an initial disruption of the lever-
pressing activity, the light flash became infor-
mationally neutral and the rate of lever-
pressing again stabilized. When this point was
reached, the rat was considered ready for the
experimental procedure. Concentrations of
from 58 to 1,150 mg/m3 (50 to 1,000 ppm)
CO were used. A train of light flashes was
presented to the rat while the lever was being
pressed. Evoked potentials generated as a re-
sult of the flash stimuli were fed into an elec-
tronic monitoring system.
In an experiment in which the rat breathed
115 mg/m3 (100 ppm) CO for 2 hours, no
significant change in lever-pressing activity
was detected when the animal was presented
with a retractable lever. During this period,
however, changes in the activity of the brain
were recorded. These can be summarized as
an increase in the amplitude of the primary
component and a decrease in amplitude with
an increase in latency of the secondary
component. The increase in the amplitude of
the first downward deflection was about 60
percent of the control value (cf. 80 percent in
an experiment with 1150 mg/m3).
At 58 mg/m3 (50 ppm) for 1 hour, the
amplitude increased by about 20 percent of
control together with an increase in the
latency of the second component. At 58 mg/m3
for 2 hours, these same effects were enhanced
- about a 50 percent increase in amplitude of
the first downward deflection. Repeated ex-
posures to 58 mg/m3 for 1 to 5 hours each
day for 4 days resulted in a progressive de-
terioration of the secondary component, as
well as an associated increase in amplitude of
the primary component. A post-exposure
period of about 48 hours was required before
these alterations in central nervous system
activity returned to pre-exposure baseline
level.
In an extensive series of studies on the
effects of chronic low-level exposure to CO,
Stupfel41 exposed mice to 58 mg/m3 (50
ppm) for periods of 3 months to 2 years and
compared his results with appropriate
controls. Animals were placed 5 days a week,
24 hours a day, into exposure chambers in
groups of 3 to 10 mice. No differences
between treated and control mice were found
with respect to fertility, fetal survival, body
growth, food intake, weight and water
content of various organs, heart rate,
amplitude of the QRS deflection in
electrocardiographic tracings, nocturnal
output of CO from the animals, and blood
chemistries (including hemoglobin, glucose,
proteins, lipids, cholesterol, calcium,
magnesium, SCOT, and SGPT). The lethal
dose of a virulent strain of bacteria was the
same for exposed and control mice. Similarly,
no differences were found when exposed and
control mice were first vaccinated and then
challenged with a larger lethal dose of the
same bacteria. Mice conceived and born in
exposed or control chambers were enclosed in
a small air-tight chamber. At the 30th and
53rd hour of the progressive hypercarboxic
hypoxia, the mortality was the same for the
mice born in either chamber. Tumor growth
of grafted tumors showed no differences in
exposed and control animals.
The same negative results as described
above were found when tests were repeated
after 2 years of exposure to 58 mg/m3 (50
ppm).
Back and Dominguez42 performed a series
of studies designed to show the effects of
long-term CO exposure on performance tasks
of trained monkeys. Twelve trained adult
Rhesus monkeys were exposed to 55 mg/m3
(48 ppm) CO in air for 100 days, and then to
8-13
-------
55 mg/m3 at a simulated altitude of 27,000
feet (5 psia in a two-gas system of 68 percent
oxygen and 32 percent nitrogen) for 105
days. Successive study phases consisted of
doubling the concentration of CO each 7 days
following the last day of exposure to 55
mg/m3, while maintaining the same simulated
altitude. Thus, CO concentrations of 110
mg/m3 (95 ppm), 220 mg/m3 (190 ppm), and
440 mg/m3 (380 ppm) were used.
Performance tasks consisted of pressing levers
in response to visual and auditory stimuli;
avoidance of electrical shock provided the
motivation to respond to the stimuli. All
animals were trained on the performance
tasks to a stabilized level during a period of
several months prior to the CO exposure.
In the two experiments conducted at 55
mg/m3 CO exposure, COHb saturation
stabilized after the first 48 hours of exposure
at 3.7 percent at sea level, and at 4.7 percent
for a simulated altitude of 27,000 feet. There
was no observable decrement in performance
under either sea level or higher-altitude
conditions. Exposure to 110, 220, and 440
mg/m3 caused mean COHb saturations of 8.3,
19.5, and 30.1 percent, respectively. These
levels produced performance decrements, in
terms of reaction times and lever presses per
minute, in only 2 of the 12 monkeys. Most
animals performed well even under conditions
where COHb attained levels of 30 percent
saturation and even though changes in
appetite and outward appearance occurred in
6 of the 12 animals.
These results suggest that this stimulus-
response pattern of a group of well-trained
monkeys was apparently not altered
by levels of COHb that are clearly detrimental
to humans. It does not seem reasonable,
therefore, to extrapolate these results to any
possible human tolerance for CO.
2. Human Data
There are several reports concerning the
possibility of CO-induced impairment of
higher nervous functions resulting in the im-
pairment of human performance. One of the
earliest of these experiments was conducted
8-14
by Forbes4 3 et al. They reported that eight
normal men who were given simple perform-
ance tests simulating automobile driving were
unaffected by exposure to CO until their
blood COHb level reached 30 percent or
more. The subjects felt normal at a COHb
level of 30 percent; the two subjects who
reached 45 percent COHb felt unequal to
driving a car and near collapse, even though
their test performance was only slightly im-
paired.
Schulte44 has employed a number of
psychological test procedures to determine
whether any impairment can be observed at
COHb levels lower than those that produce
subjective symptoms. He has also sought the
minimum level at which a measurable altera-
tion in function can be detected. The follow-
ing set of physiological and psychological
tests was performed, and constitutes one test-
ing cycle:
1. Pulse, respiratory rate and blood pres-
sure.
2. Color stimulus response test.
3. Letter stimulus response test.
4. COHb determination (Scholander and
Roughton method).
5. Plural noun underlining test.
6. Test of neurological reflexes.
7. Static steadiness test.
8. Arithmetic test.
9. Muscle persistence test.
10. ^-crossing test.
Forty-nine healthy male adults aged 25 to 55
years were exposed to approximately 115
mg/m3 (100 ppm) CO for exposure times
sufficient to produce COHb levels of up to
20.4 percent. Their responses were evaluated
during four consecutive testing cycles. The
subjects did not know during which cycle
they were being exposed to CO.
Table 8-3 shows the relationships found
between the COHb levels and the tests em-
ployed. Note that there was no correlation
between percent COHb and any of the
physiological activities or the reaction time on
the simple choice response tests (No. 1 to 8,
-------
Table 8-3. RESULTS OF PHYSIOLOGICAL AND PSYCHOLOGICAL TESTS ON SUBJECTS
EXPOSED TO 345 mg/m3 (300 ppm) CO*4
Test
1 . Pulse rate
2. Systolic blood pressure
3. Diastolic blood pressure
4. Respiratory rate
5. Muscle persistence time, left leg
6. Muscle persistence time, right leg
7. Letter responses
8. Color responses
9. Errors in letter response
1 0. Errors in color response
11. Completion time, plural-noun underlining
12. Completion time, arithmetic
13. Completion time, f-crossing
14. Errors in plural-noun underlining
15. Errors in arithmetic
1 6. Errors in f-crossing
Number of
observations
156
156
156
156
156
156
167
167
167
167
196
196
196
196
196
196
Mean (range)
72(55-102)/min.
1 22 (102-1 55) mm Hg
78 (5 5-90) mm Hg
12(9-17)/min.
27(19-47)/min.
28(1 9-5 l)/min.
69.6 (49-98)/min.
71.2(51-99)/min.
18.0(0-116)
18.7(0-115)
186.8 (87-3 17) sec
835 (501-1453) sec
123 (43-329) sec
17.7(1-46)
4.6(0-12)
3.4(0-14)
Correlation
coefficient
(between
test and
COHb level)
-0.047
-0.004
-0.025
-0.020
0.035
0.035
0.001
0.078
0.9063
0.847a
0.8 12a
0.665a
0.792a
-0.053
0.590a
0.539a
aSignificant at the 0.001 level.
and 14). There was no apparent difference be-
tween the test results of the nonsmokers and
those of the smokers, although Schulte con-
siders that the number of nonsmokers in his
study was too small to draw statistically signi-
ficant conclusions. No data on the smoking
habits of the subjects were supplied in the
report, nor was there any information on the
basal COHb levels of these subjects.
When the results obtained from each of the
tests were further divided into 20 groups ac-
cording to COHb level (0 to 0.4, 0.5 to 1.4
percent, 1.5 to 2.4 percent, etc.), it was found
that the number of errors in tests 9 through
13, and 15 and 16 increased with increases in
COHb level (see Figure 8-7). Schulte con-
siders that an effect should be detectable at a
COHb level of between 2 and 3 percent; how-
ever, the Scholander and Roughton method
of analysis for COHb does not discriminate
accurately levels below 5 percent, and hence
the lower COHb measurement categories used
by Schulte cannot be considered entirely ac-
curate.
Grudzinska4 5 studied the results of electro-
encephelograms (EEC) and other parameters
of 60 workers occupationally exposed to not
more than 115 mg/m3 (100 ppm) of CO. A
control group of 30 workers similarly em-
ployed but not exposed to CO was also
studied. The mean level of COHb was 7 per-
cent in the exposed group (levels of 11 sub-
jects exceeded 10 percent) and 3 percent in
the control group. Smokers from both groups
had higher COHb levels than those of non-
smokers. EEC's were made at rest and after
unspecified activities. A neurasthenia syn-
drome, which was based on subjective com-
plaints, was diagnosed in 63 percent of the
exposed group and 40 percent of the control
8-15
-------
ERRORS IN CHOICE LETTER RESPONSE TEST
ERRORS IN CHOICE COLOR RESPONSE TEST
100
80
60
40
20
T
I
0 5 10 15 20 25
ERRORS IN ARITHMETIC TEST
10
8
6
4
T
T
I
_L
0 5 10 15 20 25
COMPLETION OF ARITHMETIC TEST
I I
I T
1200
1100
1000
900
800
700
350
300 —
250 -
200 —
150 -o
100
= 196
5 10 15 20 25
PLURAL-NOUN UNDERLINING TEST
+ 140.1
70.5
SE = ± 3.47
CC = 0.812
5 10 15 20
COHb, percent
25
OL
o
o:
100
so
60
40
20
1 T
LU
CD
5
5 10 15 20 25
ERRORS IN t-CROSSING TEST
z
<
UJ
UJ
o
tx
7
5
3
1
300
250
200
150
100
50
0 5 10 15 20 25
COMPLETION OF t-CROSSING TEST
I To T
= ±3.83
= 0.792
I I I
5 10 15 20 25
COHb, percent
N = NUMBER OF OBSERVATIONS
PC = PREDICTION CURVE
SE =STANDARD ERROR
CC = CORRELATION COEFFICIENT
Figure 8-7. Effects of small concentrations of COHb on certain psychomotor tests.44
3-16
-------
group; but there was a statistically significant
increased incidence of headache and general
debility in the exposed group. There was a
significantly higher proportion of flat low-
voltage tracings with a scanty alpha rhythm in
the EEC's of the exposed group (p < 0.01).
Since the neurasthenia syndrome had no
well-defined clinical manifestations and be-
cause of the uncertainty as to whether the
investigation was carried out in a double-blind
fashion, these data are difficult to interpret.
Beard and Wertheim have found that CO
causes an impairment of temporal discrimina-
tion.39 Their 18 subjects were young adult
university students, all of whom were non-
smokers. The subjects, seated in a soundproof
booth, were presented with a 1,000-hertz
tone signal, the volume of which was adjusted
to well above the auditory threshold. The first
or "standard" signal was of 1-second dura-
tion, and the second or "variable" signal was
modulated in 18 steps between 0.675 and
1.325 seconds. The subjects were asked to
indicate whether the second signal was
shorter, longer, or of the same duration as the
first. The comparison stimuli were presented
in blocks of 25 trials; 8 were identical, 8
longer, and 9 shorter than the standard. A
total of 600 trials was presented to each sub-
ject in a single session, and each subject par-
ticipated in at least 15 sessions.
Figure 8—8A shows the mean percent re-
sponse after exposure to 0, 58, 115, 201, and
288 mg/m3 (0, 50, 100, 175, and 200 ppm)
CO. Each point on the graph represents the
mean performance at each CO dose (based
upon three determinations per subject) during
the second and third hours of the session, i.e.,
during 0.5 to 2.5 hours of CO exposure, since
exposure began after the first 0.5 hour. Com-
parison of performance in sessions during and
prior to CO exposure revealed significant im-
pairment by "t"-test at all doses (0.01 < p <
0.02 at 58 mg/m3; 0.001 < p < 0.01 at
higher concentrations). When discrimination
in the differences in the duration of 125 and
325 milliseconds was considered separately,
100
90
1 80
u
Q>
Q. 70
UJ
CO
Z
O
Q.
in
UI
o:
u
UJ
a:
a:
o
u
60
50
40
30
20
10
A.
DURING DISCRIMINATION OF TWO
TONES PRESENTED SUCCESSIVELY
I
I
58 115 201
CO CONCENTRATION, mg/m3
100
288
I I
B. WHEN TONES WERE
DIFFERENT
50 100 175 250
CO CONCENTRATION, ppm
| I I I
50 100 175
CO CONCENTRATION, ppm
250
58 115 201
CO CONCENTRATION, mg/m3
288
Figure 8-8. Mean percent correct responses (± one standard deviation) to 1,000-hertz
tone by 18 human subjects during exposure to CO.39
8-17
-------
the overall decrement for the latter was slight-
ly greater (60 percent) than that for the
former (35 percent), as is shown in Figure
8-8B. The percent of correct responses for dis-
crimination of differences in tone duration of
325 milliseconds was 95 percent at 0 mg/m3
of CO, compared with 50 percent when the
difference was 125 milliseconds.
Data for the time taken to obtain a signifi-
cant impairment of auditory discrimination
are shown in Figure 8-9. A fall in the percent
of correct responses was considered signifi-
cant when the mean percent of correct re-
sponses fell below 2 standard deviations of
the mean performance without CO. Figure
8-9 shows that only 90 minutes of exposure
to 58 mg/m3 CO may produce such a re-
sponse. Unfortunately, the blood COHb levels
100
UJ
u
QL
o
LL
cc.
LLJ
°- s
S!
u •=
LL. Q;
ou
.UJ
o
UJ
90 ~
80
70
60
50
40
30
20
10
0
50 100 175
CO CONCENTRATION, ppm
_| I I
250
58 115 20 1
CO CONCENTRATION, mg/m3
288
Figure 8-9. Time after initial exposure to
each concentration of CO that mean correct
response fell two standard deviations from
mean performance level in absence of CO. 3
in the studies are not available; any possible
relationship between temporal impairment
and COHb could not, therefore, be measured
directly. From the length of exposure and the
concentrations given, an increase in COHb of
about 2 percent can be inferred. Assuming a
background level of approximately 0.5 per-
cent COHb, an impairment in timing behavior
can be expected to occur at COHb levels of
about 2.5 percent.
Stewart46 et al. exposed human volunteers
to CO at concentrations of: less than 1, 29, 58,
115, 230, 575, and 1,150 mg/m3 (less than 1,
25, 50, 100, 200, 500, and 1,000 ppm).
Studies were conducted in an air-
conditioned exposure chamber in which CO
concentrations were recorded continuously
by an infrared spectrometer. Eighteen healthy
males ranging in age from 24 to 42 years of
age participated in the study. Only three of
the subjects were smokers, and these subjects
abstained from smoking for the duration of
the study. Prior to and 16 hours after each
exposure, blood samples were obtained for a
complete blood cell count, sedimentation
rate, sodium, CO2, chloride, potassium, cal-
cium, total serum protein, alkaline phos-
phatase, bilirubin, BUN, glucose, SCOT, and
COHb determinations. Over the range of CO
exposures from less than 1 to 115 mg/m3,
physiologic performance tests were periodic-
ally conducted during 8 hours of continuous
exposure to the same CO concentration.
These performance tests consisted of: hand
and foot reaction time in the AAA driving
simulator, Crawford screw test, hand steadi-
ness in the AAA steadiness test, Flanagan
coordination test, orthorator visual test, and
time-estimation hand-reaction-time test. The
latter test consisted of a series of nine tone
stimuli, followed by nine light stimuli of ap-
proximately 1, 3, or 5 seconds duration pre-
sented in a random sequence. At the termina-
tion of each stimulus, the subject depressed a
push-button for an interval estimated by the
subject to be equal in duration to the original
auditory or light stimulus. Standard EEC and
visual evoked response recordings were also
8-18
-------
obtained during exposure. Following each ex-
posure, serial venous blood samples and simul-
taneous alveolar breath samples were col-
lected for COHb saturation and CO
concentration.
No untoward subjective symptoms or
objective signs of illness were noted during
the 8 hours of exposure or in the 24-hour
period following exposure. All of the clinical
chemistries, including the repeat battery 16
hours after exposure, remained within normal
limits. There was no detectable change from
control values for any of the physiologic per-
formance tests during an 8-hour constant CO
exposure over the range of 1 to 115 mg/m3.
The latter concentration produced a blood
COHb level of 11 to 13 percent.
Three subjects were exposed to 230 mg/m3
(200 ppm) CO for 4 hours. COHb levels
reached 24.8 percent within 2 hours and were
associated with mild frontal headaches. All
clinical chemistries remained within normal
limits, but changes were observed in the visual
evoked potential. The severity of headaches
and changes in the visual evoked potential in-
creased during 2 hours of exposure to CO
concentrations of 575 mg/m3 (500 ppm); this
exposure p/oduced COHb levels of 22 to 25.4
percent. During a final exposure, subjects
were exposed to a constantly rising CO con-
centration over 2 hours until a level of 1,150
mg/m3 (1,000 ppm) was reached. This peak
concentration was maintained for an addi-
tional 30 minutes, during which the COHb
level reached 31.8 percent. Although severe
headaches were reported, no changes in clin-
ical chemistries or EKG and no impairment of
time-estimation ability were found. Perfor-
mance on the Crawford collar-and-pin test
deteriorated dramatically, and subjects
reported marked fatigue of hands and fingers
while performing the test. Changes in the
visual evoked potential were more marked
than with previous exposures.
The COHb levels were found to be so pre-
dictable and reproducible for sedentary males
from one experiment to the next that they
were able to be expressed mathematically as a
function of exposure time and concentration.
These relationships are used elsewhere in the
present report.
There is some question about the sensi-
tivity of the hand reaction-time estimation
test used in the above study as a measure of
performance response to CO exposure. The
fact that test performance did not deviate
from control even with a COHb level of 31.8
percent implies a marked degree of insensi-
tivity, especially when noticeable fatigue of
hands and fingers accompanied performance
of the manual dexterity test under the same
conditions. Thus, it is doubtful that these re-
sults can be used to refute the contrasting
data obtained by Beard and Wertheim,39 who
employed a different performance measure
for time-interval discrimination and who
found consistent deterioration of perform-
ance over the range of CO exposure from 58
to 288 mg/m3 (50 to 250 ppm). The time-
interval discrimination test of Beard and
Wertheim was very sensitive to CO exposure,
but the different measure of time estimation
employed by Stewart et al. was evidently in-
sensitive to relatively high COHb levels.
Nine male nonsmokers, ages 19 to 22 years,
were exposed to CO concentrations of 0, 58,
and 144 mg/m3 (0, 50, and 125 ppm) for 3
hours in a dome-shaped enclosed environmen-
tal system by Mikulka47 et al. at the Wright-
Patterson Air Force Base. Tests of psy-
chomotor performance, including a time-
estimation test, a tracking task, and tests of
vestibular function (balance and coordina-
tion) were administered, utilizing a double-
blind procedure. The exposure schedule was
systematically varied to remove any effect
due to training. The time-estimation test re-
quired subjects to estimate 10-second inter-
vals on an electronic switch repeatedly for 3
minutes. Each series of tests was administered
6 times during a 3-hour exposure to each con-
centration of CO. Following completion of
this sequence, five subjects were exposed to
230 mg/m3 (200 ppm) and three to 288
mg/m3 (250 ppm), and the same tests were
administered. COHb levels averaged 0.96,
2.98, 6.64, 10.35, and 12.37 percent in the
group of subjects after 3 hours exposure to 0,
8-19
-------
58, 144, 230, and 288 mg/m3 (0, 50, 125,
200, and 250 ppm), respectively. One subject
reported a slight headache during exposure to
288 mg/m3 (250 ppm), but no other subjec-
tive symptoms were reported. Group perform-
ance scores obtained during each of the 6
times the tests were administered within the
3-hour exposure period were compared with
CO exposure levels of 0, 58, and 144 mg/m3
(0, 50, and 125 ppm). CO exposures, and the
associated ultimate COHb levels of 2.98 and
6.64 percent, had no effect on tests of time
estimation, tracking task, or vestibular func-
tion of the group. Within each exposure level,
there was also no group or consistent indi-
vidual trend toward poorer performance on
these tests over the course of the 3-hour ex-
posure. The same pattern of negative results
was reported for exposures to 230 and 288
mg/m3 (200 and 250 ppm), although these
results are not actually tabulated in the text
of the report.
Important methodologic differences must
be considered in the comparison of the results
of the preceding three studies. Each group of
investigators-Beard and Wertheim, Stewart
et al., and Mikulka et al.—employed a differ-
ent method for testing time estimation. In
addition, the Stewart and Mikulka studies
were conducted in a group setting where ele-
ments of competition and other stimuli to
performance were present. In the Mikulka
study, external distractions that might com-
pete for the attention of the study subjects
were carefully eliminated or minimized. In
contrast, individual subjects in the Beard and
Wertheim study were tested in an isolated
booth for 4 hours; boredom or fatigue may
well have added to the effect of CO to pro-
duce deviations from baseline performance
when exposure and nonexposure situations
were compared. The stressful element of dis-
traction, boredom, or fatigue has been demon-
strated by Mackworth to be itself detrimental
to human performance of repetitive tasks.4 8
The synergism between a stressful test situa-
tion, as may have been present in the Beard
and Wertheim study but not in the other two
studies, and CO exposure at low concentra-
8-20
tions may account for the differences in re-
sults. Thus, differences in the method for
testing time estimation and differences in con-
ditions under which the test was administered
are possible reasons for the apparently contra-
dictory results of these three studies. The rele-
vance of the various study results to more
complex modes of behavior, particularly to
automobile driving, cannot be readily judged.
Although Stewart et al. and Mikulka et al. did
perform tests of more complex behavior,
these tests were administered in a highly arti-
ficial setting. The failure to obtain significant
changes from baseline even when COHb con-
centrations of 12 and 33 percent were reached
suggests that the undistracted attention of the
subjects to the experimental setting could
overwhelm the possible subtle effects of CO
on performance. The same phenomenon was
observed by Forbes43 et al. in the study of
the influence of CO on the ability to drive
automobiles, discussed earlier in this section.
Two subjects who attained COHb levels of 47
and 50 percent, respectively, were able to
concentrate on their tests and perform reason-
ably well even though both reported that they
were well aware that they were unable to
drive a car; one of the subjects became un-
concious for a few seconds after walking up a
few steps during the test. Beard and
Wertheim, on the other hand, tested a rela-
tively simple performance task, but may have
added a relevant factor, namely boredom or
monotony. Apparently test method and test
conditions must be considered when con-
firmatory studies are designed or when com-
parisons between studies are made. In this
light, the results of these three studies are not
contradictory. Until more evidence is ob-
tained, each of the results must be considered
to be highly specific to the method and condi-
tions of testing, and extrapolations to other
modes of behavior should be restricted.
Investigators other than Beard and Wert-
heim have reported deterioration of perform-
ance at low COHb levels. Ray and Rock-
well4 9 tested various automobile driving tasks
performed by three young males at COHb
-------
levels of 0, 10, and 20 percent. The sub-
jects were required to drive a car during night
hours on an interstate highway while CO was
administered to maintain one of the above
COHb saturations. The subjects had been
previously trained in the performance of each
test procedure. COHb levels of either 10 or 20
percent increased the time needed to respond
to taillight intensities (brakelight) and to
changes in speed. These increases also altered
their ability to maintain a constant speed of 65
miles per hour, to maintain a constant center-
of-lane position, or to maintain a 200-foot sep-
aration from the car in front. Performance of
these tasks required attention to multiple
stimuli, some of which distracted the driver
and prevented him from concentrating on any
single task for prolonged time periods.
McFarland50 et al. used a visual discrimi-
nometer to test effects of CO and altitude on
visual thresholds of trained male subjects age
16 to 25. In this test, the subject looked
through a microscope and fixed on a red
point of light in an illuminated background.
Measurements were made of the lowest in-
tensity of light, presented in flashes of 0.1
second, that could be distinguished against
the illuminated background. Carbon mon-
oxide or gas mixtures containing different
percentages of oxygen to simulate various alti-
tudes were administered through a closely
fitting mask during the test procedure. The
concentration of COHb in finger-prick blood
at the beginning of the experiment and 10 to
15 minutes after each CO administration was
determined by the microgasometric method
of Scholander and Roughton. COHb level dur-
ing CO administration ranged from 5 to 20
percent. As shown in Figure 8—10, the visual
threshold increased (i.e., the light had to be
more intense to be distinguished against the
background) as COHb levels increased over
the entire range of exposure. The effects of
CO hypoxia and simulated altitude were prac-
tically equivalent in this test. That is, the
effect of a given COHb level was the same as
that of an equal loss of percent O2Hb from
high altitude. These results clearly showed
changes in visual threshold at COHb levels as
0.4
UJ — 0.3
UJ 1- Z
a: u D
I UJ 0 0.2
i- a: °
_ tx o
-OO 0.1
to
I
I I
I
0 5 10 15 20 25 30 35 40
COHb, percent
Figure 8-10. Relation between COHb and
visual threshold.^
low as 5 percent; the same magnitude of
change in visual threshold was produced by a
simulated altitude of approximately 8,000
feet.
Beard and Grandstaff5' recently reported
the results of CO exposure on a second test of
timing function. While individually isolated in
a noise-insulated exposure chamber, seven
subjects estimated the passage of 10- and
30-second intervals. Estimation of 10-second
intervals was not affected by CO exposure. A
highly significant dose-related performance
decrement occurred, however, with attempts
to estimate 30-second intervals. Exposures of
64 minutes at 58 nig/m3 (50 ppm) produced
significant impairment. In the same report,
studies of Wertheim on the effects of CO
exposure upon visual performance were re-
ported. Four tests of visual function at
various levels of brightness were conducted.
Four subjects were exposed in random order
to CO concentrations of 0, 58, 173, and 288
mg/m3 (0, 50, 150, and 250 ppm), for a total
exposure time of 1 hour on each test day.
Exposures were always preceded and followed
by performance testing without CO. Subjects
were individually isolated in exposure booths
for a period of 2-1/2 hours on each study day.
Results of these studies, shown in Table 8—4,
indicate consistent impairment of visual per-
formance for three of the four measures of
visual function. COHb levels were estimated
from expired air samples. At each CO concen-
tration, there was a rapid recovery in perform-
ance subsequent to the exposure; test results
returned to normal more quickly than did the
CO concentrations in the expired air.
8-21
-------
Table 8-4. EFFECTS OF VARYING CO EXPOSURE ON VISUAL PERFORMANCE51
Test of visual performance
Relative brightness threshold
Critical flicker fusion frequency
Visual acuity
Absolute threshold for light
CO exposures producing significant impairment
Concentration,
mg/m^
58
173
173
288
288
58
173
288
58
58
0 to 290
Concentration,
ppm
50
150
150
250
250
50
150
250
50
50
0 to 250
Time,
min.
49
17
49
17
49
50
50
50
27
60
17 to 60
Estimated
COHb
level,
%
3.0
3.0
5.0
4.0
7.0
3.0
5.0
7.5
3.0
3.3
._
Degree of
impairment,
%
4.4
5.0
8.0
3.6
8.6
5.0
8.0
2.0
5.5
17.5
No consistent
effect
Halperin52 et al. exposed four healthy
male adults aged 16 to 25 years to measured
amounts of pure CO ranging from 100 to 300
milliliters. The CO was injected slowly into
the intake tube of a close-fitting mask. The
usual duration of the experiment was from 3
to 4 hours. The total length of exposure to
CO was from 10 to 15 minutes, and this re-
sulted in COHb levels of up to almost 20 per-
cent. Visual threshold determinations were
made at 10-minute intervals throughout the
experiments. The subjects sat in a darkened
room and looked with one eye into a micro-
scope. Each subject saw a large circular field,
uniformly illuminated at an intensity of about
0.002 foot-candle. The center of the field
contained a small point of red light to serve as
a fixation point. Just below the latter, a 1 x 1
degree object was presented in flashes of 0.1
second. The lowest intensity distinguishable
against the dim background was determined
from the mean of 10 measurements in each
test. As can be seen in Figure 8—11, a measur-
able impairment in visual function was detect-
able when the blood COHb concentrations
reached 4 to 5 percent; at higher COHb con-
centrations, greater degrees of impairment
were measured. Control experiments, in
which innocuous odors were introduced into
the intake tube of the facial mask, showed no
significant change in visual discrimination.
8-22
In the same series of experiments, a study
of hypoxic anoxia was made in which normal
air was replaced by nitrogen-oxygen mixtures.
The oxygen concentrations ranged from 16 to
9 percent, thus producing simulated altitudes
ranging from 7,000 to 20,000 feet. During
recovery from the CO exposure or the anoxia,
the subjects breathed either room air, 100
percent oxygen, or "carbogen" (consisting of
93 percent oxygen and 7 percent carbon di-
oxide). No visual determinations were made
on the subjects while they breathed
"carbogen," since the latter induced respira-
tory movements which interfered with foveal
fixation and thus influenced the visual tests.
The subjects were not told which gas mixture
they were breathing. (However, it can be
assumed that "carbogen" produced some
hyperventilation of which the subjects were
aware.) The blood COHb was determined by
the gasometric method of Scholander and
Roughton.30 Measurements were taken at the
beginning of the experiment, at 10 to 15
minutes after each CO administration, and at
20- to 30-minute intervals during the post-
exposure period. The results of a typical
experiment are shown in Figure 8—11.
One of the most important findings was
that recovery from the detrimental effects of
CO on visual function lags behind the elimina-
tion of CO from the blood; this impairment
-------
o
1/5
LLI
OS
I
4.0
3.9
3.8
ROOM AIR
11.0% 02 (SIMULATING
15,400 ft, 4,694 m)
100% 02
"CARBOGEN"
> e
o
6"
o
3.7
3.6
3.5
3.4
I I
0.5
ROOM AIR
100% 02
I I I I I I I I I I I I
I I
COHb, percent
— 4.5 -w- 9.4 ••»• 15.8 •*• 19.7
1 I
I
i i li i fi
14.2
ROOM AIR
I I
8.0
15
30
60
90 120 150
TIME, minutes
180
210
240
Figure 8-11. Effect of progressive increases of blood COHb on visual threshold, and of oxygen
and carbogen (93% 02 + 7% C02) in counteracting this effect.52 (-— Indicates time during
which CO exposure occurred; I indicates point at which blood was taken for COHb determina-
tion).
appears to be determined by the duration of
the presence of CO as well as by its concentra-
tion. The time course followed by the COHb
and visual impairment appears to depend on
the composition of the gas during the post-
anoxic period. "Carbogen" was 2-1/2 times
more effective than 100 percent oxygen in
promoting CO elimination and an associated
drop in the visual threshold. Subsequent ex-
posure to room air caused an increase in the
visual threshold (i.e., further impairment in
visual perception), although the COHb levels
began to fall (Figure 8-11). When a single
subject was exposed to CO at simulated alti-
tudes, his pattern of results was similar to that
at sea level. The latter series of experiments is
discussed more fully in Section H.
The results reported in Halperin's paper are
selected from individual subjects. No data are
given to indicate the degree of variation
among subjects, or the degree of variation for
an individual from day to day. There is no
indication as to whether an individual's
threshold level when breathing unpolluted
room air remains the same over a period of 3
to 4 hours. In addition, no statistical level of
significance was applied to the elevation of
the visual threshold above the basal level,
though standard deviations are shown for the
graphed data. Data on smoking habits of these
subjects was not given in the report; however,
in a preliminary series of experiments on one
of the same subjects, it was observed that
inhalation of the smoke of one cigarette pro-
duced a blood level of 2 percent COHb and
caused a distinct impairment of visual sensi-
tivity. After three cigarettes the blood COHb
was 4 percent, and the effect on visual sensi-
tivity was equal to that produced by hypoxic
8-23
-------
anoxia simulating an altitude of almost 8,000
feet.50
In a study by Hanks53 performed at the
Rancho Los Amigos Hospital environmental
control chamber, groups of five nonsmoking
healthy young males were exposed in random
order to CO continuously for 4 hours. CO
concentrations ranged from 0 to 115 mg/m3
(100 ppm). A critical tracking task and visual
pursuit tasks were unaffected by the exposure
to CO. Test subjects were untrained in per-
formance of these tasks, and both learning
effects and effects of competition within
groups were reported.
3. Discussion
Several reports on psychomotor effects of
CO exposure appear to be in conflict, but
explanations have been presented to account
for the apparent inconsistencies. It is quite
likely that some of the performance impair-
ment associated with CO exposure can be
overcome by attention to the task assigned.
The major tasks of importance with which CO
might interfere, e.g., those involved in driving
on a highway or a street, could very well arise
unexpectedly and not be subject to extra
attention by the exposed individual. Perhaps
what one really should be testing, then, is
vigilance.
The sensitivity of the results obtained by
Beard and Wertheim,39 Ray and Rockwell,49
and McFarland5 ° are in marked contrast to
many other studies. Again it should be
emphasized that their results should be con-
sidered highly specific to the methods and
conditions of testing. It is likely that external
stimuli may have to be examined along with
CO exposure to detect the subtle effects of
the latter. Subsequent studies should, there-
fore, account for the effects of extraneous
factors such as sounds, fatigue, boredom, and
other distractions, and should further evaluate
the possibility of an interaction between such
stimuli and the task performance thought to
be affected by exposure to CO.
Since it is amply demonstrated that
subjects smoking cigarettes are likely to have
measurable and possibly significant increases
8-24
in COHb levels, it is important to carry out
studies either on nonsmokers or on indi-
viduals whose smoking exposures are clearly
defined and whose baseline COHb levels are
established. At the present time, it is uncer-
tain to just what extent smokers do adapt to
prolonged increases in blood COHb levels.
F. EFFECTS OF CARBON MONOXIDE
ON CARDIOVASCULAR SYSTEM
1. Animal Data
a. Short-Term Exposure
Lindenberg38 exposed 27 dogs to concen-
trations of CO greater than 1,150 mg/m3
(1,000 ppm) for 1 to 4 hours. A second group
of 11 dogs was exposed to an air-nitrogen
mixture producing an oxygen deficit equiva-
lent to that caused by CO inhalation. In
animals exposed to CO, the COHb levels
reached 37 to 40 percent. In all animals where
EKG's were recorded (13 out of 27), a depres-
sion of the R-wave, elevation of the ST seg-
ment, an occasional increase in the T-wave,
and deepening of the Q- and S-waves were
recorded. In some animals, these changes in
EKG and associated irregularities of the heart
action (premature ventricular contractions re-
sulting in the abolition of arterial pulsation)
persisted for several days. In the dogs sub-
jected to severe hypoxia, the EKG changes
were essentially the same as those seen in dogs
exposed to CO. At autopsy, the hearts of
several animals revealed dilatation of the
ventricles, especially the right one. In four
CO-exposed and two hypoxic animals, small
areas of muscle necrosis were observed, as
well as fine granular fatty degeneration of
muscle fibers in certain areas, particularly in
the interventricular septum and in the outer
wall of the right ventricle.
b. Long-Term Exposure
Two studies have revealed that continuous
exposure of animals to low levels of CO can
cause cardiac changes. Ehrich5 4 et al. exposed
four dogs to about 115 mg/m3 (100 ppm) CO
for 5-3/4 hours a day, 6 days a week for 11
weeks. The resulting average COHb level was
-------
21 percent. A second group of six dogs was
exposed to air in which the oxygen content
was reduced to 10 percent. The authors con-
sidered that this led to a PQ2 in the blood
approximating that which would be present at
a blood level of 21 percent COHb. These ex-
posures were continued for 4-1/2 hours a day,
6 days a week for 11 weeks. All animals were
sacrificed 3 months after the termination of
the experiment. No EKG changes were ob-
served during the first week. After the second
week, however, one CO-poisoned dog and one
hypoxic dog exhibited inversion of normally
upright T-waves. Another hypoxic dog devel-
oped an elevation of the ST segment. A
second CO-poisoned dog developed an in-
verted cone-shaped T-wave during the tenth
week. These EKG changes appeared to be
irreversible, since they continued unabated
until about 3 months after the exposures
when the animals were sacrificed. The authors
noted the resemblance of these EKG changes
to those typically seen in myocardial anoxia.
The gross appearance of the hearts was
normal, but microscopic examination revealed
that all four CO-poisoned animals and one
oxygen-deficient animal had marked degene-
rative changes in individual muscle fibers. It
should be noted that one control dog showed
similar changes, although the number of con-
trol dogs used in this study was not reported.
Lindenberg38 exposed 15 dogs to 58
mg/m^ (50 ppm) CO for 6 weeks. Seven of
the dogs were exposed for 6 hours a day for 5
days a week. Eight were exposed continu-
ously for 24 hours a day, 7 days a week. A
second group of eight dogs was exposed to
115 mg/m^ (100 ppm) CO on a similar sched-
ule, four intermittently and four continu-
ously. Five dogs were used as controls. All
dogs were sacrificed a few days after the end
of the experiment. The dogs exposed to 58
mg/m^ developed blood COHb levels of from
2.6 to 5.5 percent. There were no changes in
the hemoglobin content or hematocrit. Five
intermittently and five continuously exposed
dogs developed EKG changes during the third
week similar to, but less severe than, those
observed from short-term exposures to higher
concentrations. Higher COHb levels in dogs
after exposure to 58 mg/m^ (50 ppm) CO
were reported by Musselman5 s et al. in
another study (see below).
The dogs exposed to 115 mg/m^ developed
COHb levels of from 7 to 12 percent. Some-
what higher COHb levels would have been ex-
pected in man after similar exposures.3 8 All
dogs showed abnormal EKG recordings after
about 2 weeks, with depression of the R-wave
voltage, elevation of the ST segment, occa-
sional deepening of the Q-wave, and occa-
sional premature ventricular contractions. At
autopsy, the most frequent finding was a dila-
tation of the right heart chambers, and also,
occasionally, of those on the left side of the
heart. Histologically, some hearts showed
degeneration of muscle.
In contrast, Musselman5 5 et al. exposed
100 rats, 40 rabbits, and 4 dogs to 58 mg/m^
(50 ppm) CO for 24 hours a day, 7 days a
week for 3 months. No changes were noted in
the EKG's or the pulse rates of the dogs.
Moreover, pathologic examination of organs
and tissues revealed no differences between
exposed and control animals in any of the
three species. The average COHb levels
reached were 7.3 percent for dogs, 3.2 per-
cent for rabbits, and 1.8 percent for rats. The
dogs showed significant increases in hemo-
globin levels (12 percent), hematocrit (10 per-
cent), and red blood cell (RBC) counts (10
percent). It should be noted that the increase
in the RBC count in one dog alone accounted
for over half the total increase established by
the whole group (Table 8-5).
Roussel56 et al. have detected reversible
EKG changes in rodents exposed to CO. Rats
were exposed to 17 and 58 mg/m^ (15 and 50
ppm) CO for 24 hours a day for 3 months.
The exposures to 58 mg/m^ caused a slight
decrease in the QRS voltage during the first 2
weeks of exposure; this subsequently returned
to normal despite continued exposure. No
changes in heart weights were observed.
Although there were increases in hemoglobin
level, hematocrit, and RBC counts, they were
significant only at thep = 0.10 and p = 0.15
levels.
8-25
-------
Table 8-5. PERCENT CHANGE IN BLOOD VALUES OF INDIVIDUAL DOGS IN
RESPONSE TO 58 mg/m3 (50 ppm) CO INHALATION DAILY
FOR 3 MONTHS55
Dogs
Unexposed
Mean
Exposed
Mean
Statistical signi-
ficance of change
Dog ID
numbera
191
192
124
185
188
193
Hemoglobin
-2
-2
-2
+7
+10
+14
+16
+11.75
p<0.05
Hematocrit
-6
-5
-5.5
+5
+8
+14
+11
+9.5
p<0.10
RBC count
-2
-5
-3.5
+6
+4
+8
+22
+10.0
aEach line of data is from a single animal.
Astrup57 et al. have recently reported that
cholesterol-fed rabbits continuously exposed
to CO for 10 weeks (with exposure levels suf-
ficient to produce COHb levels of 15 percent
for 8 weeks and 30 percent in the last 2
weeks) developed cholesterol deposits in
aortic tissue at a rate 2.5 times faster than
nonexposed cholesterol-fed animals. Intermit-
tent CO exposures for 8 hours a day for 10
weeks (sufficient to produce COHb levels of
20 percent) resulted in a fivefold excess in the
cholesterol content of aortic tissue of exposed
versus control rabbits. Cholesterol feeding and
hypoxia (10 percent oxygen in nitrogen) pro-
duced similar effects, but to a lesser degree.
Carbon monoxide exposure without choles-
terol feeding induced arterial lesions consist-
ing of endothelial hypertrophy and prolifera-
tion and focal subintimal edema; these lesions
could not be distinguished from those associ-
ated with spontaneous arteriosclerosis occur-
ring in rabbits. The authors speculated that
CO or hypoxia enhanced the development of
atheromatosis by increasing vascular perme-
ability to lipoproteins.
8-26
The effects of acute high-level and chronic
low-level exposure to CO on cardiovascular
and cerebral function and morphology in dogs
has been studied by Preziosi.58 Acute expo-
sure to CO concentrations exceeding 1,150
mg/irp (1,000 ppm) and producing maximum
COHb levels of 3 to 40 percent, resulted in
high mortality and, in survivors, sudden rises
in cerebrospinal fluid (CSF) pressure and EKG
changes (consisting of depression of R-waves,
elevation of the ST segments, and deeping of
the Q-waves). Major voltage depression and
complete abolition of electrical potentials of
the EEC occurred only after the EKG showed
severe changes. No gross pathology was ob-
served in the brains of surviving dogs, but
histologic alterations were noted, ranging
from microglial reactions to extensive necrosis
of the white matter. In the heart, small areas
of muscle necrosis and fine granular fatty de-
generation of muscle fibers were found.
Chronic intermittent and continuous expo-
sure of 15 animals to 58 mg/m^ (50 ppm) CO
and of 8 animals to 115 mg/m^ (100 ppm)
CO for 6 weeks resulted in EKG changes
-------
similar to, but of lesser magnitude than, the
changes in the acute exposure studies in the
majority of dogs. COHb concentrations
reached 2.6 and 5.5 percent in dogs inter-
mittently or continuously exposed to 58
mg/m3 (50 ppm), respectively, and 7 and 12
percent in the 115 mg/m3 (100 ppm) expo-
sure group, respectively. At autopsy, the most
frequent finding was a dilatation of the right
cardiac chamber and dilatation of the lateral
ventricles of the brain.
2. Human Data
a. Studies of Oxygen Debt
As a result of observations that the oxygen
debt* accumulation in response to exercise is
significantly greater in smokers than in
nonsmokers,5 9 - 60 Chevalier61 et al. have at-
tempted to determine the cause of the dif-
ference. In their study, CO was inhaled by ten
nonsmokers to raise blood COHb levels to the
range seen in a control group of'nine smokers.
Pulmonary function measurements were made
before and after a 2.5- to 3.5-minute period,
during which gas containing 5,750 mg/m3
(5,000 ppm) CO in compressed air was in-
haled. A standard excercise test consisting of
a 5-minute exercise period on a bicycle
ergometer was employed; the work load was
the same for each subject. Measurements of
oxygen uptake were obtained at 30-second
intervals during a 4-minute period of rest, a
5-minute period of exercise, and another
10-minute period of rest following work.
Heart rates were obtained for a continuous
EKG. In addition, several measurements of
pulmonary function were performed: pul-
monary diffusing capacity (DL^o), inspira-
tory capacity, inspiratory reserve volume,
expiratory reserve volume, tidal volume, vital
capacity, minute ventilation, airway resist-
ance, respiratory frequency, functional resid-
*The oxygen debt (O2D> = ®\ - °\> where °2 is the
oxygen uptake during a resting period before exercise
and Oj is the increased oxygen uptake after exercise
has ceased. Because of the individual differences in
the increase of oxygen uptake with exercise, the
oxygen debt may also be expressed as a ratio.
ual capacity, residual volume, and total lung
capacity.
Following CO inhalation, a level of 3.95 ±
1.87 percent COHb was obtained, compared
with 3.5 ± 1.8 percent COHb observed in the
group of smokers used as controls. Individual
data on oxygen uptake and oxygen debt be-
fore and after inhalation are shown in Table
8—6. Following CO inhalation, no significant
change was observed in the mean oxygen
uptake, although there was a statistically non-
significant increase in the mean oxygen debt.
There was a significant increase when the
oxygen debt was related to the total increased
oxygen uptake. The mean oxygen debt ratio
increased 14 percent, from 0.213 to 0.243 (p
< 0.05). The mean heart rate was significantly
less after inhalation of CO, both at rest and
during exercise (Table 8—7). There was a
statistically significant decrease in the
mean DL(^Q at rest after inhalation of CO (p
< 0.05), although all values remained within
normal limits. The difference was not appar-
ent during exercise. In pulmonary function
studies, significant changes (p < 0.05)
occurred in inspiratory capacity, total lung
capacity, and maximal voluntary ventilation
(Table 8—8). These findings could partially
represent the effects not related to CO expo-
sure, since sham exposure and double-blind
technique were not used.
b. Studies of Hemodynamic Responses
Changes in gas exchange following expo-
sure to CO are dictated by changes in the
O2Hb dissociation curve in the presence of
various concentrations of COHb, as is illus-
trated in Figure 8—1. Because the dissociation
curve is shifted to the left, maintenance of the
pre-exposure arterio-venous oxygen difference
and oxygen delivery requires that the venous
oxygen tension be decreased. This decrease in
mixed venous oxygen tension has been shown
to occur experimentally by Ayres62 et al.
Cardiorespiratory responses of five subjects to
brief exposures of relatively high levels of CO
were determined by transvenous catheteriza-
tion of the heart. Intracardiac pressures and
8-27
-------
Table 8-6. TOTAL INCREASED OXYGEN UPTAKE (VO2), OXYGEN DEBT (O2D), AND RATIO OF
02D TO V02 BEFORE AND AFTER CO INHALATION BY TEN NONSMOKERS61
Subject
1
2
3
4
5
6
7
8
9
10
Mean
SD
P
Before CO inhalation
V02,
ml of O2
5520
6160
5840
6080
5840
6160
6400
6360
5680
5860
5990
±290
°2D,
ml of O2
1240
2580
1000
1360
1800
1480
1880
2040
1660
1440
1648
±452
02D/V02
0.183
0.295
0.146
0.183
0.236
0.194
0.227
0.243
0.226
0.196
0.213
±0.042
After CO inhalation
Work Vo2,
ml of O2
5940
5940
5660
5920
5200
6340
5560
5860
5880
5640
5794
±301
<0.10
02D,
ml of O2
1060
2680
1900
1040
1840
2020
1760
1860
2420
1840
1842
±510
<0.20
02D/V02
0.151
0.310
0.251
0.174
0.261
0.265
0.240
0.240
0.291
0.246
0.243
±0.48
<0.05
Table 8-7. HEART RATE AND PULMONARY DIFFUSING CAPACITY (DLCO) BEFORE
AND AFTER CO INHALATION BY TEN NONSMOKERS61
Heart rate,
beats/min.
Mean
SD
P
DL^Q, ml/min x
mm Hg
Mean
SD
P
Before CO inhalation
Rest
90.0
±8.9
33.9
±5
2 min.
exercise
137.8
±9.7
45.4
±7
5 min.
exercise
143.6
±11.0
48.3
±8
3 min.
after
exercise
102.4
±13.5
37.4
±6
After CO inhalation
Rest
82.0
±7.2
<0.01
31.3
±3
<0.05
2 min.
exercise
129.2
±8.7
<0.02
45.5
±6
5 min.
exercise
135.8
±11.3
<0.01
46.3
±8
3 min.
after
exercise
94.8
±14.1
<0.10
36.7
±5
8-28
-------
Table 8-8. MEAN PULMONARY FUNCTION STUDIES BEFORE AND AFTER CO
INHALATION BY TEN NONSMOKERS61
Inspiratory capacity ml
Inspiratory reserve
volume, ml
Expiratory reserve
volume, ml
Tidal volume, ml
Vital capacity, ml
Residual volume, ml
Total lung capacity, ml
Functional reserve
capacity, ml
Max. breathing
capacity, liter/min.
Max. expiratory flow
rate, liter/min.
Airway resistence,
cm H2O/liter-min.
Before
3655±415
2745 ± 606
2075 ± 799
915 ±352
5820 ±740
1975 ±524
7705 ± 1083
4050+ 1100
175 ±23
585 + 60
0.89 ±0.22
After
3380 ±419
2580 + 650
2155 ±788
805 + 482
5530 + 740
2010 ±495
7545 ± 993
4160 ±930
185 ±27
590 ±53
1.06 ±0.62
Direction
of
change
.
+
.
.
+
+
+
+
+
P
<0.05a
<0.02
<0.60
<0.20
<0.10
<0.80
< 0.02a
<0.46
<0.05a
<0.50
<0.40
a Differences statistically significant.
mixed venous blood samples were obtained
by using a cardiac catheter positioned in the
main pulmonary artery. Arterial blood was
sampled from a brachial artery. Oxygen ten-
sions were measured before, and 5 to 7
minutes after, inhalation of 0.4 percent
(4,600 mg/m3 or 4,000 ppm) CO in air. The
data are shown in Table 8-9. Oxygen ten-
sions of arterial and mixed venous bloods
decreased an average of 7.3 and 13.3 percent,
respectively, when the COHb rose to between
5 and 10 percent. The difference in arterial
and venous blood, which reflects extraction
of oxygen by the tissues, increased in all five
subjects. In the fifth subject, who received the
greatest amount of CO, the left atrial pressure
rose and the cardiac output fell, indicating
development of abnormal left ventricular
function (such changes occur with the onset
of congestive heart failure). Intracardiac pres-
sures, cardiac output, oxygen consumption,
and ventilation did not change in the remain-
ing four subjects.
Ayres63 et al. have also reported on a
study of 26 patients, each of whom had a
catheter placed in the ascending aorta and
pulmonary artery. Samples of mixed expired
air and arterial, mixed venous, and coronary
sinus (venous) blood were obtained before
exposure. The subjects breathed a mixture of
5 percent (57,000 mg/m3 or 50,000 ppm) CO
in air for a period of 30 to 120 seconds. Ten
minutes after exposure, repeat samples of
blood and mixed expired air were collected
while the subjects breathed room air. Coro-
nary blood flow was measured immediately
before and 10 minutes after exposure.
Table 8—10 shows mean values for selected
cardiorespiratory measurements in the 26
subjects before and after CO inhalation. The
significant increase (p < 0.01) in average
8-29
-------
Table 8-9. HEMODYNAMIC AND RESPIRATORY RESPONSES OF FIVE
SUBJECTS TO CO INHALATION62
Subject
1-
Before
After
2_
Before
After
3-
Before
After
4-
Before
After
5-
Before
After
COHb,
%
0.48
8.84
6.29
0.37
4.95
0.96
9.69
Pressure, mm Hg
LAa
28
28
3
3
9
9
7
11
PAb
9
9
14
12
13
13
12
18
P c
ao2
89
81
86
80
74
68
84
79
77
72
PV
45
42
37
30
42
37
49
42
41
35
A-V diff6
percent
by volume
3.40
3.82
3.96
4.55
3.92
4.24
4.00
4.66
4.02
4.81
Cardiac
output,
liters/min.
5.23
4.46
4.37
4.35
4.31
4.17
5.32
6.54
6.00
4.68
Vent/
liters
4.23
4.23
4.68
5.72
2.55
3.11
5.43
7.36
4.87
4.24
PC02>
mm Hg
34
36
36
36
36
40
39
38
36
39
KEY:
aLA =
V02
eA-V diff
'Vent =
C02
Left atrium (wedge).
Pulmonary artery (mean).
Arterial oxygen tension.
Mixed venous oxygen tension.
Arterial-venous difference.
Ventilation per square meter of body
surface area per min.
Carbon dioxide tension.
oxygen extraction ratio indicates a more com-
plete extraction of oxygen from perfusing
arterial blood in the presence of increased
COHb. There was a mean decrease of 20 per-
cent in the venous oxygen tension, and this
can be associated with the increase in COHb
concentration. This decrease implies a similar
decrease in tissue oxygen tension and suggests
the possibility that some cellular processes
that are particularly sensitive to oxygen ten-
sion could have been inactivated. The de-
crease in the mixed venous oxygen tension
was regarded as a major primary response to
CO inhalation, and Ayres believes that other
hemodynamic changes must be considered as
secondary. The associated increases in cardiac
output were considered a compensatory
mechanism for tissue hypoxia, since they re-
8-30
semble the physiologic response to hypox-
emia.
Peripheral tissues normally extract about
25 percent of the oxygen present in arterial
blood; the remaining 75 percent serves as a
reserve supply for increased oxygen needs.
The mixed venous oxygen tension is normally
about 40 mm Hg, but during exercise it may
drop to 20 mm Hg. In contrast, the myo-
cardial oxygen requirements are such that,
even at rest, 75 percent of the oxygen is ex-
tracted from the coronary circulation. Cor-
onary venous blood is, therefore, only about
25 percent saturated, corresponding to an
oxygen tension of about 20 mm Hg. No sub-
stantial reserve of oxygen is available to tissue
supplied by the coronary vasculature unless
the coronary artery dilates in response to low
-------
oxygen tensions. The coronary circulation is
thus capable of increasing the flow rate in
response to increased oxygen needs, rather
than increasing the percent of oxygen extrac-
tion. Coronary vascular disease, however, may
prevent an increase in coronary blood flow in
response to need, and the myocardium may
be forced to attempt to extract more oxygen
at the expense of an already reduced coronary
venous and tissue oxygen tension.
The responses of the myocardium to in-
creased oxygen requirements induced by CO
inhalation in patients both with and without
coronary disease have also been studied by
Ayres63 et al., by means of an additional
parameter to measure the response to CO.
During periods of insufficient oxygen supply,
the citric acid (Krebs') cycle, important in
glucose metabolism, is impaired; the utiliza-
tion of pyruvate produced by glycolysis is
decreased, and results in an accumulation of
pyruvate in the cytoplasm and the resultant
transformation of pyruvate into lactate. In-
creasing cellular concentrations of lactate and
pyruvate decrease in normal extraction of
these metabolites from the coronary blood.
The extraction ratio of either lactate or
pyruvate (the arterio-coronary sinus differ-
ence divided by the arterial concentration)
can thus be a useful index for expressing oxi-
dative metabolism; these parameters are rela-
tively independent of arterial concentrations.
The extraction ratios for both metabolites
range from 15 to 30 percent when oxygen is
plentiful. During periods of inadequate oxy-
genation, however, extraction decreases, and
lactate and pyruvate may actually be pro-
duced by the myocardium. Under these con-
ditions, coronary sinus concentrations exceed
arterial concentrations.
Myocardial metabolic studies were con-
ducted on seven patients with noncoronary
heart disease and four patients diagnosed as
having coronary artery disease. All patients
had a catheter placed in the proximal coro-
nary sinus. The data from this study are
shown in Table 8—11. In contrast to the
systemic gas exchange studies, the oxygen ex-
traction decreased for both groups and could
be correlated with an increase in COHb. The
oxygen extraction ratio also decreased in each
of the two groups (cf. an increase in the sys-
temic studies). Coronary blood flow in-
creased significantly in the patients with non-
coronary heart disease, but did not in those
with coronary heart disease. Lactate extrac-
tion ratios changed to production in both
groups, but the change was statistically signifi-
cant only for the patients with coronary heart
disease. Figure 8—12 shows the responses of
three representative subjects, one with coro-
nary artery disease, one with mitral stenosis,
and a third with emphysema. Changes similar
to those already described occurred in the
patients with mitral stenosis and coronary
artery disease. The emphysematous patient
was hypoxemic at rest (PaO2 ~ 47 mm Hg);
and, when the COHb level increased 6 to 7
percent, there was an increase in coronary
blood flow and a drop in the mixed venous
and coronary sinus oxygen tensions from 20
and 20 mm Hg to the extremely low levels of
12 and 2 mm Hg, respectively. It can be noted
from the examination of Table 8—11 that the.
average blood COHb concentrations of all 11
subjects at the time these effects were meas-
ured were about 8.5 to 9 percent. From
examination of Figure 8—12, however, it can
be noted that at least two representative
patients had blood COHb levels considerably
lower than the average (cf. 5.58 percent
COHb levels above 5 percent, such as those
disease and 6.37 percent COHb in the patient
with emphysema).
From these studies, it would appear that
persons with coronary heart disease and
emphysema may be particularly susceptible to
exposures of CO that could lead to blood
COHb levels about 5 percent, such as those
that may be encountered in smoking or, less
frequently, in community air pollution. Be-
cause in this experiment there was only a
brief exposure to very high CO levels, the ob-
served effects are difficult to relate to equi-
librium conditions or longer exposures.
Both of Ayres' studies62-63 show that in-
creased COHb lowers the arterial oxygen ten-
sion (Tables 8—9 and 8-10). The more recent
8-31
-------
Table 8-10: SYSTEMIC CARDIORESPIRATORY MEASUREMENTS
IN 26 SUBJECTS BEFORE AND AFTER CO INHALATION63
Measurements
COHb, percent
Arterial PO^C. mm Hg
Venous PQ mm Hg
Arterial PrO-A mm Hg
2
Ventilation, liters/min.
Cardiac output, liters/min.
Oxygen extraction,6 ml/ 100 ml
Oxygen extraction ratiof
Alveolar-arterial O2 difference
Control
mean
0.98
81
39
40
6.86
5.01
4.30
0.27
20
CO
mean
8.96
76
31
38
8.64
5.56
4.56
0.32
29
Fa
22.1
94.5
4.2
4.1
4.4
2.7
31.2
7.0
pb
<0.01
<0.001
<0.05
<0.05
<0.05
<0.20
<0.01
<0.05
aF = variance ratio calculated for paired data with interaction as denominator.
"p = probability that observed difference between control and CO means is due to
chance.
cPOo = oxygen tension.
PCOT = carbon dioxide tension.
eOxygen extraction = arteriovenous oxygen content difference.
Oxygen extraction ratio = oxygen extraction divided by arterial oxygen content.
one63 also shows that the alveolar-arterial
oxygen difference (A-aDQ2) is increased
(Table 8-10); this difference is an index of
the inefficiency of oxygen transfer from the
lungs to the blood. Brody and Coburn64 have
recently shown, both theoretically and experi-
mentally, that under some conditions an in-
creased A-aDQ2 results from changes in the
sigmoid shape of the C^Hb dissociation curve
induced by CO. These investigators have calcu-
lated the effect of 0 to 50 percent COHb on
the A-aDQ2 under conditions of veno-arterial
shunting and ventilation and perfusion im-
balance, and have compared this to the effect
of an equivalent degree of anemia (which does
not alter the sigmoid shape of the O2Hb dis-
sociation curve). The results have indicated
that an increase of 10 percent in the COHb
causes an increase in the A-aDQ2 in the
presence of shunts as small as 2 percent of the
cardiac output, but there were no significant
8-32
changes when the shunts were less than 1 per-
cent of the cardiac output. The effect of an
equivalent anemia was considerably less. The
changes in A-aDQ2 with perfusion abnormal-
ities were smaller than those with veno-
arterial shunts, the effect of an equivalent
anemia being less than that of increased
COHb. The results of these calculations were
verified experimentally by exposing five
normal subjects, two patients with intra-
cardiac shunts, and two patients with per-
fusion imbalance to sufficient CO to give an
increase in COHb of about 10 percent. These
results are tabulated in Table 8-12. Brody
and Coburn consider that their findings have
important implications, since the tissue
hypoxia produced by increased COHb may be
augmented by arterial hypoxemia in the
presence of abnormal perfusion relationships
or veno-arterial shunts. Arterial hypoxemia
may play an important role in CO-poisoning
-------
+ 100
+ 50
x
UJ
-50
-100
20
PATIENT WITH
MITRAL STENOSIS
~~i—r
LU
O
>-
X Dl
O X
in E
O E
02
O
u
Oo
10
tO £
£^ 100
O -1
U"-
1 T
OXYGEN
PYRUVATE
J ±
I I
PATIENT WITH
CORONARY ARTERY
DISEASE
I
I
OXYGEN
PYRUVATE
LACTATE
I I
i i r
I I
PATIENT WITH
EMPHYSEMA
I I I I
OXYGEN
12 15 0 3 6 9 12 15 0 3
COHb, percent
LACTATE
PYRUVATE
I I I
1 I I I
I I
i i
j i
12 15
Figure 8-12. Myocardial metabolic measurements in three representative patients before and
after CO inhalation;63
8-33
-------
Table 8-11. MYOCARDIAL METABOLIC MEASUREMENTS IN
11 SUBJECTS BEFORE AND AFTER CO INHALATION63
Measurements
Control
mean
Group 1 — non-coronary heart disease (7 patients)
COHb, %
QM,b ml/min- lOOg
Oxygen extraction,0 ml/ 100 ml
Oxygen extraction ratio"
MVO2;e ml/min- lOOg
PcsO2>f mm Hg
Lactate extraction ratio"
Pyruvate extraction ratio
0.95
129
11.84
0.75
14.3
21
-0.01
0.28
Group 2 — coronary heart disease (4 patients)
COHb, %
QM, ml/min - 100 g
Oxygen extraction, ml/ 100 ml
Oxygen extraction ratio
MVO2, ml/min- lOOg
P f
rcsO2, mm Hg
Lactate extraction ratio
Pyruvate extraction ratio
0.66
102
12.71
0.75
12.9
19
0.12
0.39
CO
mean
9.00
186
8.89
0.64
15.9
17
-0.19
0.24
8.69
127
8.82
0.58
11.3
17
-0.36
-0.07
Fa
6.5
52.7
42.1
0.4
2.9
0.7
0.3
0.5
34.7
419
0.5
12.9
19.6
25.6
P
<0.05
<0.001
<0.001
<0.20
<0.01
<0.01
<0.05
<0.05
<0.05
aF = variance ratio calculated for paired data with interaction as a denominator.
QM = coronary blood flow.
cOxygen extraction = arterio-coronary sinus oxygen difference.
dOxygen, lactate, and pyruvate extraction ratios = respective extraction divided by arterial
concentration.
within the muscle fiber, serving to tide the
muscle over from one contraction to the next.
Two studies of the interaction between CO
and myoglobin have been undertaken, one
employing human myoglobin in vitro, and the
other with dogs. Rossi - Fanelli and Antonini
have recently studied the oxygen and CO
equilibria of human myoglobin in vitro.65
The oxygen dissociation curve of human myo-
globin was found to be hyperbolic. It differs
from that of hemoglobin in that it is not af-
fected by the hydrogen-ion concentration, the
ionic strength, or the concentration of myo-
globin. Both the shape and the properties of
the oxymyoglobin (O2Mb) dissociation curve
reflect the difference in structure and func-
tion between myoglobin and hemoglobin.
Although the relative affinity of myoglobin
for CO is not as high as that of hemoglobin, it
i = myocardial oxygen consumption.
pcsO2 = coronary sinus oxygen tension.
of subjects with normal lungs if they develop
perfusion imbalance or veno-arterial shunts
when unconscious. Persons with these ab-
normalities may therefore face unusual risks
from exposure to CO.
G. NONHEMOGLOBIN ABSORPTIVE
SYSTEMS
1. Myoglobin
Myoglobin is structurally related to hemo-
globin, and hence can be expected to react
with CO in a manner similar to hemoglobin.
Because myoglobin contains only 1 heme per
molecule, the reaction occurs without the
formation of intermediates. In vivo, its func-
tion may be to act as a reservoir for oxygen
8-34
-------
is still sufficient to cause appreciable forma-
tion of carboxymyoglobin (COMb) in non-
fatal CO poisoning.
The proportion of inhaled CO that binds to
myoglobin has been studied in dogs by
Luomanmaki.66 In the calculation of his re-
sults, Luomanmaki assumed that the CO was
equilibrated between an intravascular and an
extravascular pool, and that the latter was
comprised mostly of myoglobin. The extra-
vascular CO capacity was determined from
the difference between the separately meas-
ured total body CO capacity and the intra-
vascular CO capacity. The total body CO
capacity was determined using the dilution
principle. A known amount of CO was in-
jected into the inspiratory tube of a rebreath-
ing system. The increase in blood COHb was
measured at intervals, and total body CO
capacity was calculated as follows:
Total body CO capacity (ml STPD)
Jnjected CO (ml STPD) x 100
Increase of blood COHb
The equation assumes that the increase in
COHb is estimated at the time when there is
no more net transfer between the different
CO pools. The measured COHb levels must be
extrapolated to the time of CO injection to
correct for any increase in COHb due to
endogenous production of CO.
Data relating COHb values to extravascular
CO capacities, half-times, and equilibrium
time of CO transfer from the intravascular to
the extravascular pool are shown in Table
8—13. The mean extravascular CO capacity
was 22.9 percent of the total body CO
capacity. There was no significant linear cor-
relation between the extravascular CO capac-
ities and the COHb levels, although only 3 of
the 11 dogs had COHb levels exceeding 10
percent. The mean of the half-time to equi-
librium between the two pools was 12.5
minutes, and the mean of the equilibrium
times was 29.2 minutes. There was no linear
correlation between either the half-time or
the equilibrium time and the COHb level. The
transfer of CO from the intravascular to the
extravascular CO pool occurs within the time
needed for circulatory mixing, as detected
by 5 * Cr-labeled red cells. The distribution of
CO between intravascular and extravascular
CO pools was independent of PQ2 m the PQ2
range of 65 to 440 mm Hg.
Table 8-12. EFFECT OF CO ON ALVEOLAR-ARTERIAL OXYGEN DIFFERENCE (A-aDo ) IN NINE
SUBJECTS AFTER EXPOSURE SUFFICIENT TO INCREASE COHb ABOUT 10 PERCENT64
Subject
Normal subjects (5)
SD
p value
Intracardiac shunts
Subject 1
Subject 2a
Perfusion imbalance
Subject 3
Subject 4
COHb, %
Initial
0.9
±0.1
<0.005
2.1
1.0
2.1
1.7
Final
11.7
±4.7
12.8
12.7
12.8
11.5
A-aDQ mm Hg
Initial
12.1
±4.9
>0.5
36.5
56.7
38.0
39.8
Final
11.6
+5.9
46.9
62.8
41.0
42.6
a2,3-diphosphoglycerate was elevated in this patient, which suggests that the O2Hb dissociation curve was shifted
to the right. This shift might, in part, counteract the effect of COHb on the A-aD0 .
8-35
-------
oo
u>
OS
Table 8-13. EXTRAVASCULAR CO CAPACITIES, HALF-TIMES, AND EQUILIBRIUM TIMES FOR TRANSFER
OF CO FROM INTRAVASCULAR POOL TO EXTRAVASCULAR POOL, AND LEVELS OF BLOOD COHb
AT END OF TRANSFERS^
Dog No.
1
5
6
7
9
10
11
12
14
18
21
Mean
SD
Extravascular CO
capacity,
% of total
body CO capacity
14.6
29.0
20.9
17.5
16.0
16.3
15.6
31.8
37.5
27.5
26.0
22.9
7.4
Half-time
of
CO
transfer,
minutes
14
9
18
12
12
14
8
8
8
17
17
12.5
3.7
Equilibrium
time
of
CO
transfer,
minutes
35
19
45
30
28
33
17
15
22
40
37
29.2
9.4
COHb,a
%
5.35
10.50
0.75
30.95
1.16
7.42
35.00
2.54
2.32
2.42
5.00
_
-
Body
weight,
kg
12.9
15.0
15.9
16.4
15.5
15.9
15.0
13.2
10.6
17.5
13.6
14.68
-
Body myoglobin content,
g
28.4
60.0
44.0
35.8
35.1
32.8
26.9
55.2
36.6
83.5
46.3
44.05
-
g/kg body wt
2.20
4.00
2.77
2.18
2.26
2.06
1.79
4.18
3.45
4.77
3.40
3.01
0.98
aCOHb values extrapolated to the time of CO injection because of endogenous formation of CO.
-------
2. Cytochrome Oxidases
Cytochrome oxidases are hemoproteins
that, in vitro, are capable of reacting with CO.
The reaction between the heme moiety of
these compounds and CO appears to be
similar to the reaction of CO with hemoglobin
and myoglobin. Reversible binding, photoly-
sis, and competition between oxygen and CO
are characteristics of cy to chrome oxidases.
Nevertheless, the evidence at this time sug-
gests that interactions between CO and cyto-
chrome oxidases in the mammalian cell are of
minor significance when compared to the
effects of CO on hemoglobin and myoglobin.
Although all three types of Cytochrome
oxidases that are important in the oxygen
consumption system of the mammalian cell
can be blocked in some part by CO, only the
terminal member of the electron transfer
system (which is located in the mitochondria)
combines with CO; the other members do not
combine unless they are denatured. This term-
inal member is known as cytochrome 33 .
The reaction between cytochrome 33 and
oxygen accounts for about 90 percent of the
total oxygen consumption by the cell. In the
presence of oxygen, the reaction of CO with
cytochrome 33 is competitive, and the CO up-
take depends on the concentration of the
enzyme and the ratio of CO to ©2, rather
than on the concentration of CO alone. For
50 percent inhibition, the required ratio of
CO to O2 is between 2.2 and 28.67'69 Be-
cause the ratio is usually so much lower, these
conditions give oxygen a substantial advan-
tage in competition with CO.
A more likely candidate for CO inhibition
in vivo is cytochrome P-450. The latter,
located in the microsomal fraction of the cell,
is the terminal member of the chain of mixed
function oxidases that catalyze the incorpora-
tion of atmospheric oxygen into organic com-
pounds and for such reactions as the hydroxy-
lation of acetanilide, demethylation of
codeine, and hydroxylation of 17-hydroxy-
progesterone at carbon-21. The experimental
evidence that the CO-binding pigment of the
microsomes is in the terminal oxidase of
mammalian tissues was provided by Cooper7 °
et al. These investigators reported that the
ratio of CO to O2 required for 50 percent
inhibition is approximately 1 to 1 (range 0.5
to 1.5).
All of the above data were obtained in
vitro. Whether similar events occur in vivo is
uncertain. Root71 considers that at a PCQ
compatible with life, only nonsignificant
blocking of the oxygen consumption systems
occurs. Although the PCQ in the cell never
exceeds a few tenths of a mm Hg before fatal
blocking of hemoglobin occurs, the intra-
cellular PQ2 is als° l°w- Forster72 estimates
the intracellular PQ2 to be about 1 mm Hg in
the mitochondrial region. In vitro, the mini-
mum PQ2 f°r isolated rrtdtochondrial func-
tion is 0.5 mm Hg. At equilibrium, 1,150
mg/m^ (1,000 ppm) CO should result in a
PCO °f approximately 0.7 mm Hg in the
blood. The gradient, if any, in PCQ from the
erythrocyte to the intracellular organelles is
unknown. Even if there is a complete transfer
of CO to an intracellular locus, however, con-
centrations of CO commonly found in com-
munity air pollution are likely to be of little
relevance concerning either cytochrome 33 or
cytochrome P-450. In terms of the total dis-
tribution throughout the body of an inhaled
dose of CO, the amounts bound to these
hemoproteins are small when compared with
hemoglobin and myoglobin.
Most of the useful information concerning
the distribution of CO in the body has been
summarized by Coburn73 et al. Figure 8-13
is a diagrammatic representation of the
factors influencing body CO stores.
H. EFFECTS OF CARBON MONOXIDE AT
HIGH ALTITUDE
The effects of CO and of hypoxia induced
by high altitude are similar. Most experi-
mental data suggest that when high altitude
and CO exposures are combined, the effects
are additive. In vivo, there is an interaction
between the two factors so that exposure to
one may induce a physiological response that
influences the response of the body to the
other. For example, Forbes et al. have shown
8-37
-------
AMBIENT
PCO i
ALVEOLAR
PCO
EXOGENOUS
ENDOGENOUS
HEMOGLOBIN
CATABOLISM
OTHER HEME
0.3 ml/hr
0.1 ml/hr
*- CARBON MONOXIDE STORES
HEMOGLOBIN
8 ml
MYO-
GLOBIN
1.5 ml
OTHER
<0.5 ml
0.2%/hr
METABOLISM
CO -COn
Figure 8-13. Diagramatic summary of current concepts regarding variables that influence body
CO stores.73
that during light activity, their subjects had an
increased rate of CO uptake at an altitude of
16,000 feet compared to that at sea level, be-
cause of the hyperventilation that results
from the decreased ?O2-29 When the venti-
lation rate was corrected to its value at sea
level, the rate of uptake of CO decreased to a
value within 10 percent of the sea level value.
Although the effects of hypoxia and CO
appear to be additive, individually they do
seem to provide different physiological re-
sponses. This is because they have different
effects on blood PQ2> on the affinity of ©2
for blood hemoglobin, on the extent of O2Hb
saturation, and on ventilation. The presence
of COHb increases the affinity of hemoglobin
for O2, but lowers the total O2Hb saturation.
The ventilation rate appears to be influenced
by receptors in the carotid and aortic bodies
that are responsive to blood PQ2 an(i
PCO2-71 Hypoxia results in a lowering of the
PQ2 and increased ventilation ensues; in CO
exposure, the PQ2 apparently does not
8-38
change sufficiently to induce the necessary in-
creased ventilation.
Several different physiological and psycho-
motor tests have been used to determine the
effects of altitudes with and without CO. Pitts
et al. have observed the physiological re-
sponses to exercise when blood COHb levels
were increased by 6 percent and 13 percent in
a group of ten men at simulated altitudes (sea
level, 7,000, 10,000, and 15,000 feet).74 The
parameters measured were pulse rate, respira-
tory rate, and minute ventilation. A previous
study had indicated that in subjects at rest,
the pulse showed no change with altitude up
to 16,500 feet. After regulated exercise at
altitudes from sea level up to 21,000 feet,
however, it showed a steep, almost linear, in-
crease. Of the parameters measured in both
these studies, mean pulse rate during exercise
and for the 5 minutes immediately following
exercise showed the closest correlation with
blood COHb and ambient Po2- At sea level,
an increase of 13 percent in COHb increased
-------
the mean excercise pulse rate from 105 to
112 and the recovery pulse rate from 91 to
98. An increase of 6 percent COHb had no
effect at sea level; at 7,000 feet, however, an
increase of 6 percent COHb produced a signif-
icantly higher exercise pulse rate compared to
that produced by altitude alone. Pitts calcu-
lated that for every 1 percent increase in
blood COHb in normal subjects, up to 13 per-
cent COHb, the increase in exercise pulse rate
is equal to that which would be produced by
a 335-foot rise in altitude throughout the
range 7,000 to 10,000 feet. It is likely that
some of the subjects were smokers, since the
group mean control COHb level ranged from
2.88 to 3.64 percent on different days. Since
the smokers would have been preconditioned
in part to the effects of CO, their responses to
additional small quantities of CO might be ex-
pected to be lowered. This could have masked
the additive effect of CO and hypoxia.
A more recent study has compared the
effects of CO exposure and altitude.75 Eight
healthy male subjects were divided randomly
into two groups of four each; each group fol-
lowed a different daily schedule. The subjects
were briefly exposed daily for 10 days to con-
centrations of 5 percent CO (57,500 mg/m^
or 50,000 ppm) at 4-hour intervals between
the hours of 7 a.m. and 11 p.m. The doses
were sufficient to give an average COHb level
of 15 percent, although values ranging be-
tween 5 and 25 percent were recorded. A
variety of circulatory, ventilatory, and renal
function tests were performed during the
course of the experiment. The same experi-
mental protocol was also carried out on the
same eight subjects after spending 10 days at
an altitude of 11,225 feet. This altitude gave
roughly, a degree of hypoxemia equivalent to
that given by 15 percent COHb. The data ob-
tained from the two studies are compared in
Table 8—14. Of great significance are the
circulatory and ventilatory responses to the
two types of hypoxic conditions. As ex-
pected, CO hypoxemia shifted the O2Hb dis-
sociation curve to the left, whereas high alti-
tude caused a shift to the right, the latter
occurring during the first 24 hours. At in-
creased altitude, both the cardiac output and
the ventilatory rate increased within the first
24 hours, whereas CO had no consistent
effect on these parameters.
The lowered arterial Pc«2 at high altitude
most likely stimulated the chemoreceptors in
the aortic and carotid bodies, with the re-
sultant regulatory changes in ventilation. Mills
and Edwards76 have recently shown that
these chemoreceptors are also stimulated dur-
ing CO inhalation. These investigators have
suggested that the lack of ventilatory response
during CO hypoxemia is a result of depression
of respiratory centers in the central nervous
system. The effects of the two types of hypox-
emia at the cellular level can be estimated by
comparing the PQ? °f the mixed venous
blood under both circumstances, since this re-
flects tissue PQ2- The data in Table 8-14
show that the average PQ2 °f mixed venous
blood in CO hypoxemia is lower than in
hypoxic (high altitude) hypoxemia. In both
types of hypoxemia, a lowered tissue PQ2 is
expected; as indicated by the mixed venous
P()2> this is more pronounced in CO hypox-
emia. At increased altitude, the shift of the
O2Hb curve to the right and the circulatory
and ventilatory responses compensate for
most of the associated tissue hypoxia during
the first 24 hours. Such regulatory mecha-
nisms do not appear to be stimulated by CO
hypoxemia, and hence the latter may be con-
sidered to be more of a physiological burden.
Other studies on the combined effects of
CO and altitude have, used psychomotor tests.
Variable results have been reported, but some
of these may be explained by the use of dif-
ferent tests and others by the lack of proper
controls. The flicker fusion frequency (FFF)
and the critical flicker fusion (CFF), often
employed in these studies, have recently been
criticized because of their lack of reliabil-
ity.
77
McFarland5 ° et al. have used the increased
threshold of visual perception as an index of
the effect of both CO and high altitude.
8-39
-------
Table 8-14. AVERAGE DATA FOR EIGHT SUBJECTS (DIVIDED INTO TWO GROUPS OF FOUR)
TO COMPARE EFFECTS OF CO AND HIGH ALTITUDES ON VARIOUS PHYSIOLOGICAL
PARAMETERS75
Test
Effect of 15% COHb
Effect of 11,225-ft altitude
O2Hb saturation curve
Affinity of Hb for O2
Mixed venous oxygen ten-
sion, by estimation
Shift to left
Increased (within 12 hr)
10 to 20% decrease throughout
exposure period
Shift to right
Decreased (within 24 hr)
20% increase on first day, 10%
decrease on second day, re-
turn to normal for rest of
experimental period
Ventilation
VESTPDa rest
work
VEBTPSb rest
work
Respiratory rate rest
work
No change
Slight increase on first day
No change
No systematic change
No change
No change
15 to 20% decrease
Slight decrease
30% increase
35% increase on first day; 50%
increase by tenth day
15 to 35% increase
15 to 35% increase
Circulation
PaCO2C rest
pvC02d rest
Cardiac output
Mixed venous-arterial
CO2 difference, by
estimation rest
work
Almost unchanged
Almost unchanged
Group 1 increased 27% on first
day, followed by return to
normal; no change in Group 2
Group 1 decreased 20% on first
day; Group 2 showed no change
Group 1 increased 20% percent on
third and fifth days; no other
changes noted
Continuous decrease from 90
to 75% of control
Continuous decrease from 90
to 75% of control
Group 1 increased 35 to 45%
for the entire 10-day period;
Group 2 increased 25% by
fourth day and returned to
normal by end of stay
Group 1 decreased 15 to 20%
for the entire 10-day period;
Group 2 decreased on fourth
day only
15 to 25% increase for the en-
tire 10-day period
Renal function
Glomerular filtration
50% increase on first day, return
to normal on second day, re-
main within 20% of control for
rest of experimental period
Very slight decrease, but close
to control value
840
-------
Table 8-14 (continued). AVERAGE DATA FOR EIGHT SUBJECTS (DIVIDED INTO TWO GROUPS
OF FOUR) TO COMPARE EFFECTS OF CO AND HIGH ALTITUDES ON VARIOUS
PHYSIOLOGICAL PARAMETERS
Test
Effect of 15% COHb
Effect of 11,225-ft altitude
Renal plasma flow
Diuresis
40% increase on first day, return close
to pre-exposure value on second
day, remain < 15% below control
value for rest of experimental period
Increase of 400 to 500 ml
Very slight decrease, but close to
control value
Increase to more than twice con-
trol by sixth day
Serum lipids (cholesterol)
Hematocrit
Reticulocyte count
No significant change for first 4 days;
6% increase in last 2 days (p < 0.05)
No change
Threefold increase on third day; nearly
fourfold increase by sixth day
6 to 9% increase in first 2 days
Very slight increase (43.5 to 47)
Twofold increase on third day;
nearly threefold by ninth day
aVESTPD (liters/min) -ventilation at 0° C, 760 mm Hg, dry.
bvgBTPS (liters/min) - ventilation at body temperature and ambient pressure saturated with water vapor.
cp - alveolar carbon dioxide tension.
- mixed venous carbon dioxide tension.
Although studies of visual perception have al-
ready been discussed in Section E.2, it is
pertinent to note at this point that McFarland
et al. documented an impairment in visual
perception in a single subject with a COHb of
about 5 percent at sea level that was equiva-
lent to the impairment associated with the
low PQ2 at an altitude of 7,000 feet.
In another experiment, a group of four
trained subjects was used to study the time
course of recovery from CO and altitude.52
Data from a single subject suggest that it takes
longer to recover from a given COHb level
than from an equivalent lowering of PQ2 due
to altitude. The difference could not be ac-
counted for wholly by the presence of COHb.
It is possible that the compensatory mecha-
nisms normally activated by lowered PQ2 were
not activated when CO caused the drop in
O2Hb saturation. Alternatively, it is also pos-
sible that CO exerts a specific toxic effect on
the central nervous system that is unrelated to
the COHb level.
In both studies just described, the investiga-
tors imply that the subjects exhibited similar
responses, but they do not supply supporting
data. Other investigators have commented on
the great variability in response between sub-
jects when similar tests have been used.
Lilienthal7 8 et al. demonstrated an impair-
ment in FFF in five subjects at altitudes of
10,000 to 12,000 feet. The combined ex-
posure to CO (COHb increases of 5 to 9 per-
cent) and an altitude of 5,000 to 6,000 feet
produced an impairment in FFF, although
neither of these stresses alone affected the
FFF. The data indicate that an increase in the
COHb level of 8 to 10 percent above resting
values caused the tolerance for altitude to be
lowered by 4,000 feet or more. It should be
noted that impairment in FFF is not neces-
sarily consistent with a given COHb percent-
age. For example, at 5,000 feet one subject
showed a depressed FFF at 8.7 percent
COHb; yet in another experiment at the same
altitude, his FFF remained constant at 10.5
percent COHb. There is a possibility that
COHb determinations in this experiment were
inaccurate. The subjects' resting COHb levels
varied from 1.0 to 3.5 percent, indicating that
there were smokers in the group. Since
smokers may have higher hemoglobin values
than nonsmokers,7 9 the assumed hemoglobin
8-41
-------
value used in this experiment may not be
valid.
By contrast, Vollmer80 et al. have found
that the effects of CO and altitude are not
additive. Twenty subjects were used to study
the effect of CO and increased altitude
(10,000 and 15,000 feet) on FFF, body sway,
and size of the red visual field - all during light
activity. Compared with performance at sea
level, there was a significant impairment at
increased altitude, with and without exposure
to CO. There was no significant difference be-
tween the mean test scores during hypoxia
alone and the mean test scores following ad-
ministration of CO. The increases in COHb
were from 9 to 19 percent, with a final COHb
ranging from 12 to 22 percent. This suggests
that the resting COHb was 3 percent, and in-
dicates that some of the subjects were
smokers. Vollmer suggests that during
hypoxia at 15,000 feet, any additional burden
imposed by the presence of small amounts of
COHb is masked by compensatory mecha-
nisms. Alternatively, he considers that it is pos-
sible that 9 to 19 percent COHb does not
impose an important additional stress. At
15,500 feet, however, 4 of 17 subjects col-
lapsed after being exposed to CO. The tests
used in this study appear inadequate for pre-
dicting a serious cardiovascular reaction; nor
can their sensitivity be ranked very high.
Most of the above studies were conducted
before or during World War II. Recently, Den-
ison81 demonstrated a significant effect of
hypoxia alone on complex reaction times at a
simulated altitude of 5,000 feet during light
work. At 5,000 feet, eight of ten subjects
showed slower reaction times than nine of ten
matched controls (p < 0.05). This effect of
hypoxia was observed only during the early
stages of learning the complex experimental
task. Once the task had been learned, a
simulated altitude up to 8,000 feet had no
effect. The effect of small amounts of CO on
•
the learning of a new task at increased alti-
tude remains to be determined.
8-42
I. ADAPTATION
A subject may be considered to be adapted
(acclimatized) to a new environment when,
after repeated or prolonged exposure to that
environment, he shows a significant decrease
in the amount of reaction experienced per
unit intensity of the offending factor without
an increase in other types of reaction. Adap-
tation thus implies some short-range benefit
to the organism concerned. Individuals living
at high altitude are considered to be adapted
to their environment, since it has been shown
that they can perform physical labor there
which low-altitude residents cannot do as
readily at similar elevations. High-altitude in-
habitants, however, show a greater incidence
of pulmonary hypertension and patent ductus
arteriosis,8 2 both of which are associated
with an increased need to maintain an ade-
quate PaO2- Thus, not all high-altitude resi-
dents are adapted in the formal sense, but
they are well compensated. Since most studies
of adaptation are of brief duration, the ulti-
mate costs in terms of parameters such as
health impairment (i.e., the development of
pulmonary hypertension) can easily be over-
looked.
Some experimental studies suggest that re-
peated exposures to low levels of CO result in
an adaptation of the subject to additional ex-
posures. In animal studies, the long-term ex-
posure of dogs to low levels of CO for periods
of up to 3 months (described in Section F)
has resulted in increased hematocrits, hemo-
globin, and RBC counts.54 In studies of heart
size after prolonged exposure to CO, cardiac
enlargement has been found, presumably re-
flecting an increased work load on the
cardiovascular system.4 9 Such changes can be
considered as compensatory mechanisms lead-
ing to adaptation.
Astrup83 et al. have demonstrated an in-
crease in hemoglobin concentration in
cholesterol-fed rabbits during the first 5
weeks of an 8-week exposure to 195 mg/m^
(170 ppm) CO. The hemoglobin level then
stabilized, but when the CO concentration
-------
was increased to 405 mg/m3 (350 ppm) a fur-
ther increase in hemoglobin was observed.
The compensatory mechanisms that may have
been responsible were not discussed by the
authors. The degree of visible aortic athero-
matosis and the content of total cholesterol in
the aortic tissue was significantly higher in the
rabbits exposed to CO than in the controls.
This factor may be relevant to the pathogene-
sis of arteriosclerosis in man.
Wilks84 et al. acclimatized dogs to CO
doses ranging from 920 to 1150 mg/m3 (800
to 1,000 ppm). This resulted in increased
RBC, hemoglobin, and blood volume. When
these dogs, together with a control group of
unacclimatized dogs, were exposed to 575
mg/m3 (550 ppm) CO for 15 hours, blood
levels of COHb were the same in both groups.
This suggests that at equilibrium there is no
change in CO saturation with increasing
hemoglobin.
Russian studies on animals in which hy-
poxia was created by oxygen deficiency indi-
cate that adaptation may occur through com-
pensations of systems other than the cardi-
opulmonary system. Such changes include in-
creased myoglobin stores in the tissues, in-
creased vascularization of tissues (especially
brain tissue), and changes in the oxygen-
consumption of enzyme systems. Whether
similar changes can be induced by adaptation
to CO exposure remains to be determined.
Only one investigator has reported that
adaptation to CO can be demonstrated exper-
imentally in humans. Killick86 exposed her-
self to 220 to 520 mg/m3 (190 to 450 ppm)
CO in air for periods of 5 to 7 hours at ap-
proximately weekly intervals for a period of 6
months. The resulting COHb level at equili-
brium ranged from 16.5 percent at 255
mg/m3 (220 ppm) CO to 39.5 percent at 460
mg/m3 (400 ppm) CO. COHb was determined
with a reversion spectroscope; this method
permits subjective errors, and the COHb levels
reported in this paper may be inaccurate. CO
was measured by the iodine pentoxide meth-
od. Killick considered adaptation to have
taken place when (1) there was a diminution
in symptoms with repeated exposure to the
same concentration of CO, and (2) a dis-
crepancy between the observed COHb at the
end of an exposure was less than the COHb
obtained in vitro when the subject's blood
was equilibrated with a mixture containing
oxygen and CO at the same partial pressure as
in the alveolar air. The conclusions of this
study are open to question, since a basis for
determining the development of adaptation
was a difference between observed and calcu-
lated COHb levels. The methods used for
calculation resulted in a calculated arterial
P()2 as much as 100 mm Hg above alveolar
PC<2- Thg irregular pattern of exposure, pos-
sible erroneous calculations, and subjective
methods for COHb determination render
limited value to this study. In contrast to
Wilks' study in dogs, however, Killick found
no change in the RBC count or in the blood
volume.
In summary, it can only be stated that the
available data concerning physiologic adapta-
tion of humans to CO are inconclusive. It is
expected that some adaptation will take
place, but the mechanism is unclear.
J. ENDOGENOUS FORMATION OF
CARBON MONOXIDE
The first claims that CO could be formed
within the mammalian body were reported by
French investigators in the period 1898 to
1925,87"91 but an exogenous source of the
CO could not be ruled out. In 1945, Rough-
ton and Root9 2 demonstrated that there was
a small, but measurable, amount of CO in nor-
mal human blood. In 1949, Sjostrand93
observed that the expired air of human sub-
jects who were not exposed to exogenous CO
contained consistently more CO than the in-
spired air, suggesting that CO was being
produced in the body. Sjostrand's findings
were confirmed by Coburn94 et al.; with the
use of a sensitive anlytical method for blood
CO, these workers were able to measure di-
rectly the rate of CO formation by using a
rebreathing system. The average rate of CO
production in man was found by Coburn et
al. to be 0.42 ± 0.07 ml per hour; this is
8-43
-------
slightly lower than Sjostrand's value of 0.5 to
1.0 ml per hour in the normal adult female.
Utilizing a rebreathing system and the
Haldane equation, Sjostrand estimated an in-
direct value for COHb from the rebreathing
gas samples at the end of the rebreathing peri-
od.21 Both Sjostrand95 and Engstedt96 have
noted that the COHb level thus calculated is
positively correlated with the presence of
hemolytic disease or other states associated
with increased hemoglobin breakdown, such
as extensive trauma or mismatched transfu-
sions.97'98 These findings have been more
precisely confirmed by Coburn94'99 et al.
with their improved analytical techniques.
Sjostrand100 has also demonstrated that
solutions of hemoglobin and myoglobin liber-
ate CO upon standing, and that maximal pro-
duction of CO from such solutions cor-
responds to the CO-binding capacity of the
initial solution. Injections of hemolyzed
blood and hemoglobin solutions into humans,
dogs, and rabbits have been observed to cause
an increased endogenous production of
Co.101,102 By injecting damaged erythro-
cytes, Coburn99 et al. have demonstrated a
molar ratio between the amount of heme
destroyed and the amount of increase in CO
formation. The increase in CO formation
occurs simultaneously with rising levels of
serum bilirubin, a metabolic product of hemo-
globin.
The experimental data indicate that
endogenous CO is a by-product of heme ca-
tabolism. In vivo, the end products of hemo-
globin catabolism are the bile pigments, which
arise specifically from the heme group of the
hemoglobin. Heme, which is a cyclic tetrapyr-
role, loses its a-methene-bridge carbon atom
to form bilirubin, which is linear tetrapyrrole.
Libowitzky and Fischer1 ° 3 have been unable
to recover this missing one-carbon fragment in
vitro as either formic acid or formaldehyde.
Sjostrand1 °°"1 °2 has suggested that the miss-
ing carbon atom is incompletely oxidized,
forming CO which is then excreted in the
expired air. Ludwig104 et al. have confirmed
this suggestion by using ^c-labeled heme.
8-44
Other heme-containing proteins are also
likely sources of endogenous CO, provided
that the initial steps of their catabolism are
similar to those of hemoglobin. It is known
that approximately 10 to 15 percent of the
total bile pigment production comes from
sources other than circulating red cell hemo-
globin. These sources105 may be:
1. Myoglobin heme catabolism.
2. Catabolism of heme-containing enzymes
(cytochromes, catalases, etc.).
3. Excess production of heme in marrow
and other sites.
4. Production of bilirubin through anabolic
pathways.
5. Early death of red blood cells within the
marrow or shortly after their
release (ineffective erythropoiesis).
6. A scarf of hemoglobin around the ex-
truded nucleus of the normoblast.
In their radioactive tracer studies, White et
al. have demonstrated that labeled CO was
produced within the first few days following
injection of glycine-2-^C. This radioactive
amino acid specifically labels that omethene
-bridge carbon atom of heme. The amount of
labeled CO recovered was of the correct order
of magnitude to account for the excess
CO.1 °6 Similar results have been reported in
studies of heme catabolism in rodents.107 In
addition, White108 et al. have demonstrated
the production of CO from liver slices in
vitro, with the simultaneous production of
bilirubin. This has confirmed earlier stud-
ies1 O9.no demonstrating that nonhemo-
globin hemes in the liver are important
sources of bile pigment. Schwartz111 et al.,
using hypertransfused mice in which erythro-
poiesis was nearly 100 percent suppressed,
have estimated that about 40 percent of the
early appearing bile pigment (and CO) was
due to catabolism of nonhemoglobin hemes.
Recently, direct evidence of increased CO
production in states associated with increased
ineffective erythropoiesis has been ob-
tained.112
An appreciation of the importance of endo-
genously produced CO in clinical and experi-
mental conditions is developing. It has been
-------
noted that patients presumably not exposed
to CO do, when undergoing anesthesia, pro-
duce CO levels within rebreathing anesthesia
apparatus; these CO concentrations often ex-
ceed 58 to 115 mg/m3 (50 to 100 ppm).113
This concentration exceeds the maximum
allowable levels for industrial workers who are
exposed to CO for 8 hours. It has been sug-
gested that these closed rebreathing systems
be opened and flushed periodically during the
operative procedure in order to remove the
excess CO. Some of this increase in CO during
anesthesia may be due to the increased oxy-
gen tension of inspired air, which, according
to the Haldane equation,114'115 will pro-
mote the dissociation of COHb. Increased
COHb levels are also seen in newborn in-
fants,114>11S because of both normal and
abnormal hemolysis. The endogenous produc-
tion of CO in the newborn leads to increased
COHb levels (up to 12 percent) and results in
relation impairment of oxygen-transport func-
tion.
It has long been known that CO arising
from internal combustion engines, tobacco
smoke, and other conventional sources in sub-
marines is an important cause of atmospheric
pollution in the crew's quarters. In other
closedf systems containing men or animals, the
puzzling production of CO has been noted.
Toxic or fatal CO levels have even occurred in
some animal experiments when the con-
taminant was not specifically removed. It is
implied that the crew members (or the experi-
mental animals) themselves are an important
source of CO pollution in closed systems.
Greater attention is now being focused on the
endogenous production of CO in closed sys-
tems that are being evaluated for use in space
flights and undersea exploration.
It is conceivable that animal-plant cycles
proposed for long space flights as oxygen
producers and waste-product removers may
themselves turn out to be an additional source
of CO. This could result from the decomposi-
tion of chlorophyll - the green pigment of
plants - which contains a cyclic tetrapyrrole
structure similar to heme. Mature leaves have
been shown to produce large quantities of
CO, presumably from degradation of chlo-
rophyll.116
There is the possibility that a CO cycle ex-
ists in nature, since it has been demonstrated
that many animal and plant species produce
this compound.116'120 Carbon monoxide
can also be utilized for metabolic purposes in
certain bacteria121 and plants,122 and may
even be oxidized to CO2 at slow rates in
animals123 and in man.66 A more detailed
discussion of possible biological sources of CO
appears in Chapter 2.
K. SUMMARY
Carbon monoxide is absorbed exclusively
via the lungs, and most of its toxic properties
are a result of its reaction with hemoproteins.
The primary effect of CO is mediated by its
reaction with hemoglobin to form carboxy-
hemoglobin (COHb), thus reducing the
oxygen-carrying capacity of the blood and
accounting for about 80 percent of an inhaled
dose of CO. The affinity of hemoglobin for
CO is over 200 times that for oxygen, indica-
ting that COHb is more stable than oxyhemo-
globin (O2Hb). The presence of COHb also
shifts the O2Hb dissociation curve to the left,
implying that, at the tissue level of the circu-
lation, less oxygen is available to the cells be-
cause of the decrease in oxygen tension (PQ2)-
About 20 percent of a given dose of CO
passes from the intravascular to the extravas-
cular pool, reacting primarily with myoglobin
to form carboxymyoglobin (COMb). About 1
percent or less reacts with the heme-
containing cytochromes, and at CO concen-
trations commonly encountered in commun-
ity air pollution, this reaction is unlikely to be
of any physiological significance.
The most accurate analysis of relatively low
blood COHb concentrations results from the
spectrophotometric determination (NDIR
method) of the CO liberated from the blood
when the hemoglobin is destroyed. The neces-
sary equipment is quite costly, a tedious
procedure is involved, and relatively large
blood samples are required. Several other
good methods exist for the determination of
8-45
-------
low blood CO levels. The normal "back-
ground" concentration of blood COHb is
about 0.5 percent, and this is attributed to
endogenous sources such as heme catabolism.
The body uptake of exogenous CO increases
with the concentration, length of exposure,
and ventilatory rate. When the concentration
remains constant, a state of equilibrium is
reached in which the partial pressure of CO
(PCQ) m tne pulmonary capillary blood is al-
most equal to that in the alveolar and ambient
air. The rate of uptake of CO is fairly con-
stant with respect to blood COHb until about
one-third of the equilibrium value is reached,
and then this uptake proceeds at a slower and
slower pace. Human exposure to 35 mg/m3
(30 ppm) CO has shown that about 80 per-
cent of the equilibrium value of 5 percent
COHb is reached within 4 hours, and the re-
maining 20 percent is achieved slowly over
the next 8 hours. It is estimated that exposure
of a previously nonexposed individual to 23
mg/m3 (20 ppm) CO for about 8 or more
hours would result in a blood COHb level of
about 3.7 percent; exposure to 12 mg/m3 (10
ppm) for a similar period of time would prob-
ably result in a blood COHb level of about 2.1
percent.
The observed toxic effects of CO in both
animals and humans reflect the impairment of
the oxygen transport system. The data on
experimental exposures of animals and
humans are shown in tables 8-15 and 8-16.
Long-term exposure of animals to CO may
produce morphological changes in the heart
and brain. Dogs exposed intermittently or
continuously to 58 mg/m3 (50 ppm) for 6
weeks have developed abnormal EKG's after
the third week. At autopsy, these same dogs
have shown mobilization of glia and dilatation
of the lateral ventricles of the brain. In an-
other study, continuous exposure of dogs to
58 mg/m3 for 3 months has failed to show
such changes, but significant increases in he-
moglobin levels, hematocrits, and RBC counts
were observed. Continuous and intermittent
exposure of dogs to 11 5 mg/m3 (100 ppm)
for 6 weeks has produced a dilatation of the
chambers of the right heart and, occasionally,
of the left heart, and some degeneration of
heart muscle has also been noted. Dogs ex-
posed to 115 mg/m3 for 5% hours a day, 6
days a week for 11 weeks have developed a
consistent disturbance of the postural reflexes
and of gait, although no changes in the elec-
troencephalogram (EEC) or the peripheral
nerves were reported. At autopsy, there was
some indication of cortical damage.
The effects of CO on the hematological
system of animals suggest the possibility of
adaptation to CO. Cholesterol-fed rabbits that
were adapted (acclimatized) by exposure to
195 mg/m3 (170 ppm) CO for 8 weeks have
shown an increase in the hemoglobin level
during the first 5 weeks of exposure; the level
stabilized during the following 3 weeks. When
the CO concentration was increased to 405
mg/m3 (350 ppm), a further increase in
hemoglobin was observed.
Short-term exposure of animals to low
levels of CO have produced effects on the
central nervous system. Rats exposed to 58
mg/m3 (50 ppm) for 1 hour have developed
alterations in the electroencephalogram
(EEC), which have increased in severity with
longer periods of exposure. These changes
have returned to normal 48 hours after the
end of the exposure. After exposure to 58
mg/m3 for 48 minutes, rats have developed an
impairment in time discrimination. Short-
term exposure to higher CO concentrations
has produced similar effects, but with in-
creased severity.
No long-term human studies on experi-
mental CO exposures have been reported, al-
though there are data on occupational ex-
posures. Brief exposures to high levels of CO
have produced effects on the central nervous,
vascular, and respiratory systems. Central
nervous system effects appear to occur at
COHb levels above 2 percent. Exposure of
nonsmokers to 58 to 290 mg/m3 (50 to 250
ppm) CO for up to 2 hours has produced a
significant impairment in time discrimination,
statistically significant at about 58 mg/m3 for
90 minutes (approximately 2.5 percent
8-46
-------
Table 8-15. SUMMARY OF EFFECTS OF CARBON MONOXIDE IN ANIMALS
Species
Dogs
Rats
Rabbits
Dogs
Rats
Rats
Dogs
Dogs
CO level
58 mg/m3
(50 ppm)
5 8 mg/m3
(50 ppm)
58 mg/m3
(50 ppm)
58 mg/m3
(50 ppm)
115 mg/m3
(100 ppm)
115 mg/m3
(100 ppm)
Length of exposure
6 hrs/day, 5 days/wk,
for 6 wk
24 hr/day, 7 days/wk,
for 6 wk
24 hr/day, 7 days/wk,
for 3 mo
24 hr/day, 7 days/wk,
for 3 mo
Ihr
1 to 5 hr/day for
4 days
6 hr/day, 5 days/wk,
for 6 wk
24 hr/day, 7 days/wk,
for 6 wk
5-3/4 hr/day, 6 days/wk,
for 1 1 wk -.
COHb, %
2.6 to 5.5
Rats 1.8
Rabbits 3.2
Dogs 7.3
7 to 12
up to 21
Effect
Brain: Mobilization of glia and dilatation
of lateral ventricles. Necrosis and
dilineation absent.
Heart: 10/15 developed EKG changes in third
week.
Dogs: No changes in EKG's and pulse rates.
No histologic difference between ex-
posed and control animals. Significant
increases in hemoglobin levels, hema-
tocrits, and RBC counts.
EKG changes in the first 2 weeks returning to normal
in third week. Slight increase in hemoglobin levels,
hematocrits, and RBC counts.
Changes in EEG increasing in severity with length of
exposure.
Progressive deterioration in EEG returning to normal
48 hours after end of exposure.
Brain: Mobilization of glia and dilatation of
lateral ventricles. Necrosis and demye-
lination absent.
Heart: 8/8 developed abnormal EKG's after about
2 weeks. Autopsy: dilatation of right
heart and occasionally of left heart;
some degeneration of heart muscle.
Brain: No changes in EEG or in peripheral nerves.
Consistent disturbance of postural reflexes
and gait. Autopsy: 6/6 showed some indication
of cortical damage.
Heart: 1/4 had inverted T-wave after second week
2/4 had inverted T-wave by tenth week
Autopsy: 4/4 showed degenerative changes in
muscle fibers.
Reference
Lindenberg
etal.
Musselman
etal.
Roussel56
etal.
Xintaras40
etal.
Lindenberg
etal.
Lewey and
Drabkin37
oo
-------
oo
-K
oo
Table 8-15 (continued). SUMMARY OF EFFECTS OF CARBON MONOXIDE IN ANIMALS
Species
Rats
Rabbits
Dogs
Dogs
Dogs
Mice
Monkeys
CO level
115 to
11 ,500 mg/m3
(100 to
10,000 ppm)
195 mg/m3
(170 ppm)
920 to
1150 mg/m3
(800 to
1000 ppm)
> 1,1 50 mg/m3
(1,000 ppm)
115 mg/m3
(100 ppm)
58 mg/m3
(50 ppm)
58 mg/m3
(50 ppm)
55 mg/m3
(48 ppm)
Length of exposure
up to 48 min.
8 weeks
6 to 8 hi/day, 7 days/wk,
for 36 wks
n.a.
6 wk, continuous
and intermittent
6 wks, continuous
and intermittent
3 mo to 2 yr
n.a.
COHb, %
n.a.
19.7 at end
of first week
3 to 40
7 to 12
2.6 to 5.5
n.a.
3.7 to 4.7
Effect
Impairment in time discrimination.
Decrease in % COHb from 19.7 to 15.1. Increase in hemo-
globin level in first five weeks followed by stabiliza-
tion. Exposure to 400 mg/m3 (350 ppm) caused further
increase in Hb. Rats were cholesterol fed. Increased
total cholesterol in aortic tissue in rabbits exposed to CO.
Increased RBC counts, hemoglobin, and blood volume.
Challenge with 575 mg/m (500 ppm) in these dogs
produced the same % COHb as in non-acclimatized
controls.
Prominent EKG changes. High mortality rate. Alter-
tions in cerebral and myocardial histology.
EKG changes, more marked with continuous than
intermittent exposure. Dilatation of right
cardiac chamber. Dilatation of lateral ven-
tricles of the brain.
Same changes as noted with exposure to 115 mg/m3,
except EKG changes were not as prominent.
No changes noted in fertility, fetal survival, body
growth, food intake, weight and water content
of various organs, EKG, or blood chemistries.
No decrement in performance, even at simulated alti-
tude of 27,000 feet.
Reference
Beard and
Wertheim39
Astrup57'75
etal.
Wilks85
etal.
Preziosi58
Preziosi
Stupfel41
Back and
Dominguez
-------
Table 8-16. SUMMARY OF EFFECTS OF CARBON MONOXIDE IN HUMANS
No.
subjects
7
10
4
1
1
49
18
CO level
115 to
23,000 mg/m3
(100 to
20,000 ppm)
35 mg/m3
(30 ppm)
100%
(100 to
300 ml)
n.a.
(1 cigarette)
n.a.
(3 cigarettes)
n.a.
58 to 230 mg/m3
(50 to 250
ppm)
Length of exposure
Up to 5 hr
24 hr
10 to 15 min
n.a.
n.a.
n.a.
Up to 2 hr
COHb, %
Up to 35.0
5
Up to 20
2
4
Up to 20.4
2.5
Effect
1 . Uptake of CO increases with (a) concentration
of CO, (b) length of exposure, (c) ventilation
rate.
2. Rate of uptake of CO as measured by increase
in blood % COHb is constant up to 1/3 of
equilibrium COHb.
3. Rate of uptake decreases with increased PQ^
and apparently increases with decreased YQ^
due to hyperventilation. When the latter is corrected
for, rate of uptake is unaltered.
Approximate equilibrium value of COHb reached by 12
hours; 60% of equilibrium value reached in 2 hours, 80%
in 4 hours, and the remainder over 8 hours.
Impairment of visual function detectable at approx-
imately 4.5% COHb and increases with increase in COHb.
Recovery lags behind excretion of CO. Latter depends
on composition of gas during post-exposure period.
Experiments at simulated altitudes gave a similar
pattern of results. Data given for one subject only.
Impairment of visual function
Impairment of visual function similar to that pro-
duced by an altitude of 8,000 ft.
Impairment in response to certain psychomotor
tests, detectable at 5% COHb. No effect on
pulse, respkatory rate, blood pressure, neuro-
logical reflexes, muscle persistence, and
static steadiness test.
Significant impairment in time-interval
discrimination after exposure to 58 mg/m
(50 ppm) for 90 minutes.
Reference
Forbes29
etal.
Smith33
TT 1 -52
rlalperin
etal.
MacFarland5 °
etal.
Schulte44
Jeard and
Wertheim39
oo
-------
9°
ui
o
Table 8-16 (continued). SUMMARY OF EFFECTS OF CARBON MONOXIDE IN HUMANS
No.
subjects
4
18
5
26
11
CO level
58 to 230 mg/m3
(50 to 250
ppm)
29 to 1,150 mg/m3
(25 to 1,000)
Up to 115 mg/m3
(100 ppm)
n.a.
n.a.
n.a.
Length of exposure
Up to 2 hr
Up to 16 hr
8hr
Up to 2 min
Up to 2 min
Up to 2 min
COHb, %
3
Up to 31.8
11 to 13
Above 5
Above 5 (aver-
age 8.96).
Above 5 (aver-
age 8.5 to
9).
Effect
Consistent impairment in 3 of 4 parameters of
visual function after exposure to 58 mg/m
for 50 minutes
No impairment of time estimation. No change in
blood chemistries.
No impairment in psychomotor test performance.
Decreased PaO2 an(* PvO2
Increased oxygen extraction in the presence of
COHb.
Increased lactate production in patients with
coronary heart disease; in patients with non-
coronary heart disease, increased coronary
blood flow, and fall in mixed venous and coronary
sinus POO-
Reference
Beard and
Grand-
staff51
Stewart46
et al.
Ay res62
et al.
Ayres63
etal.
-------
COHb). At blood COHb levels of about 3 per-
cent (estimated by expired air analysis after
exposure to 58 mg/m3 of CO for 50 minutes),
significant changes in relative brightness thresh-
old and visual acuity have been observed.
Impairment in the performance of certain
psychomotor tests has occurred at about 5
percent COHb. Exposure of four subjects to
100 to 300 ml of pure CO for several minutes
has produced an impairment in visual func-
tion, which was significant when the blood
COHb level in one subject reached about 4.5
percent.
Changes in the cardiovascular system of
humans have been measured at COHb levels
greater than those associated with central
nervous system effects. Exposure to CO af-
fects oxidative metabolism of both systemic
and myocardial circulatory beds. Blood COHb
levels above 5 percent in five subjects have
produced a mean decrease of 13.3 percent in
mixed venous oxygen tension and 7.3 percent
in arterial oxygen tension. In 26 subjects
whose mean COHb was 8.9 percent, there was
a mean decrease in the venous PQ2 that could
be correlated with an increase in COHb. There
were also associated increases in oxygen ex-
traction ratios, ventilation, and cardiac out-
put.
Myocardial metabolic studies have demon-
strated that concentrations of CO sufficient
to produce significant increases in COHb may
produce a severe burden in subjects who al-
ready have increased demands on their oxy-
gen supply, such as persons with coronary
artery disease. Eleven cardiac patients, four of
whom had coronary artery disease, were ex-
posed to CO that produced a mean COHb
level of almost 9 percent, with several patients
having blood COHb levels in the range of 5.5
to 6.5 percent. Patients with noncoronary
heart disease showed a compensatory increase
in coronary blood flow in response to the in-
creased myocardial oxygen needs; this re-
sponse did not occur in the four patients with
coronary heart disease. In addition, the inade-
quate oxygen supply to the myocardium was
reflected in the lactate extraction ratio,
which changed to production in these four
patients. It thus appears that persons with cer-
tain forms of heart disease may be particu-
larly susceptible to exposures of CO that
could lead to blood COHb levels in excess of
5 percent.
The effects of CO are especially important
at altitude because of the lowered PQ2- Both
physiological and psychomotor tests have
been employed to demonstrate these effects.
As indicated by the increase in exercise pulse
rate, each increase of blood COHb of 1 per-
cent, up to 13 percent, has been shown to be
equal in effect to about 335 feet of altitude,
applied over the altitude range of from 7,000
to 10,000 feet. Impairment of visual thresh-
old perception in a single subject at 7,000
feet was equivalent to that produced by 5 per-
cent COHb at sea level. In five subjects, a
COHb level of 8 to 10 percent has produced a
mean impairment in flicker fusion frequency
(FFF) that was equivalent to lowering the
altitude tolerance 4,000 feet (from about
10,000 to 6,000 feet).
In many of the human studies, the brief
exposures to very high levels of CO make it
difficult to relate the observed effects to equi-
librium COHb levels. For long-term exposure
to CO, certain effects such as increased
hematocrits, hemoglobin levels, and blood
volume may be present, but the available data
are inadequate to draw firm conclusions con-
cerning the significance of all of these
changes.
In summary, appraisal of short-term experi-
mental exposures of humans to CO shows
the following results in terms of the blood
COHb levels observed:
l.No human health effects have been
demonstrated nor have they been ob-
served for COHb levels of 0 to 1 percent,
since endogenous CO production makes
this a physiological range.
2. The following effects on the central
nervous system have been observed at 2
to 5 percent COHb:
a. At an estimated level of about 2.5 per-
cent COHb in nonsmokers (based on
exposure to 58 mg/m3 CO for 90
8-51
-------
minutes), an impairment in time-inter-
val discrimination has been demon-
strated.
b. At COHb levels of about 3 percent
(based on exposure to 58 mg/m^ for
50 minutes), changes in visual acuity
and relative brightness threshold have
been documented.
c. At about 5 percent COHb, an impair-
ment in the performance of certain
other psychomotor tests, and an im-
pairment in visual discrimination, have
been demonstrated.
3. The following cardiovascular changes
have been observed at COHb levels above
5 percent:
Increased cardiac output, systemic
arterio-venous oxygen-content differ-
ence, systemic oxygen extraction
ratios, myocardial arterio-venous
oxygen-content difference, and coro-
nary blood flow in patients without
coronary heart disease. In patients
with coronary heart disease, lactate
extraction changes to production and
the compensatory increase in coro-
nary blood flow is absent.
The concentrations of CO necessary to result
in such blood COHb levels are a function of
ventilatory rate and length of exposure.
Long-term experimental exposure of
humans to CO may produce certain adaptive
effects such as increased hemoglobin levels
and hematocrits, but the available data are in-
adequate to draw firm conclusions. Such
effects have been observed in animals. There
is a definite need to further evaluate the ef-
fect of cigarette smoking on the central
nervous system and cardiovascular system, as
well as the possible "adaptation" of the ciga-
rette smoker to CO.
L. REFERENCES
1. Carlsten A. et al. Relationship Between Low
Values of Alveolar Carboxyhemoglobin Per-
centage in Human Blood. Acta Physiol. Scand.
(Stockholm). J7(l):62-74, June 21, 1954.
2. Adair, G. S. The Hemoglobin System: VI. The
Oxygen Dissociation Curve of Hemoglobin. J.
Biol. Chem. 63(2):529-545, March 1925.
3. Roughton, F. J. W., A. B. Otis, and R. L. J.
Lyster. The Determination of the Individual
Equilibrium Constants of the Four Inter-
mediate Reactions Between Oxygen and Sheep
Haemoglobin. Proc. Roy. Soc., Series B
(London). 144(9l4):29-54, August 16, 1955.
4. Roughton, F. J. W. and R. C. Darling. The Ef-
fect of Carbon Monoxide on the Oxyhemo-
globin Dissociation Curve. Amer. J. Physiol.
747(1):17-31, March 1, 1944.
5. Klausen, K. et al. Circulation Metabolism and
Ventilation During Prolonged exposure to
Carbon Monoxide and to High Altitude. Scand.
J. Clin. Lab. Invest. 22(Suppl. 103):26-38,
1968.
6. Lilienthal, J. L. et al. The Relationships Be-
tween Carbon Monoxide, Oxygen and Hemo-
globin in the Blood of Man at Altitude. Amer.
J. Physiol. 745(3):351-358, January 1, 1946.
7. Mulhausen, R. O., P. Astrup, and K. Mellem-
gaard. Oxygen Affinity and Acid-Base Status of
Human Blood During Exposure to Hypoxia and
Carbon Monoxide. Scand. J. Clin. Lab. Invest.
22(Suppl. 103):9-14, 1968.
8. Baumberger, J. P., H. C. Leong, and J. R.
Neville. Oxygen Delivery Rate of Human
Blood. J. Appl. Physiol. 2J(l):40-46, July
1967.
9. Amenta, J. S. The Spectrophotometric Deter-
mination of Carbon Monoxide in Blood. In:
Standard Methods of Clinical Chemistry,
Seligson, D. (ed.). Vol. 4. New York, Academic
Press, 1963. p. 31-38.
10. Tuddenham, W. J. and M. Hitchcock. Evalua-
tion of Spectrophotometric Methods for the
Determination of Blood Carboxyhemoglobin.
California Dept. of Public Health. Berkeley.
AIHL Report Number 64.
11. Commins, B. T. and P. J. Lawther. A Sensitive
Method for the Determination of Carboxy-
hemoglobin in a Finger-prick Sample of Blood.
Brit. J. Ind. Med. 22(2): 139-143, April 1965.
12. Vignoli, L. et al. Observations on the Use of
Reactive Tubes of the Draeger Type for the
Determination of Blood Carbon Monoxide
[Observations au Sujet de 1'Emploi de Tubes
Reactifs Types Draeger pour le Depistage de
1'Oxyde de Carbone Sanguin]. Arch. Mai. Prof.
(Paris). 27:201-204, April-May 1960.
13. Allen T. H. and W. S. Root. Colorimetric De-
termination of Carbon Monoxide in Air by an
Improved Palladium Chloride Method J. Biol.
Chem. 276(1):309-317, September 1955.
14. Van Slyke, D. D. and J. M. Neill. Determination
of Gases in Blood and Other Solutions by
Vacuum Extraction and Manometric Measure-
8-52
-------
ment. J. Biol. Chem. 67(2):523-584, September
1924.
15. Horvath, S. M. and F. J. W. Roughton. Im-
provements in the Gasometric Estimation of
Carbon Monoxide in Blood. J. Biol. Chem.
744(3):747-755, August 1942.
16. Scholander, P. F. and F. J. W. Roughton. Micro
Gasometric Estimation of the Blood Gases. II.
Carbon Monoxide. J. Biol. Chem.
74S(3):551-563,June 1943.
17. Roughton, F. J. W. and W. S. Root. The Esti-
mation of Small Amounts of Carbon Monoxide
in Air. J. Biol. Chem. 160(1): 135-148, Sep-
tember 1945.
18. Coburn, R. F. et al. Carbon Monoxide in
Blood: Analytical Method and Sources of
Error. J. Appl. Physiol. 79:510-515, May 1964.
19. Schuette, F. J. Method of Analysis of Carbon
Monoxide in Blood. California Dept. of Public
Health. Berkeley. AIHL Report Number 9.
20. Hackney, J. D. et al. Rebreathing Estimate of
Carbon Monoxide Hemoglobin. Arch. Environ.
Health. 5(4): 300-307, October 1962.
21. Sjostrand, T. Method for the Determination of
Carboxyhemoglobin Concentrations by Analy-
sis of Alveolar Air. Acta Physiol. Scand. (Stock-
holm). 7
-------
1968. AMRL-TR-68-175, Aerospace Medical
Research Laboratories, Wright-Patterson AFB,
Ohio, 1968.
43. Forbes, W. H. et al. The Influence of Moderate
Carbon Monoxide Poisoning Upon the Ability
to Drive Automobiles. J. Ind. Hyg. Toxicol.
7P(10):598-603, December 1937.
44. Schulte, J. H. Effects of Mild Carbon Monoxide
Intoxication. Arch. Environ. Health.
7(5):524-530, November 1963.
45. Grudzinska, B. Electroencephalogic Patterns in
Cases of Chronic Exposure to Carbon Mon-
oxide in Air. [Obraz Elektroencesalograficzny
w Przypadkach Przewleklej Ekstozycji na Male
Stezenia Tlenku Wegla w Powietrzu]. Folia
Med. Cracov. 5(3):493-515, 1963.
46. Steward, R. D. et al. Experimental Human Ex-
posure to Carbon Monoxide. Reported under
Contract CRC-APRAC. Project No. CAPM-
3-68. Coordinating Research Council, Inc.,
1969.
47. Mikulka, P. et al. The Effect of Carbon Mon-
oxide on Human Performance. Paper presented
at the Fifth Annual Conference on Atmos-
pheric Contamination in Confined Spaces, Air
Force Aerospace Medical Research Laboratory.
Wright-Patterson Air Force Base. Dayton, Ohio.
1969.
48. Mackworth, N. H. Researches on the Measure-
ment of Human Performance. Medical Research
Council. Special Report Series No. 268.
London: Her Majesty's Stationery Office. 1950.
49. Ray, A. M. and T. H. Rockwell. An Explora-
tory Study of Automobile Driving Performance
Under the Influence of Low Levels of Carboxy-
hemoglobin. Ohio State University. Dept. of In-
dustrial Engineering. Columbus. Report
Number lE-i, August 1967.
50. McFarland, R. A. et al. The Effects of Carbon
Monoxide and Altitude on Visual Thresholds.
Aviation Med. 15(6):381 -394, December 1944.
51. Beard, R. R. and N. Grandstaff. CO Exposure
and Cerebral Function. Paper Presented at the
New York Academy of Sciences Conference on
Biological Effects of Carbon Monoxide. New
York City. January 12-14, 1970.
52. Halperin, M. H. et al. The Time Course of the
Effects of Carbon Monoxide on Visual Thresh-
olds. J. Physiol. 146(3): 583-593, June 11,
1959.
53. Hanks, T. B. Analysis of Human Performance
Capabilities as a Function of Exposure to
Carbon Monoxide. Paper presented at the New
York Academy of Sciences Conference on Bio-
logical Effects of Carbon Monoxide. New York
City. January 12-14, 1970.
54. Enrich, W. E., S. Bellet, and F. H. Lewey.
Cardiac Changes from CO Poisoning. Amer. J.
Med. Sci. 208(4):5l 1-523, October 1944.
55. Musselman, N. P. et al. Continuous Exposure of
Laboratory Animals to a Low Concentration of
Carbon Monoxide. Aerospace Med.
50:524-529, July 1959.
56. Roussel, A., M. Stupfel, and G. Bouley. Trends
of Experimental Research on Air Pollution in
France. Arch. Environ. Health. 75:613-622,
April 1969.
57. Astrup, P., K. Kjeldsen and J. Wanstrup. Effects
of Carbon Monoxide on the Arterial Walls.
Paper presented at the New York Academy of
Sciences Conference on Biological Effects of
Carbon Monoxide. New York City. January
12-14, 1970.
58. Preziosi, T. An Experimental Investigation in
Animals of the Functional and Morphologic
Effects of Single and Repeated Exposures to
High and Low Concentrations of CO. Paper pre-
sented at the New York Academy of Sciences
Conference on Biological Effects of Carbon
Monoxide. New York City. January 12-14,
1970.
59. Chevalier, R. B. et al. Circulatory and Ventila-
tory Effects of Exercise in Smokers and Non-
smokers. J. Appl. Physiol. 7£(2):357-360,
March 1963.
60. Krumholz, R. A., R. G. Chevalier, and J. C.
Ross. Cardiopulmonary Function in Young
Smokers: A Comparison of Pulmonary Func-
tion Measurements and Some Cardio-
pulmonary Responses to Exercise Between a
Group of Young Smokers and a Comparable
Group of Nonsmokers. Ann. Int. Med.
60:603-610, April 1964.
61. Chevalier, R. B., R. A. Krumholz, and J. C.
Ross. Reaction of Nonsmokers to Carbon
Monoxide Inhalation: Cardio-pulmonary Re-
sponses at Rest and During Exercise. J. Amer.
Med. Assoc. 198(10): 1061 -1064, December 5,
1966.
62. Ayres, S. M., S. Gianelli, Jr., and R. G. Arm-
strong. Carboxyhemoglobin: Hemodynamic
and Respiratory Responses to Small Concentra-
tions. Science. 149(3680): 193-194, July 9,
1965.
63. Ayres, S. M. et al. Systemic and Myocardial
Hemodynamic Responses to Relatively Small
Concentrations of Carboxyhemoglobin
(COHB). Arch. Environ. Health. 18:699-709,
April 1969.
64. Brody, J. S. and R. F. Coburn. Carbon Mon-
oxide-Induced Arterial Hypoxemia. Science.
764(3885):1297-1298, June 13, 1969.
3-54
-------
65. Rossi-Fanelli, A. and E. Antonini. Studies on
the Oxygen and Carbon Monoxide Equilibria of
Human Myoglobin. Arch. Biochem. Biophys.
77(2):478-492, October 1958.
66. Luomanmaki, K. Studies on the Metabolsim of
Carbon Monoxide. Ann. Med. Exper. Biol.
Fenniae (Helsinki). 44(Suppl. 2): 1-55, 1966.
67. Keilin, D. and E. F. Hartree. Cytochrome and
Cytochrome Oxidase. Proc. Roy. Soc., Ser. B.
(London). 727(847): 167-191, May 18, 1939.
68. Wald, G. and D. W. Allen. The Equilibrium Be-
tween Cytochrome Oxidase and Carbon Mon-
oxide. J. Gen. Physiol. 40(4):593-608, March
20, 1957.
69. Warburg, O. Uber die Katalytischen Wirkungen
der Lebendigen Substanz. Berlin, Julius
Springer, 1928, 528 p.
70. Cooper, D. et al. Photochemical Action Spec-
trum of the Terminal Oxidase of Mixed Func-
tion Oxidase Systems. Science.
747(3656):400-402, January 22, 1965.
71. Root, W. S. Carbon Monoxide. In: Handbook
of Physiology, Section 3: Respiration, Fenn, W.
O. and H. Rahn. (eds.). Washington, B.C., Amer-
ican Physiological Society, 1965. p. 1087-1098.
72. Forster, R. E. Diffusion of Gases. In: Hand-
book of Physiology, Section 3: Respiration,
Fenn, W. O. and H. Rahn, (ed.). Washington,
B.C., American Physiological Society, 1965. p.
839-872.
73. Coburn, R. Endogenous Carbon Monoxide Pro-
duction and Body CO Stores. Acta. Med.
Scand. Suppl. 472:269-282, March 11, 1967.
74. Pitts, G. C. and N. Pace. The Effect of Blood
Carboxyhemoglobin Concentration on Hypoxia
Tolerance. Amer. J. Physiol. 745:139-151,
January 1, 1947.
75. A Comparison of Prolonged Exposure to Car-
bon Monoxide and Hypoxia in Man. Astrup, P.
and H. G. Pauli (eds.). Scand. J. Clin. Lab. In-
vest. 24(Suppl. 103): 1-71, 1968. ,
76. Mills, E. and M. W. Edwards. Jr. Stimulation of
Aortic and Carotid Chemoreceptors Buring Car-
bon Monoxide Inhalation. J. Appl. Physiol
25(5):494-502, November 1968.
77. Lindgren, S. A. A Study of the Effect of Pro-
tracted Occupational Exposure to Carbon Mon-
oxide with Special Reference to the Occurrence
of the So-called Chronic Carbon Monoxide
Poisoning. Acta Med. Scand. (Stockholm).
7<57(Suppl. 356): 1-135, 1961.
78. Lilienthal, J. L. and C. H. Fugitt. The Effect of
Low Concentrations of Carboxyhemoglobin on
the Altitude Tolerance of Man. Amer. J.
Physiol.745(3):359-364, January 1946.
79. Eisen, M. E. and E. C. Hammond. The Effect of
Smoking on Packed Cell Volume, Red Blood
Cell Counts, Hemoglobin and Platelet Counts.
Can. Med. Assoc. J*. 75(6):520-523, September
15, 1956.
80. Vollmer, E. P. et al. The Effects of Carbon
Monoxide on Three Types of Performance at
Simulated Altitudes of 10,000 and 15,000
Feet. J. Exp. Psychol. J5(3):244-251, June
1946.
81. Bension, B. M., F. Ledwith, and E. C. Poulton.
Complex Reaction Times at Simulated Cabin
Altitudes of 5,000 Feet and 8,000 Feet. Aero-
space Med. 57:1010-1013, October 1966.
82. Hurtado, A. Animals in High Altitudes: Resi-
dent Man. In: Handbook of Physiology. Section
4: Adaptation to the Environment, Bill, B. B.
(ed.). Washington, B.C. American Physiological
Society, 1964. p. 843-860.
83. Astrup, P., K. Kjeldsen, and J. Wanstrup. En-
hancing Influence of Carbon Monoxide on the
Bevelopment of Atheromatosis in Cholesterol-
fed Rabbits. J. Atheroscler. Res. 7:343-354,
May-June 1967.
84. Wilks, S. S., J. F. Tomashefski, and R. T. Clark.
Physiological Effects of Chronic Exposure to
Carbon Monoxide. J. Appl. Physiol.
74(3):305-310, May 1959.
85. Barbashova, Z. I. Cellular Level of Adaptation.
In: Handbook of Physiology. Section 4: Adap-
tation to the Environment, Bill, B. B. (ed.).
Washington, B.C., American Physiological
Society, 1964. p. 37-54.
86. Killick, E. M. The Nature of the Acclimatiza-
tion Occurring Buring Repeated Exposure of
the Human Subject to Atmospheres Containing
Low Concentrations of Carbon Monoxide. J.
Physiol. 107:27-44, January 1, 1948.
87. de Saint-Martin, L. Sur le Bosage de Petites
Quantities d'Oxyde de Carbone dans 1'Air et
dans le Sang Normal. C. R. Acad. Sci. (Paris).
726:1036-1039, April 4, 1898.
88. Nicloux, M. Sur 1'Oxyde de Carbone Contenu
Normalement dans le Sang. C. R. Acad. Sci.
(Paris). 72(5:1526-1528, May 23, 1898.
89. Nicloux, M. Influence de 1'Asphyxie sur la
Teneur du Sang en Oxyde de Carbone: Produc-
tion d'Oxyde de Carbone dans 1'Organisme. C.
R. Acad. Sci. (Paris). 726:1595-1598, May 31,
1898.
90. Nicloux, M. Nouvelles Bemonstrations de la
Presence Normale de 1'Oxyde de Carbone dans
le Sang. C. R. Acad. Sci. (Paris).
779(26):1633-1636,Becember29, 1924.
91. Nicloux, M. L'Oxyde de Carbone et 1'Intoxica-
tion Oxycarbonique. Paris, Masson and Com-
pany, 1925. 254 p.
92. Roughton, F. J. W. and W. S. Root. The Fate of
CO in the Body Buring Recovery from Mild
8-55
-------
Carbon Monoxide Poisoning in Man. Amer. J.
Physiol. 145(2):239-252, December 1, 1945.
93. Sjostrand, T. Endogenous Formation of Carbon
Monoxide in Man Under Normal and Pathologi-
cal Conditions. Scand. J. Clin. Lab. Invest.
7:201-214, 1949.
94. Coburn, R. F., W. S. Blakemore, and R. E.
Forster. Endogenous Carbon Monoxide Produc-
tion in Man. J. Clin. Invest. 42:1172-1178, July
1963.
95. Sjostrand, T. Koloxidbildning vid Intravital
Hamolys. Nord. Med. (Stockholm).
43(5):2l 1-216, 1950.
96. Engstedt, L. Endogenous Formation of Carbon
Monoxide in Hemolytic Disease: With Special
Regard to Quantitative Comparison to other
Hemolytic Indices. Acta Med. Scand. (Stock-
holm). 759(Suppl. 332): 1-63, 1957.
97. Fretheim, F. Carcinoma Ventriculi Behandelt
med Abdominothoracal Total Gastrectomi.
Oslo; Akademisk Tryckningscentral, 1953.
98. Troell, L., O. Norlander, and B. Johanson. Red
Cell Destruction in Burns: With Special Refer-
ence to Changes in the Endogenous Formation
of Carbon Monoxide. Acta Chir. Scand. (Stock-
holm). 709(2): 158-168, June 18, 1955.
99. Coburn, R. F., W. J. Williams, and R. E.
Forster. Effect of Erythrocyte Destruction on
Carbon Monoxide Production in Man. J. Clin.
Invest. 45:1098-1103, June 1964.
100. Sjostrand, T. Formation of Carbon Monoxide
by Coupled Oxidation of Myoglobin with
Ascorbic Acid. Acta Physiol. Scand (Stock-
holm).26(4): 334-337, 1952.
101. Sjostrand, T. The Formation of Carbon Mon-
oxide by in vitro Decomposition of Haemo-
globin in Bile Pigments. Acta Physiol. Scand.
(Stockholm). 26(4):328-333, 1952.
102. Sjostrand, T. The Formation of Carbon Mon-
oxide by the Decomposition of Haemoglobin in
vivo. Acta Physiol. Scand. (Stockholm).
25(4): 338-344, 1952.
103. Libowitzky, H. and H. H. Fischer. Bile Pig-
ments: XX. Isohydfoxycoproporphyrin -1 Ester
[Uber Iso-oxykoproporphyrin I-ester. 20. Zur
Kenntnis der Gallenfarbstoffe]. Hoppe-Seyler's
Z. Physiol. Chem. 255(5/6):209-233, 1938.
104. Ludwig, G. D., W. S. Blakemore, and D. L.
Drabkin. Production of Carbon Monoxide by
Hemin Oxidation. J. Clin. Invest. 36:912, June
1957.
105. Bessis, M., J. Breton-Gorius, and J. P. Thiery.
Possible Role of the Hemoglobin Accom-
panying the Nucleus of Erythroblasts in the Or-
igin of Precociously Eliminated Stercohilin
[Role Possible de I'Hemoglobine Accom-
pagnant le Noyau des Erythroblastes dans
1'origine de la Stercobiline Eliminee Precoce-
ment]. C. R. Acad. Sci. (Paris).
252(15):2300-2302, April 10, 1961.
106. White, P. et al. Carbon Monoxide Production
Associated with Ineffective Erythropoiesis.
Blood. 24(6):845, December 1964.
107. Landaw, S. A. and H. S. Winchell. Endogenous
Production of Carbon-14 Labeled Carbon Mon-
oxide: An in vivo Technique for the Study of
Heme Catabolism. J. Nuclear Med. 7:696-707,
September 1966.
108. White, P. et al. The Formation of Carbon Mon-
oxide and Bilirubin from Hemin in Cell-free
Preparations fron Rat Liver. Blood.
25(6):992-993, December 1966.
109. Ibrahim, G. W., S. Schwartz, and C. J. Watson.
Early Labeling of Bilirubin from Glycine and
6-Aminolevulinic Acid in Bile Fistula Dogs,
with Special Reference to Stimulated versus
Suppressed Erythropoiesis. Metabolism.
75:1129-1139, December 1966.
110. Robinson, S. H. et al. Bilirubin Formation in
the Liver from Nonhemoglobin Sources. Exper-
iments with Isolated, Perfused Rat Liver.
Blood. 26(6): 823-829, December 1965.
111. Schwartz, S., G. Ibrahim, and C. Watson. The
Contribution of Nonhemoglobin Hemes to the
Early Labeling of the Bilirubin. J. Lab. Clin.
Med. 64(6): 1003, December 1964.
112. White, P. et al. Carbon Monoxide Production
Associated with Ineffective Erythropoiesis. J.
Clin. Invest. 4(5:1986-1998, December 1967.
113. Middleton, V. et al. Carbon Monoxide Accumu-
lation in Closed Circle Anesthesia Systems. An-
esthesiology. 26(6): 715-719, November-
December 1965.
114. Bjure, J. and S. P. Fallstrom. Endogenous For-
mation of Carbon Monoxide in Newborn
Infants: I. Non-Icteric and Icteric Infants With-
out Blood Group Incompatibility. Acat Paediat.
(Stockholm). 52:361-366, July 1963.
115. Oski, F A. and A. A. Altman. Carboxy-
hemoglobin Levels in Hemolytic Disease of the
Newborn. J. Pediat. 67(5):709-713, November
1962.
116. Wilks, S. S. Carbon Monoxide in Green Plants.
Science. 129(3354):964-966, April 10, 1959.
117. Loewus, M. W. and C. C. Delwiche. Carbon
Monoxide Production by Algae. Plant
Physiol.35(4):371-374, July 1963.
118. Simpson, F. J., G. Talbot, and D. W. Westlake.
Production of Carbon Monoxide in the
Enzymatic Degradation of Rutin. Biochem.
Biophys. Res. Commun. 2:15-18, January
1960.
8-56
-------
119. Westlake, D. W., J. M. Roxburgh, and G.
Talbot. Microbial Production of Carbon Mon-
oxide from Flavonoids. Nature.
759(4753): 510-511, February 11, 1961.
120. Wittenberg, J. The Source of Carbon Monoxide
in the Float of the Portugese Man-of-War,
Physalia Physalis L. J. Exp. Biol.
37(4):698-705, December 1960.
121. Yagi, T. Enzymatic Oxidation of Carbon Mon-
oxide. Biochim. Biophys. Acta. 30(1): 194-195,
October 1958.
122. Krall, A. R. and N. E. Tolbert. Comparison of
Light-Dependent Metabolism of Carbon Mon-
oxide by Barley Plants with that of Formalde-
hyde, Formate and Carbon Dioxide. Plant
Physiol. J2(4):321-326, 1957.
123. Clark, R. T., Jr. Evidence for Conversion of
Carbon Monoxide to Carbon Dioxide by Intact
Animal. Amer. J. Physiol. 162(3):560-564, Sep-
tember 1950.
8-57
-------
CHAPTER 9.
EPIDEMIOLOGIC APPRAISAL OF CARBON
MONOXIDE
A. INTRODUCTION
Studies to determine the effects of CO
upon health have usually involved short-term
high-concentration exposure to CO; therefore,
the observed clinical effects are often at-
tributable to hypoxia. Many of these effects
are considered to be reversible as CO is elim-
inated from the body.1 >2 A number of recent
clinical and laboratory studies have resulted in
the concern that subtle cardiovascular and
central nervous system effects may be asso-
ciated with elevated CO levels in the atmos-
phere.
Epidemiologjc studies, as distinguished
from toxicologic or experimental studies, deal
with the effects of pollution from the
ambient air on groups of people living or
working in a community or area. In such
studies health effects are examined as they
occur naturally, rather than in a laboratory;
but this type of study also has the dis-
advantage that all the factors of possible im-
portance cannot be controlled. Nevertheless,
the preparation of air quality criteria and air
quality standards usually relies on epidemic-
logic studies because of the limitations in-
herent in most laboratory studies.
In air pollution epidemiology, gross mor-
tality data have been an insensitive way of
measuring health effects. Further, there is
often inappropriate designation of cause of
death, variation in certification of cause of
death, and usually a lack of autopsy data.
Systematic study of morbidity associated
with exposure to CO is handicapped by this
lack of available indices of health effects.
Hospital admissions data are one form of
useful information; but problems due to varia-
bility in availability of beds, day-of-week
biases, changing medical staff, overtime, and
altered criteria for admission make this infor-
mation susceptible to misinterpretation. Some
of these problems have been dealt with by
Sterling et aL in a study utilizing Blue Cross
hospital admission data as an index of
morbidity.3'4
The problems of associating monitoring
station data with the actual impact on the
individual who is exposed to a number of en-
vironments during the course of a day has
been dealt with by Goldsmith et al.s Because
of the relative ease in determining carboxy-
hemoglobin (COHb) levels by the analysis of
expired air, the potential for using each indi-
vidual as his own monitoring system should
be considered in many cases.6 In several occu-
pational studies COHb levels have been
measured in individuals exposed to high con-
centration of CO and attempts have been
made to relate COHb levels to health effects.
These studies are discussed in the following
sections.
B. SOURCES AND MAGNITUDE OF EX-
POSURE TO CARBON MONOXIDE
The numerous sources of CO and their rela-
tive contribution to body COHb levels are just
beginning to be assessed. In addition to the
CO encountered in community air, man is
personally exposed to individual sources such
as cigarette smoke, household heaters, cook-
ing fumes, and occupational pollution. De-
tecting and estimating the contribution of
community air pollution in the presence of
multiple exposures poses a complex problem.
Fortunately, it is easy to estimate the amount
of CO in the body by expired air analysis
after 20-second breathholding.7-9 Limitations
9-1
-------
in the application of this method to non-
smokers are discussed in Chapter 8, Section
C.3.
1. Community and Residential Exposures
Because of the large number of motor ve-
hicles, CO is produced in sufficiently large
quantities in certain cities that it can no
longer be considered a problem in only the
immediate vicinity of traffic; it may now be
found throughout entire communities.10'11
A quantitative discussion on the extent of this
problem is given in Chapter 4, Section B.
Haagen-Smit has measured the CO levels to
which the commuter is exposed in Los
Angeles city traffic.1 2 He found that the aver-
age concentration was 43 mg/m3 (37 ppm)
CO and that this level increased to 62 mg/m3
(54 ppm) in slow and heavy traffic.
Goldsmith et al. have reported on the
increase in COHb in two pairs of subjects, - a
smoker and a nonsmoker in each pair - ex-
posed together to Los Angeles conditions.5'8
Some results of this work are shown in
Figures 9-1 and 9-2.
A theoretical approach has been postulated
to estimate effects of population exposure to
CO by inference from an exposure pattern
and indirect measurement of the mean COHb
0.
Q-
z~
o
(J
z
o
u
o
u
70
60
50
40
30
20
10
^ ENVIRONMENTAL CO
-— EXPIRED AIR OF NONSMOKER
•— EXPIRED AIR OF SMOKER
| INDICATES CIGARETTE SMOKED
12
6
-p.m.
10
12
-*+*-
10
12
HOUR OF DAY
Figure 9-1. Carbon monoxide levels of environmental air and of expired air of smoker and
nonsmoker, Los Angeles and Pasadena, August 1962.5
9-2
-------
AMBIENT AIR
INDICATES
CIGARETTE SMOKED
OBSERVED COHb, SMOKER
OBSERVED COHb. NONSMOKER
89 10 11 12 1 234 56789 10 11 12 1 234567
E
HOUR OF DAY
Figure 9-2. Carbon monoxide levels of environmental air and COHb levels of smoker and
nonsmoker, Los Angeles County, 1963.8
levels in the population. The application of
such a procedure would be more valid than
current methods of environmental surveil-
lance.
A recent review describes several household
sources of CO.1 3 In addition it has also been
shown that open fires and charcoal braziers
produce a substantial amount of CO.14 A
field study in New Guinea also indicates
that high levels of CO may be present in
native huts when cooking is done.1 5 Some of
the seasonal variation reported for COHb con-
centrations in individuals may be attributable
to household heating. A further discussion of
levels of CO measured in households appears
in Chapter 6, Section D.
Community CO levels have been monitored
in a variety of areas to determine the distri-
bution and magnitude of exposure. Very little
attention, however, has been directed toward
the influence of community exposure upon
household CO levels.
2. Occupational Exposures
Most epidemiologjc studies of the effects of
CO on human health have dealt with occu-
pationally exposed groups. These studies can-
not be extrapolated quantitatively to the
general population because persons with
severe anemia, cardiovascular insufficiency, or
other debilitating conditions are unlikely to
be working in places like traffic tunnels, steel
mills, or parking garages. In addition, people
occupationally exposed to CO may simul-
taneously be exposed to a number of other
9-3
-------
environmental sources of CO, and the contri-
bution of each possible source may be diffi-
cult to isolate. The effects usually observed in
occupational studies of CO are increased
levels of COHb and the disputed "chronic car-
bon monoxide poisoning syndrome,"16'17
which consists of recurrent symptoms such as
headache, dizziness, exertional dyspnea,
diarrhea, urinary frequency, sweating, thirst,
weight loss, loss of libido, and insomnia.
Grut studied drivers of vehicles propelled
with "producer gas" in Copenhagen during
World War II; he indicated that 46 percent of
721 drivers had chronic CO poisoning, char-
acterized by fatigue, headache, irritability,
dizziness, and disturbed sleep.1 6
Lindgren examined two similar groups of
workmen, one of which was occupationally
exposed to CO.17 The exposed group, with
significantly higher COHb levels, included 970
subjects; the control group included 432 sub-
jects. He found no higher frequency of
symptoms and signs typical of chronic CO
poisoning in the exposed group than in the
control group. He also found no differences in
the frequency of illness between the two
groups, based on national health insurance
records over a period of 10 years.
An important study of occupational ex-
posure to CO was conducted among em-
ployees of New York's Holland Tunnel.1 s>1 9
The average exposure through all parts of the
tunnel throughout the day was estimated to
be 80 mg/m3 (70 ppm), with peak concentra-
tions rarely higher than 230 mg/m3 (200
ppm). The levels of CO found in the blood of
traffic officers stationed in the tunnel for a
2-hour period were within the range usually
observed in cigarette smokers with no occupa-
tional exposure to CO. In addition, the
amounts of CO absorbed during tunnel duty
appeared to add to amounts acquired from
cigarette smoking. No complaints attributable
to CO exposure were noted. Hemoglobin de-
terminations were reported as normal for all
exposed individuals. Urinalysis did not reveal
abnormalities of glucose or albumin when
compared with other populations.
9-4
Hofreuter et al. studied 68 employees of a
vehicle inspection center where hourly CO
concentrations averaged 58 mg/m3 (50 ppm),
with these measurements ranging from 12 to
173 mg/m3 (10 to 150 ppm).20 The average
blood COHb level for this exposed group was
3.74 percent; this was significantly higher
(p<0.01) than the average of 2.67 percent
COHb found in a control group. Average
hemoglobin levels were also significantly high-
er in the exposed group. The high average
COHb level in the control group is attributed
to the majority of subjects in each group be-
ing smokers.
Ramsey studied 38 parking garage em-
ployees whose occupational exposure to CO
averaged 68 mg/m3 (59 ppm) during the work
day.21 COHb levels in these individuals were
significantly different from those in a control
group not exposed to motor vehicle exhaust.
Their hemoglobin levels were also significant-
ly higher than those of control subjects.
Ramsey felt that occupational exposure
appeared more important than smoking in
determining COHb level in this group (See
Table 9-1).
de Bruin measured COHb levels of police-
men and drivers in Rotterdam and Amster-
dam.22 Blood samples obtained before and
after work showed increased COHb in those
occupationally exposed. A control group
showed no such increase.
Clayton et al. found increases in COHb
levels in smoking (3.1 to 3.9 percent COHb)
Table 9-1. COHb LEVELS OF SMOKERS AND
NONSMOKERS IN EXPOSED
AND CONTROL GROUPS22
Group
Exposed (parking garage)
Nonsmokers 14
Smokers 24
Controls
Nonsmokers 1 0
Smokers 17
COHb, %
a.m.
Mean
1.5
2.9
S D
±0.83
±1.88
p.m.
Mean
7.3
9.3
0.81
3.9
S D
±3.46
±3.16
±0.54
±1.48
-------
and nonsmoking (0.8 to 1.2 percent COHb)
subjects travelling in a police scout car for 8
hours in traffic; the average CO level meas-
ured during this period was 20 mg/m3 (17
ppm) although a peak of 138 mg/m3 (120
ppm) was recorded.2 3 After also studying the
COHb levels of 237 individuals involved in
not appear to be related to impaired driving
ability. It is interesting to note that the infor-
mation presented in Table 9-2 and Figure 9-3
shows that drivers involved in accidents had
higher COHb levels than did pedestrians,
though the differences are not statistically sig-
nificant. No attempt was made to relate ac-
Table 9-2. FREQUENCY DISTRIBUTION OF CO BLOOD ANALYSES OF
INDIVIDUALS INVOLVED IN TRAFFIC ACCIDENTS23
COHb, %
1.0
1.0- 1.9
2.0- 2.9
3.0- 3.9
4.0- 4.9
5.0- 5.9
6.0- 6.9
7.0- 7.9
8.0- 8.9
9.0- 9.9
10.0-10.9
11.0-11.9
31.5
Clotted
Broken
Totals
Total number
of analyses
(cumulative percent
in parentheses)
73 (32.2)
45 (52.0)
30 (65.2)
14 (71.4)
25 (82.4)
14 (88.5)
10 (93.0)
7 (96.0)
4 (98.0)
2 (98.7)
1 (99.1)
1 (99.6)
1 (100)
7
3
237
Status of individuals involved11
Drivers
27
21
14
6
12
6
3
5
3
2
-
1
-
2
1
103
Pedestrians
30
17
11
6
6
7
4
2
1
-
-
-
-
3
2
89
Passengers
5
1
1
-
3
-
1
-
-
-
-
-
-
1
-
12
Status unknown
11
6
4
2
4
1
2
-
-
-
1
-
1
1
-
33
11.0
9.0
7.0
. 5.0
i
L 3.0
r
' 1.5
1.0
0.8
TII I I I I
ODRIVERS
(100 CASES)
APEDESTRIANS
(84 CASES)
"The difference in COHb between drivers and pedestrians is not statistically significant.
cident rate to ambient CO level in this study.
The implications of the possible relationship
between ambient levels of CO, blood COHb
levels, and the occurrence of motor vehicle
accidents suggest that this is an important
area for future research.
Chovin has studied 331 traffic policemen in
Paris. Determinations of COHb were made be-
fore and after a 5-hour work period, with
average CO exposures of 12 to 14 mg/m3 (10
to 12 ppm).24 Cigarette smokers who started
work with relatively high COHb levels but did
not smoke while at work tended to excrete
CO, whereas similar smokers who started
work with low levels tended to have an in-
crease in* COHb. Those who had COHb levels
of 3 to 8 percent at the beginning of the work
shift showed very little change (See Figure
9-5
12 5 10 20 40 60 80 90 95 9899
CUMULATIVE PERCENT INDIVIDUALS
Figure 9-3. Distribution of COHb among
individuals involved in traffic accidents.23
traffic accidents, these authors concluded that
the CO level in the Detroit urban area does
-------
99.9
99.8
99.5
99
98
95
90
80
70
60
50
40
30
20
10
5
2
1
<
O
O
z
z
UJ
u
o:
UJ
CL
<
_l
:D
u
BEFORE
EXPOSURE
(PERCENT COHb DERIVED FROM
VOLUME CO ON THE ASSUMPTION
OF 15 g HEMOGLOBIN/100 ml OF
BLOOD)
0.5 0.75 1.0 1.5 2.0 3.0 4.0 5.0 7.5 10.0
COHb CONCENTRATION (LOG SCALE), percent
15.0
25.0
Figure 9-4. COHb levels of policemen who smoke before and 5 hours after exposure
to between 12 and 23 mg/m3 (10 and 12 ppm) CO, Paris, 1963.24
9-4). Nonsmokers had an increase in COHb
that was related to the ambient exposure at
the intersection where they were directing
traffic (See Figure 9-5).
Chovin derived the equation:
ICO = 0.024C-0.07
to depict the manner in which blood CO
equilibrium is approached after a person is ex-
posed to traffic for 5 hours. ICQ is the in-
crease in blood CO (in cc of CO/100 cc
blood), and C is the average ambient CO con-
centration (ppm). This equation can be ex-
pressed in terms of change in percent COHb
as follows:
A % COHb = 0.096C - 0.28
Thus, for example, an average 5-hour expos-
ure to 22 mg/m3 (20 ppm) CO would result
in an increase of COHb of 1.64 percent, and a
5-hour exposure to 12 mg/m3 would result in
an increase of COHb of about 0.7 percent.
Breysse has conducted a study to deter-
mine potential health hazards associated with
operation of gasoline fork lift trucks in the
holds of ships.25 Carbon monoxide was de-
termined from expired air samples before
work, before lunch, after lunch, and after
work. Smoking was noted to have a marked
effect upon COHb content. Six percent of
nonsmokers had COHb levels greater than 3
percent, and 47 percent of 108 smokers ex-
ceeded this level prior to work (See Table
9-3). It was further noted that 6 percent of
9-6
-------
LJJ
U
3
U
BEFORE
EXPOSURE
AFTER
EXPOSURE
(PERCENT COHb DERIVED
FROM VOLUME PERCENT
CO ON THE ASSUMPTION OF
15 g HEMOGLOBIN/100 m
OF BLOOD)
0.5
0.75
1.0
1.5
2.0
COHb CONCENTRATION
(LOG SCALE), percent
Figure 9-5. COHb levels of policemen who
do not smoke before and 5 hours atter ex-
posure to between 12 and 23 mg/m (10 and
12 ppm) CO, Paris, 1963.24
individuals had COHb levels exceeding 10 per-
cent COHb prior to work, and 10 percent ex-
ceeded this level after work. No distinction
between smokers and nonsmokers was made
in this part of the study.
Airplane pilots flying over forest fires have
been studied to determine whether CO expos-
ure significantly affected their COHb.5 Ex-
pired-air analysis indicated that the blood
COHb levels averaged 4.5 percent, reaching a
maximum of 8.1 percent in one particular
pilot. Again, smoking resulted in a higher
range of COHb concentration than did oc-
cupation.
On the basis of several studies, then, it has
been demonstrated that continuous exposure
to relatively low levels of CO may result in
significant increases in blood COHb levels, for
exposure periods as short as 5 hours. Cigarette
smoking alone can result in similar or greater
increases in COHb levels, and smoking and ex-
posure to ambient levels of CO may both con-
tribute to increasing COHb levels.
3. Qgarette, Pipe, and Cigar Smoke
Carbon monoxide occurs in high concentra-
tion in cigarette smoke (greater than 22,400
mg/m3> 20,000 ppm, or 2 percent), and the
average concentration inhaled is about 460 to
575 mg/m3 (400 to 500 ppm or 0.04 to 0.05
percent).
The magnitude of smoking exposures has
been estimated in a population of longshore-
men examined prior to the work shift and
during periods of little community air pollu-
tion.5 Exposure estimates were based on
measurements of CO in expired air after
20-second breathholding. These estimates
were validated by measurement of COHb in a
sample of the participants. The results are
shown in Table 9-4. A level of 5.9 percent
COHb was found to be the median value in
moderate cigarette smokers who inhale. The
relatively low levels in pipe smokers and cigar
smokers are due to small amount of smoke
inhaled when tobacco is consumed in these
forms. The effect of inhaling is clearly to in-
crease the uptake of CO.
Ringold et al. have measured concentra-
tions of CO in expired air and grouped their
data according to smoking history.6 As is
shown in Figure 9-6, the amount of CO ex-
pired is quite clearly related to smoking hab-
its.
C. DEFINITION OF SENSITIVE GROUPS
The concept of a "susceptible population"
merits consideration in the study of air pol-
lution epidemiology. Human responses to
community air pollution have shown wide
variations, which contribute in no small way
to the difficulty in assessing the effects of pol-
lutants. Since air quality criteria must, unless
9-7
-------
Table 9-3. COHb LEVELS OF 108 SMOKERS AND
92 NONSMOKERS BEFORE WORK25
Nonsmokers
COHb
level,
percent
0
1
2
3
4
5
6
7
> 7
Number
26
35
21
4
2
2
2
0
0
Percent
28
38
' 23
5
2
2
2
0
0
Cumulative
percent
28
66
89
94
96
98
100
100
100
Smokers
Number
3
13
21
20
9
10
18
6
8
Percent
3
12
19
19
8
9
17
6
7
Cumulative
percent
3
15
34
53
61
70
87
93
100
Table 9-4. PROPORTION OF SMOKERS AND MEDIAN VALUES OF
EXPIRED CO AMONG LONGSHOREMEN5
Smoking pattern
Never smoked
Ex-smoker
Pipe and/or cigar smoker only
Light smoker (half pack or less per day)
Moderate smoker (more than 1/2 pack and
less than 2 packs per day)
Heavy smoker (2 packs or more per day)
Percent of study
population by
smoking pattern
23.1 (764)b
12.1 (401)
13.4 (445)
13.0 (429)
31.3 (1,035)
7.0 (233)
Median CO, ppm
3.2
3.9
5.4
Inhaler
17.1
27.5
32.4
Noninhaler
9.0
14.4
25.2
Median COHb levela,
%
1.3
1.4
1.7
Inhaler
3.8
5.9
6.9
Noninhaler
2.3
3.4
5.5
aThe percent COHb was estimated from regression.
bThe number of subjects is given in parentheses. The smoking pattern of four persons was not ascertained.
otherwise specified, consider all of the popu-
lation rather than just major segments of it,
studies must consider especially the impact of
air pollution on the "most sensitive" re-
sponders. The population group most sus-
ceptible to the adverse effects of atmospheric
CO can be predicted on a physiological basis
to include those persons most sensitive to a
decrease in oxygen supply: (1) people with
9-8
severe anemia due to the already limited sup-
ply of oxygen-carrying hemoglobin; (2) those
with cardiovascular disease and the resultant
impairment of circulation; (3) those with ab-
normal metabolic states such as thyrotoxicosis
or fever, which result in increased oxygen de-
mands; (4) those with chronic pulmonary
disease; and, (5) the developing fetus, which
may be unusually sensitive to insufficient
-------
30
20
Z
g
Z
LU
U
Z
o
U
o
U
10
^^^^
I
MEAN
STANDARD DEVIATION
5.5
0.8
3.7
3.8
18.6
7.7
29.0
'16.4
3.8
-3.9
-10
-1.1
-3.2
NEVER
OR PAST
(93 SUBJECTS)
PIPE AND
CIGAR ONLY
(9 SUBJECTS)
OCCASIONAL
AND LIGHT
(25 SUBJECTS)
MODERATE
AND HEAVY
(41 SUBJECTS)
SMOKING HABIT
Figure 9-6. Distribution of expired-air CO, according to smoking history and corrected for
ambient-air CO.6
oxygen. Several recent reviews of the patho-
physiology of CO exposure include overviews
of the population at greatest risk from such
exposure.2 6~2 8 A recent review of animal and
human studies strengthens the impression that
in patients with insufficient arterial blood
flow, small amounts of COHb impair unload-
ing of oxygen and further affect the clinical
course.29
In addition to the groups proposed as most
sensitive, individuals requiring maximal judg-
mental and functional ability may be an im-
portant group to consider in the discussion of
health effects associated with CO. Automo-
bile drivers are the largest group of individuals
in this category.
A number of studies have pointed out that
cigarette smoking may have a deleterious ef-
fect upon the fetus, most notably manifest in
an increased incidence of low birth weights
and a lower average birth weight, but the
usual emphasis has been upon components
other than CO. Haddon30 has shown that
COHb levels in maternal blood are reflected in
the cord blood at delivery. The cord blood of
infants delivered from cigarette smoking
mothers has a higher COHb level than is
found in that of infants from nonsmoking
mothers. There appears to be a similar level of
COHb in maternal and cord blood (See Figure
9-7). Whether this in itself results in any other
effect on the fetus is at this time uncertain,
but unborn infants, who during parturition
may have exceptional requirements for oxy-
genation, may well be among the population
at high risk.
9-9
-------
!§
234567
CARBOXYHEMOGLOBIN, percent
10
Figure 9-7. Percentage of hemoglobin saturated with CO in cord and maternal blood
specimens of smokers and nonsmokers.3°
D. STUDIES AND INTERPRETATION
1. Mortality Studies
Statistical approaches utilized in deter-
mining whether there is excess mortality from
atmospheric pollution have been presented by
a number of investigators.31 ~3 3 Such varia-
bles as particulates, smoke-shade index, ox-
ides of sulfur, and oxidants have been studied
with some frequency, but CO has not. This
may be due in part to the fact that CO meas-
urements are not always available.
Massey et al. compared mortality in two
"communities" in Los Angeles County, which
experienced similar daily temperature but dif-
ferent levels of air pollution.34 The pollutant
variables studied were oxidant, SO2, and CO.
The investigators had to compare areas of in-
termediate and relatively high pollution rather
than low versus high areas because it was not
possible to maximize differences in air pollu-
tion exposure and still remain within an area
of uniform temperature. Differences in daily
mortality were analyzed by means of correla-
tion and multiple-regression techniques. There
9-10
were no significant correlations between mor-
tality and pollutant levels. Another problem
involved in this use of spatial analysis was the
different characteristics of the populations re-
siding within each area. The populations of
the communities differed in median age, sex
ratio, social status, urbanization, and racial
composition. It was hoped in conducting the
two-community study that the daily differ-
ences between mortality in the low and high
area would be relatively independent from
day to day. Previous studies have indicated
that effects that must be taken into account
in time-series analyses are those of autocorre-
lation as well as cyclic seasonal variations. The
negative results of this study must be viewed
in light of these limitations.
Using data on cardiac and respiratory mor-
tality for 1956, 1957, and 1958, Hechter and
Goldsmith have shown that the number of
deaths per day in Los Angeles County varies
between 1.0 and 1.3 per 100,000 popula-
tion.35 These fluctuations were approximate-
ly 180 degrees out of phase with fluctuations
-------
for maximal daily temperature and oxidant
values, and approximately in phase with CO
maxima (See Figure 9-8). If not properly
dealt with, such phase differences can pro-
duce spurious correlations. When Fourier
curves were fitted to the data,* it was found
that a single cycle of Fourier functions fit
temperature and oxidant levels, and that two-
component Fourier curves fit CO levels and
cardiorespiratory mortality (See Figure 9-9).
When the residuals from these fitted curves
were analyzed, no significant correlations be-
*Fourier curve-fitting consists of adding successive
pairs of sine and cosine functions as variables, each
successive pair being functions of twice the angle of
the preceding pair.
tween pollutants and mortality were found
(residuals are presumed to have had removed
the major effect of time of year). In addition,
there were no significant correlations when
lag periods of 1 to 4 days were utilized in the
analysis. It is possible, however, that in an
attempt to remove a time-of-year effect, a real
effect of pollutants on mortality may also
have been removed, particularly if it was a
small effect.
Curphey et al. attempted to determine
whether there is any association between the
amount of COHb in postmortem blood and
ambient CO levels with the 24-hour period
preceding death.36 The investigators were
aware of the possibility that postmortem
30
20
z
Q
O 10
0
30
a.
a.
iiiiiiiimiiiimiimiiiiiiiiiiiiii
iiiiiiiiiiiiiiiiiniiiinLiiiiiiiiiii
UJ
o
X
O
O
z
o
01
u
20
10
Illlllllll IIIIIMIIII Mllll MIIIIIMI
liiiiiiiHiiiniiiiiiiiiniiiiiHiJii
90
. 80
UJ
o:
70
60
1.4
nnm i minium ill iii mill i mi
QL O
Q. a:
a^
|£
, .^ 1.0
o: uj
<
U
0.8
iiimiiiiiiiiiiiiiiiiiiiimiiiiiili
1956
1957
YEAR
1958
1956
1957
YEAR
1958
Figure 9-8. Comparison of maximum concentrations of oxidant and carbon monoxide,
maximum temperature, and daily death rate for cardiac and respiratory causes,
Los Angeles County, 1956-1958.35
9-11
-------
blood specimens may deteriorate and produce
falsely high COHb levels, but they did not
find that the length of the interval between
death and analysis had any effect on COHb
levels in this study.
Information concerning smoking habits was
obtained from a questionnaire mailed to next
of kin. A total of 1,075 cases for which a
COHb determination had been performed
was then classified by smoking habits. Non-
smokers consistently had lower COHb levels
than smokers. Male nonsmokers had higher
COHb levels than female nonsmokers. Varia-
bles such as age, time of day and day of week
of death, maximum and minimum tempera-
tures, and cause of death had little relation-
ship to COHb levels. There did, however,
appear to be some association between ambi-
ent CO levels and postmortem COHb levels
(See Figure 9-10).
These data have been analyzed further in
an attempt to determine whether individuals
with cardiovascular disease certified by the
coroner's office as having "myocardial infarc-
tions" have different COHb levels than
individuals dying of "other cardiovascular
disease."37 Both smokers and nonsmokers
were examined initially (Figure 9-11). The
myocardial infarction cases were noticed to
be younger than those dying of "other cardio-
vascular disease." Since COHb levels of
smokers may diminish with age (either associ-
ated with the manner in which cigarettes are
inhaled or some other factor that interferes
with the alveolar diffusion of CO), an adjust-
ment for age is required when comparisons
TEMPERATURE
\
\
OXIDANT
v/
//
//
//
//
\ .
'* /
\>^
//
//
//
\
V
20
15
10
<
O
X
o
m
"*
/ .* •
' / i
/ *
* •*
\
A--
// \
CARBON MONOXIDE
\ Is
v.'-
x/
CARDIAC AND RESPIRATORY DEATH RATE
HI MM
1.4
1.3
Si
>- i
1.2
1-1 £§
UJ o
1.0 Q 2
0.9
J FMAMJJASONDJ FMAM JJASON DJ FMAMJJASON D
4 1956 *4-« 1957 KM 1958 >4
YEAR
Figure 9-9. Fourier curves fitted to data in Figure 9-8.15
u
u
9-12
-------
z
CO
o
_l
o
o
s
UJ
X
>-
X
o
CO
OL
<
u
<
o
HI
s
5.0
4.0
*- 3.0
t>
o
o
a 2.0
1.0
0
32
' I I I I I I 1 I I I I 1 I I | |
CIGARETTE SMOKERS •
i i i
UJ .
LU O
su
UJf-
OZ
< UJ
p
24
16
- ATMOSPHERIC CARBON MONOXIDE
I
I < I
I i
JAN. FEB. MAR. APR. MAY JUN.
WEEK OF REPORT
Figure 9-10. COHb levels of coroner cases,
by smoking status and atmospheric CO con-
centrations, Los Angeles County, 1961.36
such as these are carried out. When the popu-
lation was divided into two groups, those 65
and older and those under 65, no significant
differences in COHb levels were noted be-
tween the two diagnostic categories (Table
9-5). In the male population under age 65,
however, the myocardial infarction cases had
on the average a higher COHb; but the differ-
ence was not significant.
Cohen et al. have attempted to test the
hypothesis that during periods of high CO
pollution, individuals hospitalized with acute
cardiovascular disease are adversely af-
fected.38 They have studied myocardial in-
farction admissions to 35 hospitals in Los
Angeles County during 1958. Hospital records
were abstracted by the medical librarian staff
at each hospital. Information obtained in-
cluded age, sex, date of admission, date of
discharge, discharge diagnosis, disposition of
patient (recovery or death), area of residence,
area of employment, number of days hospital-
ized, and date of onset of illness. The analysis
included 3,080 admissions for myocardial in-
farction, and involved separate calculations
for hospitals in areas of high and low CO pol-
lution.
No significant association was found be-
tween the number of admissions for myo-
cardial infarction and ambient CO levels. Sig-
nificant correlations were found, however, for
weekly myocardial infarction case fatality
rates and ambient CO levels during the week
of admission. Patients admitted to hospitals in
the areas of "high" CO pollution where the
weekly CO concentration ranged from about
9 to 16 mg/m3 (8 to 14 ppm) exhibited statis-
tically significant increases (p<0.01) in mor-
tality rates from myocardial infarction when
compared to patients admitted during weeks
with lower average CO concentrations. This
correlation was principally accounted for by
an end of the year increase in both case fatal-
ity rates and ambient CO levels. To avoid
spurious correlations, which can result from
day-of-week effects as well as autocorrelation,
separate analyses were performed for each
day of the week and by high and low pollution
areas (Table 9-6). Significant associations were
then observed only for some of the days of the
week and only in the area of the county desig-
nated as having high CO levels. The case fatal-
ity rates in the high CO area were particularly
different from those in the low CO area dur-
ing weeks of the year with the greatest mean
CO levels. The comparability of these two
areas was not documented in regard to socio-
economic characteristics.
Factors other than CO exposure, such as
hospital admission and hospital-care practices
and, most importantly, seasonal influences on
case fatality rates, may have accounted for
the observed associations. At present, it ap-
pears that an association could exist between
myocardial infarction case fatality rate and
atmospheric CO pollution, but additional
studies, particularly of COHb levels in myo-
cardial infarction patients at the time of ad-
mission, are required to draw any conclusions
about causality. Individuals dying a sudden
9-13
-------
UJ
in
<
U
L1-
o
I-
z
UJ
(J
a:
UJ
a_
60
50
40
30
20 -
60
50
40
30
20
10
MYOCARDIAL INFARCTION
OTHER CIRCULATORY DISEASES
MALE SMOKERS
I I I I I I I
FEMALE SMOKERS
I I
0 0.9 1.9 2.9 3.9 4.9 5.9 6.9
COHb, percent
T 1 1 I I I I ' l~~l•"
MALE NONSMOKERS
.L
TTI
i — ' — i — i ' ' ' r
FEMALE NONSMOKERS
J I I I
I L
0.9 1.9 2.9 3.9
COHb, percent
4.9 6.9
Figure 9-11. COHb levels in myocardial infarction deaths and in other cardiovascular disease
deaths, Los Angeles County, 1961.37
death and hospitalized myocardial infarction
patients must be examined to determine
whether the COHb levels of these two popula-
tions differ.
2. Morbidity Studies
There have been few studies in which an
attempt has been made to relate community
CO exposures to indices of health. Instead,
the approach utilized has been to study oc-
cupationally exposed groups. Because of the
limitations of generalizing from occupational
groups to the general population as previously
discussed, community morbidity studies are
becoming increasingly important.
Cassell et al. obtained daily records of ill-
ness prevalence from a panel of 1,747 persons
9-14
living within a restricted geographic area of
New York City.39 The subjects were followed
at weekly intervals for an average of 45 weeks
each, providing 61,000 person-weeks of infor-
mation. Symptoms recorded were common
cold, cough, headache, and eye irritation. Pol-
lutants under study included particulate
matter, total hydrocarbons, CO, and sulfur
dioxide. Meteorologic factors such as wind
speed, precipitation, and temperature were
also considered. Correlation analyses demon-
strated two distinct clusters of environmental
variables and their associated symptoms.
Headache and eye irritation tended to occur
with warm, humid weather and stagnant
meteorologic conditions in which there were
high levels of CO, ammonia, aldehydes, total
-------
Table 9-5. COHb LEVELS FOR CARDIOVASCULAR DISEASE CATEGORIES BY AGE,
SMOKING HABITS, AND SEX,a LOS ANGELES COUNTY, 196137
Age group and
cause of death
Under 65 years
Myocardial infarction
Other circulatory
65 and older
Myocardial infarction
Other circulatory
Smoker
Male
Mean
COHb
3.13
2.84
1.29
2.02
S D
1.70
1.52
0.64
1.40
Number
of cases
76
116
15
80
Female
Mean
COHb
(2.10)b
3.01
(2.23)b
1.43
S D
1.84
2.43
2.81
1.09
Number
of cases
8
24
3
26
Nonsmoker
Male
Mean
COHb
1.44
1.15
1.18
0.98
S D
1.30
0.83
0.86
0.69
Number
of cases
14
45
23
154
Female
Mean
COHb
b
(0.70)
0.76
0.91
0.92
S D
0.22
0.40
0.50
0.52
Number
of cases
5
27
15
194
aNone of differences within sex, age, and smoking category are statistically significant.
b Parentheses indicate mean based on samples smaller than 10 cases.
Ul
-------
Table 9-6. RELATIONSHIP BETWEEN NUMBER OF HOSPITAL ADMISSIONS FOR MYOCARDIAL
INFARCTION, MYOCARDIAL INFARCTION CASE FATALITY RATES, AND AMBIENT CO
LEVELS BY DAY OF WEEK, LOS ANGELES COUNTY, 195838
Day
of
admission
All days
Weekdays
Weekends
Sunday
Monday
Tuesday
Wednesday
Thursday
Friday
Saturday
Avg CO
concentration,
ppm
7.41
7.66
6.80
6.53
7.71
7.45
7.53
7.71
7.90
7.07
Total area
Mean
myocardial
infarction
admissions
8.46
8.94
7.26
6.94
9.54
9.41
9.13
8.08
8.56
7.58
Correlation3
coefficient-
admissions
versus CO
0.002
-0.120
-0.022
-0.251
-0.234
-0.071
0.150
-0.019
0.121
-0.040
Mean
case fatality
rate per 100
admissions
26.0
24.7
30.2
28.3
25.4
23.5
- 24.2
26.9
23.6
32.0
Correlation"
coefficient-
case fatality
rate versus
CO
0.114C
0.130C
0.177
0.049
0.019
0.134
0.273C
-0.030
0.262
0.309C
High area
Mean
case fatality
rate per 100
admissions
27.3
25.8
31.7
29.3
26.3
24.5
24.7
29.4
24.3
34.0
Correlation3
coefficient-
case fatality
rate versus
CO
0.1 62d
0.167d
0.256d
0.037
0.058
0.096
0.186
0.210
0.308C
0.466C
Low area
Mean
case fatality
rate per 100
admissions
19.1
18.4
22.0
22.8
11.7
21.8
24.1
18.4
23.5
21.2
Correlation3
coefficient-
case fatality
rate versus
CO
-0.002
0.048
-0.101
0.011
0.093
0.209
0.207
0.161
-0.111
-0.182
Correlation between myocardial infarction admissions and log CO (basin average).
''Correlation between arc sin transformation of myocardial infarction case fatality rate (x ^
the number of deaths and N is the number of admissions and log CO (basin average).
cSignificant at the 5% level.
Significant at the 1% level.
= arc sin TN+1 + arc sinTN+1 ) where x is
-------
oxidants, and organic acids, but low levels of
hydrocarbons and sulfur dioxide. The second
cluster of effects (common cold, cough, and
sore throat) were thought to occur in wintry
weather (low radiation, low humidity, low
temperature, and medium winds) with high
levels of particulate matter and oxides of sul-
fur, but virtually no oxidant or aldehydes.
The relevance of this work to actual effects of
CO is limited since the presence of CO was
probably only an index of a variety of pri-
mary pollutants. The association of headache
and increased ambient CO concentrations is,
however, quite plausible.
Sterling3 >4 et al. assembled Blue Cross ad-
missions data from Los Angeles hospitals for
the period March to October 1961. Diagnoses
were grouped according to what the authors
consider "highly relevant," "relevant," and
"nonrelevant" illnesses. After correcting for
day-of-week effects in both pollutant and ad-
mission frequencies, a statistically significant
correlation was found with CO and several
other pollutants for "highly relevant" condi-
tions such as allergic disorders, inflammatory
diseases of the eye, acute upper respiratory
infections, influenza, and bronchitis. Since
there is no biologically plausible explanation
for such an association, at the present time
such a relationship cannot be regarded as sig-
nificant in terms of CO.
Verrna40 et al. undertook a retrospective
study of absences due to illness among a
group of white-collar workers located in
metropolitan New York during a 3-year peri-
od. Any employee who had been absent be-
cause of illness reported to the company med-
ical department for appraisal prior to his
returning to work. These records were then
categorized as either respiratory or nonrespira-
tory illness, and an association was noted be-
tween respiratory illness and ambient sulfur
dioxide levels. No such association was ob-
served between respiratory illness and CO. No
association was found between nonrespiratory
illness and sulfur dioxide, smoke shade, or
CO. When time trends were removed from the
data and analyses were repeated, there were
no significant associations between absences.
and any of the pollution variables. These data
therefore demonstrate yearly cyclic behavior,
which tends to influence both pollutants and
illness absences. The authors state the models
they have developed retain their descriptive
power for respiratory illness absences, and
suggest that while no causal association can be
inferred, there is a relationship between res-
piratory illness absences, air pollution, and cli-
mate variables from one time period to the
next.
3. Possible Relevance of Carbon Monoxide
Exposure to Motor Vehicle Accidents
As noted in the prior section dealing with
magnitude and types of exposure, motor ve-
hicles contribute a large proportion of com-
munity CO exposure. The effects of CO upon
visual threshold and ability to discriminate
time intervals41-42 have been discussed in
detail in Chapter 3, Section E. In view of the
increasing evidence of sensory impairment as-
sociated with relatively low-level CO expos-
ures, it has become quite pertinent to deter-
mine whether such effects in motor vehicle
drivers predispose them to accidents. McFar-
land has reviewed the numerous factors that
must be taken into account in epidemiologic
studies of motor vehicle accidents.4 3 >44
During the period 1959 through 1963 Cho-
vin2 4 determined COHb levels in three popu-
lation groups. He analyzed 1,672 blood sam-
ples from motor vehicle drivers who were
thought to be responsible for accidents, 3,818
samples from workers who were sometimes
exposed to CO in their occupations, and
1,518 samples from individuals who were sus-
pected of having been exposed to domestic
sources of CO. Alcohol measurements were
also made in the accident category, but data
are not available. The cumulative distribution
of blood CO levels is shown in Figure 9-12.
Individuals involved in auto accidents had the
highest blood CO levels, followed by workers
with CO exposure; individuals with suspected
exposure to CO in the home had the lowest
blood CO levels. Chovin notes that smokers
and nonsmokers were present in all three cate-
gories, but no data are presented to indicate
9-17
-------
UJ
U
OH
z
LU
12.0
8.0
4.0
2.0
1.6
1.2
> 0.8
a
UJ
0.4
. Q
O
O
_1
CO
' CO
E
•3.0'
2.0
1.0
o
° 0.5
Qi
UJ
Q.
CO
_ E
u
O
U
— 0.1
0.4
0.3
0.2
0.1 0.5 510 3050 70 90 9899.5
CUMULATIVE PERCENT INDIVIDUALS
Figure 9-12. Cumulative distribution of
blood CO concentrations, based on 5-year
study of car drivers, workmen with CO ex-
posure, and private individuals suspected
of accidental CO exposure.24
whether the proportion of smokers and non-
smokers is the same in these categories. Other
questions, especially the association of in-
creased cigarette consumption with other vari-
ables, must be dealt with before any firm con-
clusions can be drawn from this study.
An additional approach that could be of
assistance in determining the relevance of CO
to automobile accidents is study of the fre-
quency of motor vehicle accidents during
periods of and in locations with different CO
levels. A statistical and epidemiological strate-
gy for this purpose has been developed and
utilized by Ury45 for studying the effect of
oxidant on automobile accidents.
E. SUMMARY
Exposures to environmental levels of CO
can increase blood COHb concentrations in
human subjects. The amount of this increase
is reasonably predictable and must be consid-
ered in relation to CO exposures from inhaled
cigarette smoke as well as from occupational
and domestic sources. Methods for estimating
COHb levels in large populations are relatively
simple.
Continuous exposure to relatively low lev-
els of CO may result in significant increases
9-18
in blood COHb levels for exposure periods of
only a few hours. Such an exposure increases
the body burden of COHb in persons who do
not already have such a body burden from
cigarette smoking. Longer exposures would
most likely produce a somewhat greater in-
crease, with greater potential for impairment
of tissue oxygenation.
Exposure of traffic policemen, in Paris, for
5 hours to between 12 and 14 mg/m3 (10 and
12 ppm) increased COHb levels in non-
smokers by about 0.7 percent. The same ex-
posures of cigarette smokers may cause those
who have elevated COHb at the start of ex-
posure to have a decrease in COHb and those
who had relatively low values of COHb at the
start of the study to have an increase in
COHb. Cigarette smoking was not permitted
during this 5-hour period of exposure.
Apart from increases in COHb, three possi-
ble effects have been a source of major con-
sideration in epidemiologic studies:
1. Continued exposure to low levels of
CO may produce some persistent tox-
ic reaction, such as a chronic CO
poisoning syndrome. The evidence for
the occurrence of such a condition is
inadequate and is based primarily on
subjective symptons.
2. The evidence to date, though incon-
clusive, suggests that weekly average
CO values in excess of from 9 to 16
mg/m3 (8 to 14 ppm) may be associ-
ated with an increase in mortality in
hospitalized patients with myocardial
infarction. Substantiation of this im-
pression will require a study of the
prognosis of myocardial infarction
patients in relationship to COHb levels
measured at admission to the hospital.
3. In two studies, persons driving motor
vehicles that were involved in acci-
dents had higher COHb levels than
"control" populations; controls were
not ideal, however. Possible mecha-
nisms by which CO might affect the
ability to drive a motor vehicle are
suggested in the available data in CO
-------
effects upon visual sensitivity, psycho-
logical test performance, and accurate
estimation of time intervals. As little
as 2.5 percent COHb has produced
these effects in laboratory studies of
nonsmokers, and the available epidem-
iologic information is consistent with
the premise that such an increase in
COHb levels among drivers might in-
fluence the frequency of accidents.
Specific areas wherein research is needed to
clarify uncertainties relating to health effects
of CO exposure are:
1. The increment of COHb that can be
produced by exposures to CO
concentrations in the range of 12 to
23 mg/m3 (10 to 20 ppm) for time
periods from 8 to 24 hours.
2. The relationship of ambient CO levels
and of COHb levels to the survival of
hospitalized patients with myocardial
infarction.
3. The prognostic significance with re-
spect to cardiovascular conditions of
elevated levels of COHb.
4. The relationship, if any, between am-
bient CO and COHb levels and the oc-
currence of motor vehicle accidents
when weather and driving conditions,
cigarette smoking, alcohol and drug
use, and other factors are adjusted and
controlled.
5. The relationship between concentra-
tions of CO measured outdoors and
inside households.
F. REFERENCES
1. Lilienthal, J. L. Jr. Carbon Monoxide. J. Pharma-
col. Exp. Therap. 99:324-354, August 1950.
2. Root, W. S. Carbon Monoxide. In: Handbook of
Physiology, Section 3. Respiration, Fenn, W. O.
and H. Rahn (ed.). Washington, D.C., American
Physiological Society, 1965. p. 1087-1098.
3. Sterling, T. D. et al. Urban Morbidity and Air
Pollution: A First Report. Arch. Environ. Health.
73(2):158-170, August 1966.
4. Sterling, T. D., S. V. Pollack, and J. J. Phair.
Urban Hospital Morbidity and Air Pollution: A
Second Report. Arch. Environ. Health.
75:362-374, September 1967.
5. Goldsmith, J. R., F. Schuette, and L. Novick.
Appraisal of Carbon Monoxide Exposure from
Analysis of Expired Air. Excerpta Med. Int.
Congr. Series. 62:948-952, 1963.
6. Ringold, A. et al. Estimating Recent Carbon
Monoxide Exposures. Arch. Environ. Health.
5(4):308-318, October 1962.
7. Jones, R.H. et al. Relationship Between Alveolar
and Blood Carbon Monoxide Concentrations Dur-
ing Breathholding. J. Lab. Clin. Med. 57:553-564,
April 1958.
8. Goldsmith, J. R., J. Terzaghi, and J. D. Hackney.
Evaluation of Fluctuating CO Exposures. Arch.
Environ. Health. 7(6):647-663, December 1963.
9. Siosteen, S. M. and T. Sjostrand. A Method for
the Determination of Low Concentrations of CO
in the Blood and the Relation Between the CO
Concentration in the Blood and that in the
Alveolar Air. Acta Physiol. Scand. (Stockholm).
22(2-3): 129-136, April 25, 1951.
10. Goldsmith, J. R. and L. H. Rogers. Health Haz-
ards of Automobile Exhaust. Public Health Rept.
74(6):551-558,June 1959.
11. Lawther, P. J., B. T. Commins, and M. Hender-
son. Carbon Monoxide in Town Air. An Interim
Report. Ann. Occup. Hyg. 5:241-248, October-
December 1962.
12. Haagen-Smit, A. J. Carbon Monoxide Levels in
City Driving. Arch. Environ. Health. 72:548-550,
May 1966.
13. Amiro, A. G. Carbon Monoxide Presents Public
Health Problems. J. Environ. Health.
32(1): 83-88, July-August 1969.
14. Sofoluwe, G. Smoke Pollution in Dwellings of
Infants with Bronchopneumonia. Arch. Environ.
Health. 7(5:670-672, May 1968.
15. Cleary, G. J. and C. R. B. Blackburn. Air Pollu-
tion in Native Huts in the Highlands of New
Guinea. Arch. Environ. Health. 77(5):785-794,
November 1968.
16. Grut, A. Chronic Carbon Monoxide Poisoning.
Copenhagen, Ejnar Munksgaard, 1949. 229 p.
17. Lindgren, S. A. A Studysof the Effect of
Protracted Occupational Exposure to Carbon
Monoxide with Special Reference to the Occur-
rence of the So-called Chronic Carbon Monoxide
Poisoning. Acta Med. Scand. (Stockholm).
767(Supp. 356):1-135, 1961.
18. Sievers, R., T. I. Edwards, and A. L. Murray.
Medical Study of Men Exposed to Measured
Amounts of Carbon Monoxide in the Holland
Tunnel for 13 Years. National Institute of
Health, Industrial Hygiene Division. Washington,
D.C. PHS Bulletin Number 278. 1942. 74 p.
19. Sievers, R. F. et al. Effect of Exposure to Known
Concentrations of Carbon Monoxide. J. Amer.
Med. Assoc. 77S(8):585-588, February 21, 1942.
9-19
-------
20. Hofreuter, D. H., E. J. Catcott, and C. Xintaras.
Carboxyhemoglobin in Men Exposed to Carbon
Monoxide. Arch. Environ. Health. 4:81-85, Jan-
uary 1962.
21. Ramsey, J. M. Carboxyhemoglobinemia in Park-
ing Garage Employees. Arch. Environ. Health.
75(5):580-583, November 1967.
22. deBruin, A. Carboxyhemoglobin Levels Due to
Traffic Exhaust. Arch. Environ. Health.
75(3):384-389, September 1967.
23. Clayton, G. D., W. A. Cook, and W. G. Fredrick.
A Study of the Relationship of Street Level Car-
bon Monoxide Concentrations to Traffic Acci-
dents. Amer. Ind. Hyg. Assoc. J. 27:46-54, Feb-
ruary 1960.
24. Chovin, P. Carbon Monoxide: Analysis of Ex-
haust Gas Investigations in Paris. Environ. Res.
7(2): 198-216, October 1967.
25. Breysse, P. A. Use of Expired Air for Evaluating
Carbon Monoxide Exposures. Presented at the
9th Conference on Methods in Air Pollution and
Industrial Hygiene Studies. Pasadena. February
7-9, 1968.
26. Dinman, B. D. Pathophysiologic Determinants of
Community Air Quality Standards for Carbon
Monoxide. J. Occup. Med. 70:446-456", Septem-
ber 1968.
27. Smith, R. G. Discussion of Pathophysiologic De-
terminants, of Community Air Quality Standards
for Carbon Monoxide. J. Occup. Med.
70:456-462, September 1968.
28. Bartlett, D. Pathophysiology of Exposure to Low
Concentrations of Carbon Monoxide. Arch. En-
viron. Health. 76:719-727, May 1968.
29. Kjeldsen, K. Smoking and Athersclerosis. Copen-
hagen, Ejnar Munksgaard, 1969. 145 p.
30. Haddon, W., Jr., R. E. Nesbitt, and R. Garcia.
Smoking and Pregnancy: Carbon Monoxide in
Blood During Gestation and at Term. Obstet.
Gynecol. 75(3):262-267, September 1961.
31. Winkelstein, W.et al. The Relationship of Air Pol-
lution and Economic Status to Total Mortality
and Selected Respiratory System Mortality in
Men. I. Suspended Particulates. Arch. Environ.
Health. 14:162-171, January 1967.
32. Glasser, M., L. Greenburg, and F. Field. Mortal-
ity and Morbidity During a Period of High Levels
of Air Pollution. Arch. Environ. Health.
75:684-694, December.1967.
33. Zeidberg, L. D., R. J. M. Horton, and E. Landau.
The Nashville Air Pollution Study: VI. Cardiovas-
cular Disease Mortality in Relation to Air Pollu-
tion. Arch. Environ. Health. 75:225-236, August
1967.
34. Massey, F. J., E. Landau, and M. Deane. Air Pol-
lution and Mortality in Two Areas of Los Ange-
les County. Presented at the Joint Meeting of the
American Statistical Association and the Biomet-
ric Society (ENAR). New York. December 27,
1961.
35. Hechter, H. H. and J. R. Goldsmith. Air Pollu-
tion and Daily Mortality. Amer. J. Med. Sci.
247:581-588, May 1961.
36. Curphey, T. J., L. P. L. Hood, and N. M. Perkins.
Carboxyhemoglobin in Relation to Air Pollution
and Smoking. Arch. Environ. Health.
70:179-185, February 1965.
37. Cohen, S. I. Carboxyhemoglobin Levels and
Myocardial Infarction. Presented at the Califor-
nia Medical Association Scientific Assembly. San
Francisco. March 27, 1968.
38. Cohen, S. L, M. Deane, and J. R. Goldsmith.
Carbon Monoxide and Myocardial Infarction
Arch. Environ. Health. 7P:510-517, April 1969.
39. Cassel, E. J. et al. Air Pollution, Weather, and
Illness in Children and Adults in a New York
Population. Arch. Environ. Health. 75:523-530,
April 1969.
40. Verma, M. P., F. J. Schilling, and W. H. Becker.
Epidemiological Study of Illness Absences in Re-
lationship to Air Pollution. Arch. Environ.
Health. 75:536-543, April 1969.
41. Halperin, M. H. et al. The Time Course of the
Effects of Carbon Monoxide on Visual Thresh-
olds. J. Physiol. 746(3):583-593, June 11, 1959.
42. Beard, R. R. and T. A. Wertheim. Behavioral Im-
pairment Associated with Small Doses of Carbon
Monoxide. Amer. J. of Pub. Health.
57:2012-2022, November 1967.
43. McFarland, R. A., G. A. Ryan, and R. Dingman.
Etiology of Motor-Vehicle Accidents, with Spe-
cial Reference to the Mechanisms of Injury. New
England J. Med. 275:1383-1388, June 20, 1968.
44. McFarland, R. A. The Epidemiology of Motor
Vehicle Accidents. J. Amer. Med. Assoc.
750:289-300, April 28, 1962.
45. Ury, H. Photochemical Air Pollution and Auto-
mobile Accidents in Los Angeles. Arch. Environ.
Health. 77(3):334-342, September 1968.
9-20
-------
CHAPTER 10.
SUMMARY AND CONCLUSIONS
A. OCCURRENCE, PROPERTIES, AND
FATE OF ATMOSPHERIC
CARBON MONOXIDE
Because of its origin from the incomplete
combustion of organic materials, carbon mon-
oxide (CO) is emitted to the atmosphere in
greater quantities than any other urban air
pollutant. The largest sources of CO in the
urban environment may be classified as tech-
nological. Several geophysical and biological
sources of this pollutant have been identified,
but their contribution to urban atmospheric
concentrations is thought to be small. Back-
ground concentrations of CO (arising from
both natural and technological sources) are
presently estimated to range from 0.029 to
1.15 milligrams per cubic meter (mg/mP), i.e.,
0.025 to 1.00 part per million (ppm).
Carbon monoxide is a colorless, odorless,
tasteless gas. Oxidation of CO to carbon diox-
ide (CO2) does occur in the atmosphere, but
the rate of the known reactions have been
shown to be very slow. The mean residence
time of atmospheric CO has been estimated to
be between 1 month and 5 years.
Removal processes for atmospheric CO
have been postulated to include: the migra-
tion of CO to the upper atmosphere, the bind-
ing of CO to porphyrin compounds in plants
and animals, and undetermined interactions
between CO and ocean water, and the adsorp-
tion and oxidation of CO on various surfaces.
Some of these removal processes are, how-
ever, highly speculative.
B. FORMATION OF
CARBON MONOXIDE
CO arises primarily from incomplete or in-
efficient combustion of carbonaceous fuels.
Oxygen concentration, flame temperature, gas
residence time, and combustion chamber
turbulence are important variables that affect
the exhaust concentrations of CO.
C. ESTIMATION OF CARBON
MONOXIDE EMISSIONS
An estimated 92 x 109 kilograms (102 mil-
lion tons) of CO were emitted in the United
States in 1968. This amounts to 50 percent
by weight of all major air pollutant emissions
that year. Fuel combustion in mobile sources
utilizing the internal combustion engine is the
principal source category of CO (58 percent).
Miscellaneous combustion sources, principally
forest fires, and industrial process sources are
the second (17 percent) and third (11 per-
cent) largest categories, respectively. Disposal
of solid wastes is the fourth (8 percent)
greatest source category of CO emissions, and
stationary fuel combustion is the fifth (2 per-
cent).
Emission estimates were derived by the use
of emission factors and activity levels. A sum-
mary of the method of estimation applied to
each source category is presented. Estimates
indicate that no further increase in magnitude
of CO vehicular emissions above the 1968
value of 59 million tons would be expected
before about 2000.
D. MEASUREMENT OF CARBON
MONOXIDE CONCENTRATIONS
IN AMBIENT AIR
Nondispersive infrared (NDIR) analyzers
are the most commonly used continuous,
automated devices for measuring atmospheric
CO concentrations and are generally accepted
10-1
-------
as the most reliable reference method. Meas-
uring ranges usually extend from 1 to 58
mg/m3 (1 to 50 ppm) CO or from 1 to 115
mg/m3 (1 to 100 ppm) CO. Water vapor and
CO2 interfere in the determination of CO by
NDIR techniques. Filter cells and treatment
of the incoming gas stream are techniques
used to minimize these interferences.
Galvanic and coulometric analyzers are
two other instruments commercially available
for continuously measuring CO concentra-
tions. The function of both instruments de-
pends on the oxidation of CO by iodine pent-
oxide (1205). These instruments are flow- and
temperature-dependent and suffer from multi-
ple interferences; consequently, they have not
been widely used.
A mercury vapor analyzer, which depends
on the liberation of mercury vapor when CO
is passed over hot mercuric oxide, has been
used as a portable, continuous-monitoring an-
alyzer. Though especially adaptable for meas-
uring low CO concentrations [0.29 mg/m3
(0.25 ppm)], this instrument does not appear
suitable for routine air monitoring because of
numerous interferences and electronic insta-
bility.
A recently developed automated gas
chromatographic system operates by quantita-
tively converting CO to methane (CIfy),
which is subsequently semi-continuously
measured by a flame ionization detector. This
arrangement shows considerable promise as a
monitoring device. Concentrations of from
0.1 to 1,150 mg/m3 (0.1 to 1,000 ppm) may
be determined, and instrument output over
this range is linear for both CO and Cffy.
Another principle for determination of at-
mospheric CO concentrations is based on the
catalytic conversion, using Hopcalite, of CO
to CO2 with a measurement of the resulting
temperature rise. These systems are widely
used in enclosed spaces, but their applicability
for ambient air monitoring is limited be-
cause they function best at high ambient con-
centrations.
Intermittent samples may be collected in
the field and later analyzed in the laboratory
by NDIR, gas chromatographic, or infrared
10-2
spectrophotometric methods of analysis.
Colorimetric techniques, generally based on
the reduction of a metallic salt, have been
used for rapid, relatively gross estimates of
CO concentrations.
Accurately prepared standard samples are
necessary for the calibration of any instru-
ment used to measure CO concentrations. Gas
samples may be standardized by volumetric,
gravimetric, and chemical techniques.
E. ATMOSPHERIC CARBON MONOXIDE
CONCENTRATIONS
Diurnal, weekly, and seasonal variations in
CO concentrations can be observed. Diurnal
and weekly variations correlate best with
community traffic patterns; seasonal variations
are most dependent on meteorologic variables.
Both macro- and micrometeorological fac-
tors play a role in the rate of dispersion of CO
emissions. Micrometeorological factors, such
as mechanical turbulence produced by auto-
mobiles and airflow around buildings, become
important in determining street-side expos-
ures. Macrometeorological factors can lead to
air stagnation, which causes high community
CO levels.
The concepts of averaging time and fre-
quency of occurrence are important when de-
scribing ambient pollutant measurements. Be-
cause of physiological considerations, the
averaging time of most interest for CO is 8
hours. Aerometric data from the Continuous
Air Monitoring Program, the State of Califor-
nia, and Los Angeles County were analyzed
for the 8-hour-averagjng-time CO concentra-
tion exceeded 0.1 percent of the time at each
available site. These values ranged from ap-
proximately 12 to 46 mg/m3 (10 to 40 ppm).
To aid in analyzing aerometric data, a sta-
tistical model has been developed. While year-
to-year mean and peak CO values may vary
markedly within a community, the model can
be used to calculate, based on any averaging
time, a statistically probable annual maximum
concentration.
Within a community, CO concentrations
vary markedly with location. Calculated an-
nual maximum concentrations in the most
-------
polluted 5 percent of the locations incorpo-
rated in a recent sample of a variety of sites
showed that CO concentrations predicted
inside the passenger compartment of motor
vehicles in downtown traffic were almost 3
times those predicted in central urban areas
and 5 times those expected in residential
areas. Occupants of vehicles traveling on ex-
pressways and arterial routes were found to
have CO exposures somewhere between those
in central urban areas and in downtown traf-
fic.
Concentrations exceeding 100 mg/m^ (87
ppm) have been measured in underground
garages, in tunnels, and in buildings con-
structed over highways.
Using emission and meteorological data,
diffusion models can be used to estimate com-
munity air quality under a variety of con-
ditions.
F. EFFECTS OF CARBON MONOXIDE
ON VEGETATION AND
MICROORGANISMS
Plants are relatively insensitive to CO at the
lower levels of concentrations that have been
found to be toxic for animals. CO has not
been shown to produce detrimental effects on
certain higher plants at concentrations below
115 mg/m3 (100 ppm) when exposed for
from 1 to 3 weeks. Nitrogen fixation by
Rhizobium trifolii innoculated into red clover
plants has been reduced by about 20 percent,
however, after exposure to 115 mg/m^ (100
ppm) CO for 1 month.
G. TOXICOLOGICAL APPRAISAL OF
ATMOSPHERIC CARBON MONOXIDE
CO is absorbed by the lung and reacts pri-
marily with hemo proteins and most notably
with the hemoglobin of the circulating blood.
The absorption of CO is associated with a re-
duction in the oxygen-carrying capacity of
blood and in the readiness with which the
blood gives up its available oxygen to the
tissues. The affinity of hemoglobin for CO is
over 200 times that for oxygen, indicating
that carboxyhemoglobin (COHb) is a more
stable compound than oxyhemoglobin
(O2Hb). About 20 percent of an absorbed
dose of CO is found outside of the vascular
system, presumably in combination with
myoglobin and heme-containing enzymes.
The magnitude of absorption of CO increases
with the concentration, the duration of ex-
posure, and the ventilatory rate. With fixed
concentrations and with exposures of suffi-
cient duration, an equilibrium is reached; the
equilibrium is reasonably predictable from
partial-pressure ratios of oxygen to CO.
Long-term exposures of animals to suffi-
ciently high CO concentrations can produce
structural changes in the heart and brain. It
has not been shown that ordinary ambient ex-
posures will produce this. The lowest expo-
sure producing any such changes has been
58 mg/m^ (50 ppm) continuously for 6
weeks.
The normal or "background" concentra-
tion of COHb in nonsmokers is about 0.5 per-
cent and is attributed to endogenous sources
such as heme catabolism. The body's uptake
of exogenous CO increases blood COHb ac-
cording to the concentration and length of
exposure to CO as well as the respiratory rate
of the individual.
In human exposure studies, continuous
exposure to 35 rng/m^ (30 ppm) CO has led
to 80 percent of the equilibrium value of 5
percent COHb being approached in 4 hours,
and the remaining 20 percent approached
slowly over the next 8 hours. Theoretical cal-
culations indicate a COHb equilibrium value
of about 3.7 percent after continuous ex-
posure to 23 mg/m^ (20 ppm) and about 2
percent after continuous exposure to 12
mg/m^ (10 ppm). The equilibrium values are
generally reached after about 8 or more hours
of exposure, although physical activity can
shorten this time period.
Interference with the accurate estimation
of time intervals has been demonstrated in
nonsmokers with exposures to as low as 58
mg/m^ (50 ppm) CO for 90 minutes. Such an
exposure is likely to lead to COHb levels in
the range of 2.5 percent. At a blood level of
10-3
-------
about 3 percent COHb, estimated by expired
air analysis after exposure of nonsmokers to
58 mg/m3 (50 ppm) CO for 50 minutes, signif-
icant changes in relative brightness threshold
and visual acuity have been observed. Evi-
dence of impairment in performance of other
psychomotor tests has been associated with
COHb levels of 5. percent in some instances.
Experimental exposures of human subjects to
CO leading to blood COHb levels above 5 per-
cent have been associated with impairment in
the oxidative metabolism of the myocardium
in subjects with pulmonary emphysema and
coronary heart disease. Persons in the latter
group are unable to compensate for CO ex-
posures by increasing coronary blood flow
and are, therefore, particularly vulnerable.
Persons with veno-arterial shunts in the circu-
lation are also probably vulnerable, as are
those with respiratory impairment. From
physiologic considerations CO would be ex-
pected to have a greater effect with increasing
altitude.
There is evidence that CO exposure increas-
es the hematocrit of the blood and probably
the circulating blood volume, although the
significance of these changes is not clear.
There is evidence that prolonged exposure to
relatively high concentrations of CO increases
the deposition of lipids in the major blood
vessels of rabbits, and this could be a factor in
the pathogenesis of arteriosclerosis.
Thus, in summary it may be stated that:
(1) no human health effects have been dem-
onstrated for COHb levels below 1 percent,
since endogenous CO production makes this a
physiological range; (2) the following ef-
fects on the central nervous system occur
above 2 percent COHb: (a) at about 2.5 per-
cent COHb in nonsmokers (from exposure to
58 mg/m3 for 90 minutes), an impairment in
time-interval discrimination, has been docu-
mented, (b) at about 3 percent COHb in non-
smokers (from exposure to 58 mg/m3 for 50
minutes), an impairment in visual acuity and
relative brightness threshold has been ob-
served, (c) at about 5 percent COHb there is
an impairment in performance of certain
other psychomotor tests; (3) cardiovascular
10-4
changes have been shown to occur at expos-
ure sufficient to produce over 5 percent
COHb; they include increased cardiac output,
increased arterial-venous oxygen difference,
increased coronary blood flow in patients
without coronary disease, decreased coronary
sinus blood PQ2 m patients with coronary
heart disease, impaired oxidative metabolism
of the myocardium, and other related effects;
these changes have been demonstrated to pro-
duce an exceptional burden on some patients
with heart disease; and (4) adaptation to CO
may occur through increasing blood volume,
among other mechanisms.
H. EPIDEMIOLOGICAL APPRAISAL OF
CARBON MONOXIDE
Those segments of the population most sus-
ceptible to the adverse effects associated with
atmospheric CO can be predicted on a physio-
logic basis to include those people most sensi-
tive to a decreased oxygen supply. These sus-
ceptible groups include, then, individuals with
anemia, cardiovascular disease, anormal meta-
bolic states such as thyrotoxicosis or fever,
and chronic pulmonary disease and the devel-
oping fetus.
A major source of CO exposure is cigarette
smoke; cigarette smokers generally have a
COHb with a median value of 5 percent,
whereas nonsmokers are usually found to
have about 0.5 percent COHb. Community
exposures of people who are cigarette smok-
ers and already have an elevated COHb will
either lead to an increase in COHb or will
slow down the excretion of CO during inter-
vals between cigarette smoking, depending
upon the initial COHb level in the smoker and
the magnitude and duration of the ambient
CO exposure. Exposure of traffic policemen,
in Paris, for 5 hours to between 12 and 14
mg/m3 (10 and 12 ppm) has increased COHb
levels in nonsmokers by about 0.7 percent.
The extent of human CO exposure from
sources other than smoking or the ambient
outdoor air has not been well documented.
Several effects of long-term exposure to CO
have been implicated. Recent data suggest
that the mortality from myocardial infarction
-------
may be increased by exposure to average
weekly CO concentrations of from 9 to 16
mg/m3 (8 to 14 ppm), although these results
are not conclusive and require replication.
The probability of involvement in motor ve-
hicle accidents may also be associated with
CO exposure. This could be related to the in-
fluence of CO exposure on visual acuity, esti-
mation of time intervals, or other psychomo-
tor parameters.
I. AREAS FOR FUTURE RESEARCH
Review of this document reveals many
areas where additional research is necessary to
fill the gaps in our present knowledge of the
behavior and effects of ambient CO.
The atmospheric reactions and fate of am-
bient CO are only vaguely understood and
therefore require further study. Improve-
ments are needed in instrument-measuring
methods, particularly with a view to eliminat-
ing interferences and to making the instru-
ments less cumbersome. Associated with this
is the need to measure the influence of
outdoor CO levels on indoor CO concentra-
tions.
Research on the physiology of CO in the
human body has provided considerable infor-
mation on both endogenous CO production
and on the effects of CO at various cellular
and microcellular levels. Our knowledge of
the effects of CO on enzyme systems and tis-
sue oxygenation, however, is far from com-
plete. In addition, mechanisms of CO catabo-
lism in the body remain undefined. The up-
take of CO during varying time periods and
with changes in activity must be further docu-
mented.
Studies of the effects of CO on human be-
havior and performance need both clarifi-
cation and replication. Definition and
sophistication of parameters sensitive to
changes in blood carboxyhemoglobin merit
considerable attention as a prerequisite to bet-
ter defining the influence of CO on human
performance.
Epidemiological information is urgently
needed on the possible effects of CO on sever-
al segments of the population which theoreti-
cally at least are at great risk to CO expos-
ure. In addition, many questions have been
raised concerning the relationship between
CO exposure and the development and/or
progression of cardiovascular disease, and our
present state of knowledge is far from com-
plete on this subject.
The relationship between CO exposure
from smoking and CO exposure from the am-
bient air is not clear at the present time. While
both exposures produce increases in blood
COHb, the associated effects are not identical.
Whether or not some method of adaptation to
CO exposure exists is a debatable issue at the
present time.
J. CONCLUSIONS
Derived from a careful evaluation of the
studies cited in this document, the conclu-
sions given below represent the National Air
Pollution Control Administration's best judg-
ment of the effects that may occur when vari-
ous levels of pollution are reached in the am-
bient air. Additional information from which
the conclusions were derived, and qualifica-
tions that may enter into consideration of
these data, can be found in the appropriate
chapter of this document.
1. Experimental exposure of nonsmokers
to a concentration of 35 mg/m3 (30
ppm) for 8 to 12 hours has shown
that an equilibrium value of 5 percent
COHb is approached in this time; a-
bout 80 percent of this equilibrium
value, i.e., 4 percent COHb, is present
after only 4 hours of exposure. These
experimental data verify formulas
used for estimating the equilibrium
values of COHb after exposure to low
concentrations of CO. These formulas
indicate that continuous exposure of
nonsmoking sedentary individuals to
23 mg/m3 (20 ppm) will result in a
blood COHb level of about 3.7 per-
cent, and an exposure to 12 mg/m3
(10 ppm) will result in a blood level of
about 2 percent (Chapter 8, Sections
D and K).
10-5
-------
2. Experimental exposure of nonsmokers
to 58 mg/m3 (50 ppm) for 90 minutes
has been associated with impairment
in time-interval discrimination (See
Chapter 8, Section E). This exposure
will produce an increase of about 2
percent COHb in the blood. This same
increase in blood COHb will occur
with continuous exposure to 12 to 17
mg/m3 (10 to 15 ppm) for 8 or more
hours. (See Chapter 8, Sections D and
E).
3. Experimental exposure to CO concen-
trations sufficient to produce blood
COHb levels of about 5 percent (a lev-
el producible by exposure to about 35
mg/m3 for 8 or more hours) has pro-
vided in some instances evidence of
impaired performance on certain oth-
er psychomotor tests, and an impair-
ment in visual discrimination (Chapter
8, Section E).
4. Experimental exposure to CO concen-
trations sufficient to produce blood
COHb levels above 5 percent (a level
producible by exposure to 35 mg/m3
or more for 8 or more hours) has pro-
vided evidence of physiologic stress in
patients with heart disease (Chapter 8,
Section F).
Table 10-1 presents these conclusion in tab-
ular form.
K. RESUME
An exposure of 8 or more hours to a car-
bon monoxide concentration of 12 to 17
mg/m3 (10 to 15 ppm) will produce a blood
carboxyhemoglobin level of 2.0 to 2.5 per-
cent in nonsmokers. This level of blood
carboxyhemoglobin has been associated with
adverse health effects as manifested by
impaired time interval discrimination. Evi-
dence also indicates that an exposure of 8 or
more hours to a CO concentration of 35
mg/m3 (30 ppm) will produce blood carbox-
yhemoglobin levels of about 5 percent in
nonsmokers. Adverse health effects as mani-
fested by impaired performance on certain
other psychomotor tests have been associated
with this blood carboxyhemoglobin level, and
above this level there is evidence of physio-
logic stress in patients with heart disease.
There is some epidemiological evidence
that suggests an association between increased
fatality rates in hospitalized myocardial
infarction patients and exposure to weekly
average CO concentrations of the order of 9
to 16 mg/m3 (8 to 14 ppm).
Evidence from other studies of the effects
of CO does not currently demonstrate an
association between existing ambient levels of
CO and adverse effects on vegetation, mate-
rials, or other aspects of human welfare.
It is reasonable and prudent to conclude
that, when promulgating air quality standards,
consideration should be given to requirements
for margins of safety that would take into
account possible effects on health that might
occur below the lowest of the above levels.
10-6
-------
Table 10-1. EFFECTS OF CARBON MONOXIDE
Environmental conditions
Effect
Comment
Reference
35 mg/m3 (30 ppm)
for up to 12
hours
Equilibrium value of 5 percent blood
COHb is reached in 8 to 12 hours;
80 percent of this equilibrium value,
(4 percent COHb) is reached within
4 hours.
Experimental exposure of nonsmokers.
Theoretical calculations suggest expo-
sure to 23 (20 ppm) and 12 mg/m3
(10 ppm) would result in COHb levels
of about 3.7 and 2 percent, respec-
tively, if exposure was continuous for
8 or more hours.
Smith
58 mg/m3 (50 ppm) for 90 minutes
Impairment of time-interval discrim-
ination in nonsmokers.
Blood COHb levels not available, but
anticipated to be about 2.5 percent.
Similar blood COHb levels expected
from exposure to 10 to 17 mg/m3
(10 to 15 ppm) for 8 or more hours.
Beard and
Wertheim
115 mg/m3 (100 ppm) intermittently
through a facial mask
Impairment in performance of some
psychomotor tests at a COHb level
of 5 percent.
Similar results may have been observed
at lower COHb levels, but blood mea-
surements were not accurate.
Schulte
High concentrations of CO were ad-
ministered for 30 to 120 seconds,
and then 10 minutes was allowed
for washout of alveolar CO before
blood COHb was measured.
Exposure sufficient to produce blood
COHb levels above 5 percent has been
shown to place a physiologic stress on
patients with heart disease.
Data rely on COHb levels produced
rapidly after short exposure to high
levels of CO; this is not necessarily
comparable to exposure over a longer
time period or under equilibrium con-
ditions.
Ayres et al.
-------
APPENDIX
CONVERSION BETWEEN VOLUME AND
MASS UNITS OF CONCENTRATION
The physical state of gaseous air pollutants
at atmospheric concentrations may be de-
scribed by the ideal gas law:
pv = nRT
(1)
where: p = Absolute pressure of gas
v = Volume of gas
n = Number of moles of gas
R = Universal gas constant
T = Absolute temperature
The number of moles (n) may be calculated
from the weight of pollutant (w) and its mo-
lecular weight (m) by:
w
n = —
m
(2)
Substituting equation 2 into equation 1
and rearranging yields:
v =
wRT
pm
(3)
Parts per million refers to the volume of
pollutant (v) per million volumes of air (V).
ppm =•
106V
(4)
Substituting equation (3) into equation (4)
yields:
ppm =
w RT
VpmlO6
(5)
Using the appropriate values for variables in
equation 5 a conversion from volume to mass
units of concentration for CO may be derived
as shown below.
T
P
m
R
298°K(25°C)
1 atm
28 g/mole
8.21 x 10'2 8-atom/mole'
'K
ppm =
w(g)xl03(mg/g) 8.21 x IP'2 (g-atm/mole°K) x 298(°K)
V(£) x I(r3(m3/e) Katm) x 28 (g/mole) x 106
1 mg/m3 = 0.87 ppm
1 ppm =1.15 mg/m3
A-l
-------
SUBJECT INDEX
Absorption in oceans, 2-6
Adaptation, 8-42-8-43
Adenosine triphosphate reduction, 7-1
Adsorption on surfaces, 2-2, 2-6
Aerobic soil bacterium, 2-5
Agriculture waste burning, 4-10
Air quality model, 6-19
Air stagnation, 6-5
Air-to-fuel ratio, 3-2-3-3
Aircraft emissions, 4-8—4-9
Ambient air-measurement, 5-1—5-9
Anaerobic methane-producing soil micro-
organisms, 2-5
Annual variations, 6-3
Ascarite-filled tubes, 5-3
Atheromatosis, 8-26
Atmospheric concentrations, 6-1—6-28
Atmospheric diffusion models, 6-27
See also Meteorological diffusion models
Atmospheric migration, 2-5
Averaging time, 6-17
B
Background levels, 2-4
See also Ingre Lehmann Station,
Greenland
Point Barrow
Solar spectral techniques
Behavioral changes, 8-11-8-24
Bilirubin, 8-43-8-44
Biochemical removal, 2-6
Biochemical sink, 2-6
Biological removal, 2-5
Biological sources, 2-2
California observations, 6-19—6-21
CAMP observations, 6-19
Car passenger exposure, 6-23
Cardiovascular system effects, 8-24-8-34
animal data, 8-24-8-27
human data, 8-27-8-34
Catalytic action, 2-6
Catalytic analysis, 5-5
Catalytic reactor, 5-5
Central nervous system effects, 8-10—8-24
animal data, 8-10-8-14
discussion, 8-24
human data, 8-14-8-24
Chemical assay, 5-2
See also Measurement methods
Chemical reactions, 2-2—2-4
Clostridium welchii, 2-5
Coal combustion, 4-9
Coal-refuse bank fired, 4-10
Collection of spot or integrated samples, 5-5
Colloidal solution, 5-6
Colorimetric analysis, 5-6
See also Measurement methods
Combustion for power and heat, 4-9
See also Sources
Combustion processes, 3-1
Continuous measurement, 5-2
See also Measurement methods
Coulometric analyzer, 5-4
See also Measurement methods
Cupola, 4-10
Cytochrome oxidases, 8-37
cytochrome A3, 8-37
cytochrome P-450, 8-37
D
Definition of sensitive groups, 9-7
Destructive methods measurement of car-
boxyhemoglobin in blood, 8-6—8-7
CO detector tubes, 8-6
gas-phase chromatography, 8-7
manometric and volumetric methods, 8-6
nondispersive infrared method, 8-7
1-1
-------
reduction of palladium chloride by the
micro-diffusion technique, 8-6
Diurnal patterns, 6-1
E
Effects
adenosinetriphosphate reduction, 7-1
atheromatosis, 8-26
behavioral changes, 8-11 —8-24
bilirubin, 8-43-8-44
cardiovascular system, 8-24—8-34
central nervous system, 8-10—8-24
cytochrome oxidases, 8-37
endogenous formation, 8-43—8-45
extravascular capacity, 8-34
femization of plants, 7-1
heme, 8-1, 8-43-8-44
heme catabolism, 8-43
hemodynamic responses, 8-27—8-34
hemoglobin breakdown, 8-43
high altitude, 8-37-8-42
higher nervous function impairment, 8-14
hypoxia, 8-22, 8-26, 8-37, 8-39, 8-43
morphological changes in CNS, 8-10
nitrogen fixation-inhibition, 7-1 —7-2
nonhemoglobin absorptive systems,
8-34-8-37
oxygen debt studies, 8-27
plants and micro-organisms, 7-1—7-2
psychomotor tests, 8-14, 8-19, 8-37, 8-39
theoretical consideration - toxicology,
8-1-8-3
time-interval discrimination test, 8-19
toxicological appraisal, 8-1—8-57
uptake by humans, 8-7—8-10
visual discriminometer, 8-21
Eight hour 0.1 percentile averages, 6-19
Electrochemical analyzers, 5-4
Emission estimates by source, 4-3
Emission levels, 4-1
See also Emissions
Emissions
air-to-fuel ratio, 3-2
aircraft, 4-8
estimates by source, 4-2—4-5
future, 4-11
future trends, 6-25
indoor levels, 6-23
internal combustion engines, 3-1
levels, 4-1
metropolitan areas, 4-5
miscellaneous combustion, 4-10
motor vehicles, 4-1—4-9
national levels, 4-1
regional levels, 4-1
stationary combustion sources, 3-3
world wide, 2-6
Endogenous formation, 8-43—8-45
Epidemiologic appraisal, 9-1—9-20
Equilibrium methods analysis of expired air
measurement of carboxyhemoglobin in
blood, 8-7
Exposure
car passengers, 6-23
definition of sensitive groups, 9-7
long-term, 8-24
relevance to motor vehicle accidents, 9-17
severe locations, 6-23
short-term, 8-24
sources and magnitude of, 9-1—9-7
special situations, 6-21—6-25
Extravascular capacity, 8-34
Femization of plants, 7-1
Filter cells, 5-2
Forest fires, 4-10
Formation, 3-1
Frequency distribution, 6-17
Fuel oil combustion, 4-9
Future CO emissions, 4-11
Future trends, 6-25
Galvanic analyzers, 5-14
Gas chromatographic analysis, 5-5, 5-6
Gas chromatographic analyzers, 5-5
Gravimetric methods, 5-1
H
Heme, 8-1,8-43, 8-44
Heme catabolism, 8-43
1-2
-------
Hemodynamic responses, 8-27-8-34
Hemoglobin, 8-1
Hemoglobin breakdown, 8-43
Hersch-type cell - modified, 5-4
High altitude - effects, 8-37-8-42
Higher nervous functions impairment, 8-14
History, 2-1
Hopcalite, 5-5
Hypoxia, 8-22, 8-26, 8-37, 8-39, 8-43
I
Incineration, 4-10
Indoor levels, 6-23
Industrial processes, 4-10
Infrared spectrophotometric analysis, 5-5
See also Nondispersive infrared analyzers
Inge Lehmann Station - Greenland, 2-4
See also Northern Greenland
Background levels
Instrument performance, 5-2
Intermittent analysis, 5-5
Internal combustion engine emissions, 3-1,
3-2
See also Emissions
Iodine pentoxide reduction, 5-2
Iron foundries, 4-10
K
Kraft pulping mills, 4-10
Length-of-stain indicator tube, 5-6
Long-term exposure, 8-24
Lower atmospheric reactions, 2-2
M
Measurement in ambient air, 5-1 —5-7
See also Measurement methods
Measurement methods
ascarite-filled tubes, 5-3
catalytic analysis, 5-5
catalytic reactors, 5-5
chemical assay, 5-2
collection of spot or integrated samples,
5-5
colloidal solution, 5-6
colorimetric analysis, 5-6
continuous measurement, 5-2
coulometric analyzers, 5-4
electrochemical analyzers, 5-4
filter cells, 5-2
galvanic analyzers, 5-4
gas chromatographic analysis, 5-5, 5-6
gas chromatographic analyzers, 5-5
gravimetric methods, 5-1
Hersch-type cells - modified, 5-4
hopcalite, 5-5
infrared spectrophotometric analysis, 5-5
intermittent analysis, 5-5
iodine pentoxide reduction, 5-2
length-of-stain indicator tubes, 5-6
measurement in ambient air, 5-1—5-7
measuring CO in atmosphere, 5-2—5-6
mercuric oxide, 5-4
mercury vapor analyzers, 5-4
molybdenum salts, 5-6
National Bureau of Standards colorimetric
indicating gel, 5-6
nondispersive infrared analysis, 5-2, 5-5
optical filters, 5-3
palladium salts, 5-6
photometric determination, 5-4
potassium palladosulfite, 5-6
p-sulfamoyl benzoate, 5-6
terms describing instrument performance,
5-2
volumetric gas dilution techniques, 5-1
Measurement of carboxyhemoglobin in blood,
8-3-8-7
Measuring CO in atmosphere, 5-2—5-6
See also Measurement methods
Mercuric oxide, 5-4
Mercury vapor analyzer, 5-4
Meteorological diffusion models, 6-25—6-28
See also Atmospheric diffusion models
Meteorological factors, 6-3
Miscellaneous combustion, 4-10
See also Emissions
Sources
Mobile combustion sources, 4-1—4-9
1-3
-------
Molybdenum salts, 5-6
Morbidity studies, 9-14-9-17
Morphological changes in CNS, 8-10-8-11
Mortality studies, 9-10-9-14
Motor vehicles emissions, 4-1—4-7
See also Emissions
Myoglobin, 8-34-8-36
See also Nonhemoglobin absorptive sys-
tems
N
National Bureau of Standards colorimetric
indicating gel, 5-6
National emission levels, 4-1
See also Emissions
Natural gas combustion, 4-9
Natural sources, 2-2
Nitrogen-fixation inhibition, 7-1
Nonbiological sources, 2-2
Nondestructive methods measurement of
carboxyhemoglobin in blood, 8-3—8-6
Nondispersive infrared analyzers, 5-2, 5-5
See also Infrared spectrophotometric anal-
ysis
Nonhemoglobin absorptive systems,
8-34-8-37
cytochrome oxidases, 8-37
myoglobin, 8-34-8-36
Nonhighway mobile sources, 4-9
Northern Greenland, 2-4
See also Background levels
Inge Lehmann Station
O
Ocean sink, 2-6
Open burning, 4-10
Optical filters, 5-3
Oxygen debt studies, 8-27
Physical properties, 2-2
Plants and micro-organisms effects, 7-1—7-2
Point Barrow, Alaska, 2-4
See also Background levels
Potassium palladosulfite, 5-6
P-sulfamoylbenzoate, 5-6
Psychomoter tests, 8-14, 8-19, 8-37, 8-39
R
Regional emission levels, 4-1
See also Emissions
Relevance of exposure to motor vehicle acci-
dents, 9-17-9-18
Palladium salts, 5-6
Petroleum refining, 4-10
Photometric determination, 5-4
1-4
Seasonal patterns, 6-3
Severe exposure locations, 6-23
Short-term exposure, 8-24
Smog, 6-5
Solar spectral techniques, 2-4
See also Background levels
Solid waste combustion, 4-10
Sources
agriculture waste burning, 4-10
air-to-fuel ratio, 3-2—3-3
biological, 2-2
coal combustion, 4-9
coal-refuse bank fired, 4-10
combustion for power and heat, 4-9
cupola, 4-10
emission estimates by source, 4-3
endogoneous formation, 8-43—8-45
forest fires, 4-10
fuel oil combustion, 4-9
incineration, 4-10
indoor levels, 6-23
industrial processes, 4-10
iron foundries, 4-10
kraft pulping mills, 4-10
miscellaneous combustion, 4-10
natural gas combustion;. 4-9
nonbiological, 2-2
nonhighway mobile, 4-9
open burning, 4-10
petroleum refining, 4-10
-------
solid waste, 4-10
stationary combustion, 3-3
structural fires, 4-10
wood combustion, 4-9
Sources and magnitude of exposure, 9-1—9-7
cigarette, pipe, and cigar smoke, 9-7
community and residential, 9-2—9-3
occupational, 9-3-9-7
Sources of urban data, 6-5
Special exposure situations, 6-21—6-25
See also Exposure
Stationary combustion sources, 3-3
Stoichiometric ratio, 3-1
Structural fires, 4-10
Studies and interpretation, 9-10—9-18
Susceptible population, 9-7—9-9
Technological sources, 2-1
Temporal variations in concentration, 6-1
Terms describing instrument performance, 5-2
Terrestrial and marine biosphere sink, 2-5
Theoretical considerations toxicology,
8-1-8-3
Time-interval discrimination test, 8-19
Toxicological appraisal, 8-1—8-57
Turnover time - atmospheric, 2-4
U
Upper atmosphere sink, 2-5
Upper atmospheric reactions, 2-4
Uptake by humans, 8-7-8-10
Urban concentrations, 6-5—6-21
Urban data analysis techniques, 6-5—6-19
Vehicle traffic variations, 6-21—6-22
Visual discriminometer, 8-21
Volumetric gas dilution techniques, 5-1
W
Wood combustion, 4-9
World wide emission totals, 2-6
1-5
------- |