AIR QUALITY CRITERIA
FOR
PHOTOCHEMICAL OXIDANTS
U. S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE
Public Health Service
Environmental Health Service
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AIR QUALITY CRITERIA
FOR
PHOTOCHEMICAL OXIDANTS
U.S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE
Public Health Service
Environmental Health Service
National Air Pollution Control Administration
Washington, D.C.
March 1970
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National Air Pollution Control Administration Publication No. AP-63
For sale by the Superintendent ol Documents, U.S. Government Printing Office, Washington, D.C., 20402 - Price $1.75
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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 presently have for determining to what
point pollution 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 ex-
perience in evaluating environmental hazards
as a guide, we can conclude that improved
knowledge will show that there are identi-
fiable 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 reviewed and, in all probability,
revised. The Congress has made it clear,
however, that we are expected, without de-
lay, to make the most effective use of the
knowledge we now have.
The 1967 amendments to the Clean Air
Act require that the Secretary of Health,
Education, 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
protection of the public health and wel-
fare .... Such criteria shall. . . reflect the
latest scientific knowledge useful in indicat-
ing the kind and extent of all identifiable
effects on health and welfare which may be
expected from the presence of an air pollu-
tion 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
technological, social, and political action to
protect the public from the adverse effects
of air pollution.
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 topo-
graphy, all of which influence the capacity
of air to dilute and disperse pollution, are
generally homogeneous.
Further, the Act requires the Secretary to
define those geographical regions in the
country where air pollution is a problem—
whether interstate or intrastate. These air
quality control regions will be designated on
the basis of meteorological, social, and polit-
ical factors which suggest that a group of
communities should be treated as a unit for
setting limitations on concentrations of at-
mospheric pollutants. Concurrently, the
Secretary is required to issue air quality
criteria for those pollutants he believes may
be harmful to health or welfare, and to
publish related information on the tech-
niques which can be employed to control
the sources of those pollutants.
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
notice to develop ambient air quality stand-
ards applicable to the region for the pollu-
tants involved, and to develop plans of
action for implementing 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
111
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National Air Pollution Control Administra-
tion has established appropriate programs to
carry out the several Federal responsibilities
specified in the legislation. Previously, on
February 11, 1969, air quality criteria and
control techniques information were pub-
lished for sulfur oxides and particulate
matter.
This publication, Air Quality Criteria for
Photochemical Oxidants, 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, univer-
sities, 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 specially selected
for their competence and expertise in the
many fields of science and technology related
to the problems of atmospheric pollution by
photochemical oxidants. These efforts, with-
out which this document could not have been
completed successfully, are acknowledged
individually on the following pages.
As also required by the 1967 amendments
to the Clean Air Act, appropriate Federal
departments and agencies, also listed on the
following 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 Control Administration to discuss
their comments.
This Administration is pleased to acknowl-
edge the efforts of each of the persons
specifically named, as well as the many not
named who have contributed to the publica-
tion of this volume. In the last analysis,
however, the National Air Pollution Control
Administration is responsible for its content.
JOHN T. MIDDLETON
Commissioner
National Air Pollution Control
Administration
IV
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NATIONAL AIR QUALITY CRITERIA ADVISORY COMMITTEE
Chairman
Dr. Delbert S. Earth, Director
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 at Riverside
Riverside, California
Dr. Adrian Ramond Chamberlain
Vice President
Colorado State University
Fort Collins, Colorado
Mr. James P. 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
Down state 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 at Green Bay
Green Bay, Wisconsin
Mr. William J. Stanley*
Director, Chicago Department of
Air Pollution Control
Chicago, Illinois
*Membership expired June 30, 1969.
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CONTRIBUTORS AND REVIEWERS
Dr. David M. Anderson
Assistant Manager
Environmental Quality Control
Bethlehem Steel Corporation
Bethlehem, Pennsylvania
Dr. Donald Bartlett, Jr.
Department of Physiology
Dartmouth Medical School
Hanover, New Hampshire
Dr. Mario C. Battigelli
Department of Medicine
The School of Medicine
The University of North Carolina
Chapel Hill, North Carolina
Mr. Francis E. Blacet
Department of Chemistry
University of California at Los Angeles
Los Angeles, California
Mr. F. W. Bowditch
Director, Emission Control
General Motors Technical Center
Warren, Michigan
Mr. Robert Bryan
Environmental Health Systems
Systems Development Corporation
Santa Monica, California
Professor R. A. Bryson
Center for Climatic Research
Department of Meteorology
The University of Wisconsin
Madison, Wisconsin
Dr. George Buell
Air and Industrial Hygiene Laboratory
California Department of Public Health
Berkeley, California
Dr. Robert E. Carroll
Professor and Chairman
Department of Preventive and Community
Medicine
The Albany Medical College of Union
University
Albany, New York
Dr. Robert J. Charlson
Associate Professor of Atmospheric
Chemistry
Department of Civil Engineering
University of Washington
Seattle, Washington
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. Robert Eckhart
Director, Medical Research Division
Esso Research and Engineering Company
Linden, New Jersey
Mr. W. L. Faith
Consulting Chemical Engineer
San Marino, California
Dr. Hans L. Falk
Associate Director for Laboratory
Research
National Institute of Environmental Health
Sciences
Research Triangle Park, North Carolina
VI
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Dr. N. F. Frank
Harvard University School of Public Health
Harvard University
Cambridge, Massachusetts
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. Bernard D. Goldstein
New York University Medical Center
Department of Medicine
School of Medicine
New York, New York
Dr. Harold H. Golz
Medical Director
American Petroleum Institute
New York, New York
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
Mr. Al Hexter
Environmental Epidemiology Unit
California Department of Public Health
Berkeley, California
Dr. Margaret Hitchcock
Air and Industrial Hygiene Laboratory
California Department of Public Health
Berkeley, California
Dr. Charles H. Hine
Clinical Professor of Occupational and
Environmental Medicine
University of California Medical School
San Francisco, 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
Mr. C. E. Kircher
Research Manager, Research Division
Detrex Chemical Industries, Inc.
Detroit, Michigan
Dr. Paul Kotin, Director
National Institute of Environmental
Health Sciences
Research Triangle Park, North Carolina
Dr. Charles G. Kramer
Associate Medical Director, Midland Division
The Dow Chemical Company
Midland, Michigan
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
Mr. Arthur Levy
Chief, Air, Water and Solid Waste
Chemistry Division
Battelle Memorial Institute
Columbus, Ohio
Mr. Benjamin Linsky
Professor, Department of Civil Engineering
West Virginia University
Morgantown, West Virginia
Dr. H. N. MacFarland
Professor and Director
Center of Research on Environmental Quality
Faculty of Science
York University
Downsview, Ontario, Canada
Vll
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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. V. W. Moore
Vice President
Research-Cottrell, Inc.
Bound Brook, New Jersey
Dr. Peter K. Mueller
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. Jay A. Nadel
University of California Medical School
San Francisco, California
Mr. Norman Perkins
Environmental Epidemiology Unit
California Department of Public Health
Berkeley, California
Mr. J. N. Pitts, Jr.
Professor of Chemistry
Department of Chemistry
University of California at Riverside
Riverside, California
Dr. Alexander Rihm, Assistant Commissioner
Division of Air Resources
New York State Department of Health
Albany, New York
Dr. Stanley Rokaw
Chief, Pulmonary Research Section
Rancho Los Amigos Hospital
Los Angeles, California
Mrs. Willie Mae Salmon
Environmental Epidemiology Unit
California Department of Public Health
Berkeley, California
Mr. Jean J. Schueneman, Chief
Division of Air Quality Control
Environmental Health Services
Maryland Department of Health
Baltimore, Maryland
Mr. Francis Scofield
Vice President, Technical Affairs
National Paint, Varnish and Lacquer
Association, Inc.
Washington, D. C.
Dr. R. W. Scott
Coordinator for Conservation Technology
Esso Research and Engineering Company
Linden, New Jersey
Dr. C. Boyd Shaffer
Director of Toxicology
American Cyanamid Company
Wayne, New Jersey
Professor Arthur C. Stern
Department of Environmental Sciences
and Engineering
The School of Public Health
The University of North Carolina
Chapel Hill, North Carolina
Dr. Edward Stephens
Air Pollution Research Center
University of California at Riverside
Riverside, California
Dr. Herbert E. Stokinger
Chief, Laboratory and Toxicology and
Pathology
Bureau of Occupational Safety and Health
Environmental Control Administration
Cincinnati, Ohio
vui
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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. Yoshiro Tokiwa
California Department of Public Health
Berkeley, 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
Mr. Lowell G. Wayne
Air Pollution Control Institute
University of Southern California
Los Angeles, California
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. Melvin Weisburd
Manager, Environmental Health Systems
Systems Development Corporation
Santa Monica, California
Mr. John E. Yocom
Director, Engineering and Technical
Programs
The Travelers Research Company
Hartford, Connecticut
Mr. John A. Zapp, Jr.
Director, Haskell Laboratory for Toxicology
and Industrial Medicine
E. I. duPont de Nemours & Company, Inc.
Wilmington, Delaware
IX
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Dr. Bernard E. Saltzman
Research Professor of Environmental
Health and Engineering
Department of Environmental Health
College of Medicine
University of Cincinnati
Cincinnati, Ohio
Mr. John A. Maga
Executive Officer
California Air Resources Board
Sacramento, California
Mr. Morton Sterling
Director
Detroit and Wayne Counties Air
Pollution Control Agencies
Detroit and Wayne County Department
of Health
Detroit, Michigan
Dr. O. Clifton Taylor
Air Pollution Research Center
University of California, Riverside
Riverside, California
Mr. Edward J. Pethus
Department of Air Pollution
Chicago, Illinois
Mr. Donald F. Phillips
Department of Air Pollution
Chicago, Illinois
Mr. William A. Munroe
Chief
Air Pollution Control Program
New Jersey Department of Health
Trenton, New Jersey
Mr. W. L. Faith
Consulting Chemical Engineer
San Marino, California
Dr. Oscar J. Balchum
Professor of Medicine
School of Medicine
University of Southern California
Los Angeles, California
Mr. Elmer Robinson
Chairman
Environmental Research Department
Stanford Research Institute
Arlington, Virginia
Dr. David Bates
Professor
Department of Preventive Medicine
McGill University
Montreal, Quebec, Canada
Dr. Leslie A. Chambers
Director
Institute of Environmental Health
School of Public Health of Houston
University of Texas
Houston, Texas
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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
Engineering
Office of Construction
XI.
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TABLE OF CONTENTS
Chapter Page'
LIST OF TABLES xvii
LIST OF FIGURES xx
CHAPTER 1. INTRODUCTION l~l
CHAPTER 2. PHYSICAL AND CHEMICAL NATURE OF PHOTO-
CHEMICAL OXIDANTS 2-1
A. INTRODUCTION 2-1
B. GENERAL DISCUSSION 2-1
C. PHYSICAL PROPERTIES 2-2
1. Ozone 2-2
2. Peroxyacetyl Nitrate 2—3
D. OXIDANT FORMATION PROCESSES 2-3
1. Nitrogen Dioxide Photolytic Cycle 2—3
2. Hydrocarbon Interaction with Nitrogen Dioxide Photolysis .... 2—6
3. Hydrocarbon Reactivity 2—8
4. Nitric Oxide and Nitrogen Dioxide 2-10
E. METEOROLOGICAL EFFECTS 2-11
1. General 2-11
2. Sunlight 2-11
3. Temperature 2—13
F. REACTANT CONCENTRATION STUDIES 2-13
1. Environmental Chamber Studies 2—13
2. Atmospheric Studies 2—15
G. FUTURE RESEARCH 2-17
H. SUMMARY 2-19
I. REFERENCES 2-19
CHAPTER 3. ATMOSPHERIC PHOTOCHEMICAL OXIDANT
CONCENTRATIONS 3_1
A. INTRODUCTION . 3_j
B. CONCENTRATIONS OF OXIDANTS IN URBAN ATMOSPHERES
1. General Discussion . 3_i
2. Oxidant Concentration Patterns 3_2
3. Seasonal and Diurnal Variations 3—4
4. Oxidant Measurement Parameters 3—6
xii
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Chapter Page
a. Sulfur Dioxide 3—6
b. Nitrogen Dioxide ATMOSPHERES 3~6
c. Nitric Oxide 3—7
C. CONCENTRATIONS OF OZONE IN URBAN ATMOSPHERE . 3-7
1. Adjusted Oxidant . . 3-7
2. Ozone Concentration Patterns 3-11
D. CONCENTRATIONS OF PEROXYACETYL NITRATE IN THE
URBAN ATMOSPHERE 3-11
E. METEOROLOGICAL FACTORS 3-14
1. General Discussion 3 — 14
2. Transport . 3—15
3. Monitoring Station Location 3 — 17
F. SUMMARY 3-17
G. REFERENCES 3-18
CHAPTER 4. NATURAL SOURCES OF OZONE 4-1
A. INTRODUCTION 4-1
B. NATURAL SOURCES OF OZONE 4-1
C. OZONE TRANSFER 4-1
D. SUMMARY 4_3
E. REFERENCES 4-4
CHAPTER 5. MEASUREMENT OF OXIDANTS, OZONE, AND PEROX-
YACETYL NITRATE IN AMBIENT AIR 5_1
A. INTRODUCTION 5-1
B. REFERENCE METHOD FOR MEASUREMENT OF TOTAL OX-
IDANTS 5-1
C. METHODS FOR MEASUREMENT OF TOTAL OXIDANTS . . . . 5-2
1. Continuous Methods Utilizing Potassium Iodide 5—2
a. Colorimetric 5—2
b. Coulometric 5—3
c. Colorimetric versus Coulometric Methods 5—3
2. Other Methods—Intermittent Sampling 5—5
a. Ferrous Ammonium Sulfate 5—5
b. Alkaline Potassium Iodide 5—5
c. Phenolphthalin 5—5
D. METHODS SPECIFICALLY FOR MEASUREMENT OF OZONE . . 5-5
1. Chemiluminescence 5—5
2. Ultraviolet Photometry 5—6
3. Trans-butene-2 Gas Phase Titration 5-6
4. Rubber Cracking 5-6
5. Other Chemical Methods 5-6
E. METHODS FOR DETERMINATION OF PEROXYACETYL NI-
TRATE 5-6
1. Long-Path Infrared Spectroscopy 5—6
2. Gas Chromatography 5-7
xiii
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Chapter
F. SUMMARY 5-7
G. REFERENCES 5-7
CHAPTER 6. EFFECTS OF PHOTOCHEMICAL OXIDANTS ON VEGE-
TATION AND CERTAIN MICROORGANISMS 6-1
A. INTRODUCTION 6-1
B. SYMPTOMS OF THE EFFECTS OF PHOTOCHEMICAL AIR POL-
LUTANTS ON VEGETATION 6-2
C. FACTORS AFFECTING RESPONSE OF VEGETATION TO PHO-
TOCHEMICAL AIR POLLUTANTS 6-3
1. Genetic Factors 6—3
2. Environmental Factors 6—4
3. Other Factors 6-5
4. Discussion 6—6
D. PROBLEMS IN DIAGNOSIS AND ASSESSMENT OF THE ECO-
NOMIC IMPACT OF PHOTOCHEMICAL AIR POLLUTION ON
VEGETATION 6-6
E. DOSE-INJURY RELATIONSHIPS OF PHOTOCHEMICAL AIR
POLLUTION AND VEGETATION 6-7
F. EFFECTS OF PHOTOCHEMICAL OXIDANTS ON MICRO-
ORGANISMS 6-12
G. EFFECTS OF OZONE ON MICROORGANISMS 6-12
H. SUMMARY 6-18
I. REFERENCES 6-20
CHAPTER 7. THE EFFECT OF OZONE ON MATERIALS 7-1
A. INTRODUCTION 7-1
B. MECHANISMS OF OZONE ATTACK 7-1
C. THE EFFECT OF OZONE ON RUBBER 7_j
D. THE EFFECT OF OZONE ON FABRICS AND DYES 7-4
1. Damage to Textile Fabrics 7__4
2. Fading of Dyes 7_4
E. THE NEED FOR FUTURE RESEARCH 7_6
F. SUMMARY 7_6
G. REFERENCES 7_7
CHAPTER 8. TOXICOLOGICAL APPRAISAL OF PHOTOCHEMICAL
OXIDANTS g_!
A. INTRODUCTION
B. OZONE
1. Animal Data
a. Acute Toxicity
b. Effects of Prolonged Exposure to Ozone
c. Interaction with Other Agents
d. Mechanisms of Ozone Toxicity in Animals
e. Summary . .
xiv
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Chapter PaSe
2. Human Data 8-18
a. Occupational Exposures to Ozone 8—18
b. Human Experimentation 8—19
c. Summary of Human Exposure to Ozone 8-24
C. OXIDANTS 8-25
1. Animal Data 8-25
a. Direct Effects of Photochemical Oxidants 8-25
b. Indirect Effects of Photochemical Oxidants 8—33
c. Summary 8—34
D. PEROXYACYL NITRATES 8-35
1. Animal Data 8-35
Lethality . 8-35
2. Human Data 8-35
Effects on Pulmonary Function . . 8—35
3. Discussion . 8-35
E. SENSORY IRRITATION 8-35
1. Animal Data 8-35
Effects of Air Pollutants on the Eye 8-35
2. Human Data 8-38
a. Olfactory Effects 8-38
b. Experimental Studies of Eye Irritation 8—38
3. Discussion 8—39
F. SUMMARY 8-40
G. REFERENCES 8-42
CHAPTER 9. EPIDEMIOLOGICAL APPRAISAL OF PHOTOCHEMICAL
OXIDANTS 9-1
A. INTRODUCTION 9-1
B. ACUTE EFFECTS OF PHOTOCHEMICAL OXIDANTS 9-1
1. Daily Mortality in Relation to Variations in Oxidant Levels . ... 9—1
a. Mortality Among Residents Age 65 Years and Older 9—1
b. Mortality and Heat Waves . 9—1
c. Mortality of Nursing Home Residents 9—4
d. Two-Community Study 9-4
e. Mortality from Cardiac and Respiratory Diseases 9—5
f. Discussion 9—6
2. Hospital Admissions in Relation to Oxidant Levels 9-7
a. Los Angeles County Hospital Admissions, 1954 .... 9—7
b. Hospital Admissions in the Los Angeles Metropolitan Area . . 9—7
c. Discussion 9—8
3. Aggravation of Respiratory Diseases by Oxidant Pollution 9—8
a. Aggravation of Asthma 9-8
b. Aggravation of Emphysema and Chronic Bronchitis 9-8
c. Discussion 9—12
4. Impairment of Performance Associated with Oxidant Pollution . . 9—12
a. Athletic Performance 9-12
b. Automobile Accidents . 9—13
c. Ventilatory Performance 9-13
xv
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Chapter Pa%e
d. Discussion A
5. Eye Irritation in Relation to Variations in Oxidant Levels 9-14
a. Panel Studies 9~!^
b. Student Nurse Study 9~16
c Evaluation of Filters for Removing Eye Irritants from Polluted
' Air 9-16
d. Photochemical Oxidant and Eye Irritation in Locations Other
Than California 9~18
q i o
e. Discussion 7
C. CHRONIC EFFECTS OF PHOTOCHEMICAL OXIDANTS 9-20
1. Mortality in Areas of High and Low Oxidant Pollution 9-21
a. Lung Cancer Mortality 9—21
b. Chronic Respiratory Disease Mortality 9—22
c. Discussion 9—23
2. General Morbidity in Areas of High and Low Oxidant Pollution. . . 9-23
a. State of California Health Survey 9-23
b. Chronic Respiratory Disease Survey of Telephone Workers . . . 9-26
c. Discussion 9—27
3. Effects of Photochemical Oxidant Pollution on Community
Satisfaction 9-27
a. State of California General Health Survey 9—27
b. Survey of Los Angeles Physicians 9—29
c. Discussion 9—30
D. SUMMARY 9-30
1. Review of Results from Cited Studies 9-30
2. Future Research Needs 9—31
3. Discussion 9—32
E. REFERENCES 9-32
CHAPTER 10. SUMMARY AND CONCLUSIONS 10-1
A. INTRODUCTION 10-1
B. NATURE OF PHOTOCHEMICAL OXIDANTS 10-1
C. ATMOSPHERIC PHOTOCHEMICAL OXIDANT CONCENTRA-
TIONS 10_l
D. NATURAL SOURCES OF OZONE 10-2
E. MEASUREMENT OF PHOTOCHEMICAL OXIDANTS 1Q-2
F. EFFECTS OF PHOTOCHEMICAL OXIDANTS ON VEGETATION
AND MICROORGANISMS 10-3
G. EFFECT OF OZONE ON MATERIALS 10-4
H. TOXICOLOGICAL STUDIES OF PHOTOCHEMCIAL OXIDANTS 10-5
1. Effects of Ozone in Animals 10—5
2. Effects of Ozone in Humans -. 10—5
3. Effects of Peroxyacetyl Nitrate 10-6
4. Effects of Mixtures Containing Photochemical Oxidants on
Animals 10—6
5. Effects of Mixtures Containing Photochemical Oxidants on
Humans 10—7
xvi
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Chapter Page
I. EPIDEMIOLOGICAL STUDIES OF PHOTOCHEMICAL OXIDANTS iQ-7
J. AREAS FOR FUTURE RESEARCH 10-8
1. Environmental Aspects of Photochemical Oxidants 10—8
2. Toxicity of Ozone, Photochemical Oxidants, and Peroxyacyl Ni-
trates 10_8
3. Epidemiology of Photochemical Oxidants 10—9
K. CONCLUSIONS 10-9
1. Human Exposure 1Q—9
a. Ozone 10—9
b. Oxidants 10—10
2. Other Exposures 10—10
a. Photochemical Oxidants 10—10
b. Ozone Effects on Susceptible-Materials 10—10
L. RESUME 10-10
APPENDIX. CONVERSION BETWEEN VOLUME AND MASS UNITS
OF CONCENTRATION A-l
SUBJECT INDEX 1-1
LIST OF TABLES
Table
1-1 Factors to be Considered in Developing Air Quality Criteria 1-2
2—1 Physical Properties of Ozone 2—3
2—2 Physical Properties of Peroxyacetyl Nitrate 2—3
2—3 Ozone or Oxidant Yields from Photooxidations of a Mixture of an
Organic Substance with Nitrogen Oxides in Air 2—9
2—4 Peroxyacetyl Nitrate Yields from Photooxidation of Hydrocarbon-
Nitrogen Oxide Mixtures in Air 2—10
3—1 Summary of Maximum Oxidant Concentrations Recorded in Selected
Cities, 1964-1967 3-2
3—2 Cumulative Frequency Distribution of Hourly Average Oxidant
Concentrations in Selected Cities, 1964-1965 3-3
3—3 Summary of Total Oxidant Concentrations Recorded at CAMP Sites,
1964-1967 3-4
3—4 Highest Monthly Mean of 1-Hour Average Oxidant Concentrations
Recorded In Selected Cities, 1964 and 1965 3-5
3—5 Monthly Mean Hourly Average Oxidant Concentrations Adjusted for
Nitrogen Dioxide for Selected Summer and Winter Months, in Four
Cities 3-8
3—6 Monthly Mean Daily Maximum 1-Hour Average Oxidant Concentra-
tions Adjusted for Nitrogen Dioxide for Selected Summer and Winter
Months, In Four Cities 3—9
3—7 Summary of Maximum Daily 1-Hour Average Ozone Concentrations
for Selected Cities 3-11
3—8 Average Hourly Ozone Concentrations in Selected Cities, 1967 3 — 12
5 — 1 Effect of Nitrogen Dioxide on Oxidant Determination in the Absence
of Ozone 5—4
5—2 Calibration Stability of Colorimeter Oxidant Monitoring Stations,
xvii
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Table
Statewide Continuous Air-Monitoring Network, California, Seven
Stations, 1963 to 1965 5~~4
6-1 Effects of PAN, Ozone, and the Photochemical Complex on the
Growth and Biochemistry of Plants 6
6-2 Susceptibility of Plants to Concentrations of PAN, the Photochemical
Complex, and Mixtures of Sulfur Dioxide and Ozone Producing Acute
Injury Symptoms ~~
6-3 Relative Phytotoxicity of Four Members of the Peroxyacyl Nitrates,
Indicated by Preliminary Fumigation on Two Species of Plants 6-10
6-4 Threshold Susceptibility of Plants to Acute Injury from Ozone 6-10
6-5 Projected Ozone Concentrations Which Will Produce, for Short-Term
Exposures, 5 Percent Injury to Economically Important Vegetation
Grown Under Sensitive Conditions 6—12
6-6 Projected Ozone Concentrations Which Will Produce, for Short-Term
Exposures, 20 Percent Injury to Economically Important Vegetation
Grown Under Sensitive Conditions 6—12
6-7 Lists of Plants in Three Sensitivity Groups by Sensitivity to Ozone ... 6-13
6—8 Summary of Effects of Ozone on Bacteria and Protozoa 6—19
7—1 Formulation of Highly Ozone-Sensitive Rubber 7—3
7-2 Effect of Ozone on Rubber 7-3
7-3 Tire Sidewall Formulation 7-3
7—4 Effects of Ozone on Sidewall Formulations Containing Various
Antiozonant Concentrations 7—3
7—5 Subjective Color Change of Dyed Cotton Exposed to Ozone Concen-
trations Between 980 and 1960jug/m3 (0.5 and 1.0 ppm) . 7-5
8—1 LDSO of Ozone for Various Species After 3-Hour Exposure 8—1
8—2 Effects of Exposure of Rats to NonLethal Concentrations of Ozone 8—2
8—3 Development of Tolerance to the Mortality-Enhancing Effect of
Ozone on Streptococcal Infection 8—12
8—4 Depression of Phagocytosis After 3-Hour Exposure to Ozone 8—13
8-5 Mortality of Mice Exposed to Streptococcal Aerosol Following a
3-Hour Ozone Exposure 8—14
8—6 Summary of the Effects of Ozone in Animals 8—17
8-7 Summary of Available Data on Occupational Exposure of Humans to
Ozone 8-20
8-8 Effect of Inhaling Either Air or 1,180 to 1,570 ngjm3 (0.6 to 0.8
ppm) Ozone for 2 Hours on Pulmonary Diffusing Capacity (DL CO)
of 11 Seated Normal Subjects 8-22
8-9 Effect of Inhaling Either Air or 1,180 to 1,570 jug/m3 (0.6 to 0.8
ppm) Ozone for 2 Hours on Vital Capacity (VC), Indirect Maximal
Breathing Capacity (FEV0.75 x 40), and Maximum Mid-expiratory
Flow Rate (MMFR), on 10 Male Subjects 8-23
8-10 Summary of Data on Human Experimental Exposure to Ozone 8-26
8-11 Chemical Agents in Exhaust-Contaminated Atmospheres 8-28
8-12 Ultrastructural Alteration in Alveolar Tissue of Mice After Exposure
to more than 780 Mg/m3 (0.4 ppm) Oxidant for 2 to 3 Hours 8-31
8-13 Ultrastructural Alterations in Alveolar Tissue of Mice After 3-Hour
Exposure to from 980 to 1,470 /ug/m3 (0.50 to 0.75 ppm) Oxidant in
xviii
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Table Page
Synthetic Photochemical Smog 8-31
8—14 Lung Tumor Incidence in Mice After Exposure to Either Ozonized
Gasoline or Washed Air 8-32
8—15 Effect of Irradiated and Non-Irradiated Exhaust on Mice Treated with
Antu 8-34
8—16 Summary of the Effects of Photochemical Oxidants in Animals 8-36
8—17 Comparisons of Means and Percentage Change in Oxygen Uptake in
Healthy Male College Students After Inhalation of 1,485 jug/m3 (0.3
ppm) Peroxyacetyl Nitrate and Filtered Air 8-37
8-18 Summary of Toxicologic Studies of Ozone Exposure 8—40
8—19 Summary of Toxicologic Studies of Oxidant Exposure on Animals . . . 8—41
9—1 Average Number of Deaths per Day Due to Cardiac and Respiratory
Causes Among Residents of Los Angeles County, Age 65 and Older,
As Related To Temperature and Oxidant Concentrations By Month,
1954-1955 9-2
9—2 Correlation of Morning and Early Afternoon Oxidant Levels with
Oxygen Consumption and Airway Resistance of 15 Patients with
Chronic Respiratory Disease 9—10
9—3 Proportion of Variation Associated with Environmental Factors in
Symptoms, Signs, and Ventilatory Tests in a Diseased and in a Control
Group 9-11
9—4 Sign-Test Data for Testing the Association of Oxidant Levels with
Accidents, Los Angeles, August Through October, 1963 and 1965 ... 9—13
9-5 Correlation of Eye Irritation with Simultaneous Oxidant Concentra-
tions, in Order of Decreasing Eye Irritation Score, for a Number of
Stations in the Los Angeles Area 9—14
9—6 Correlation as Judged by a Panel of "Experts" Between Eye Irritation
and Simultaneous Other Variables 9-16
9—7 Effect of Filter Upon Sensory Irritation and Chemical Measurements 9-18
9—8 Pearson Product-Moment Correlation Coefficients Between Eye Irrita-
tion and Environmental Factors in a Nonfiltered Room 9—20
9—9 Total Lung Cancer Mortality in an American Legion Study Popula-
tion, California, 1958-1962 9-22
9-10 Lung Cancer Deaths and Relative Risks per 100,000 Man-Years of an
American Legion Study Population, By Extent of Cigarette Smoking
and Residence, California, 1958-1962 9-22
9—11 Total Chronic Respiratory Disease Mortality in an American Legion
Study Population, California, 1958-1962 . . 9-23
9-12 Selected Respiratory Conditions Reported by General Population
Sample, California, May 1956 ... .9-25
9-13 Percent of Survey Responses of General and Working Populations
"Bothered" by Air Pollution, by Major Geographic Areas in Califor-
nia, May 1956 9-27
9—14 Percent of Survey Responses of General and Working Populations,
"Bothered" by Air Pollution, Who have Considered Moving or
Changing their Jobs for this Reason, by Major Geographic Areas in
California, May 1956 9-28
9—15 Reasons for Moving from Three Areas of California, in Response to
xix
-------
Table
General Population Survey, May 1956 9-28
9-16 Air Pollution Effects Reported in General Population Survey, by Type
of Community and by Major Geographic Areas in California, May
1956 ; 9-29
9-17 Effects of Air Pollution on Community Satisfaction, Reported in
General Population Survey, by Major Geographic Area, California,
May 1956 9"30
10-1 Projected Ozone Concentrations Which Will Produce, for Short-Term
Exposures, 5 percent Injury to Economically Important Vegetation
Grown Under Sensitive Conditions 10—4
10-2 Effects of Ozone 10-n
10-3 Effects Associated with Oxidant Concentrations in Photochemical
Smog 10-12
LIST OF FIGURES
Figure
2—1 Atmospheric nitrogen dioxide photolytic cycle 2—4
2-2 Diurnal variation of NO, NO2, and 03 concentrations in Los Angeles,
July 19, 1965 2~5
2-3 Interaction of hydrocarbons with atmospheric nitrogen dioxide
photolytic cycle 2—7
2-4 Nitrogen dioxide dissociation as a functional wavelength of light
absorbed 2—12
2—5 Maximum oxidant concentration as a function of propylene and nitric
oxide reactant concentrations during 2-hour dynamic irradiation 2—15
2—6 Maximum oxidant concentration as a function of hydrocarbon and
nitrogen oxide concentrations reacted during 1-hour dynamic irradia-
tion of automobile exhaust mixtures 2—15
2—7 Maximum oxidant concentration as a function of propylene and nitric
oxide reactant concentrations during static irradiations 2—15
2—8 Maximum oxidant concentration as a function of hydrocarbon and
nitrogen oxide reactant concentrations during 2-hour dynamic irradia-
tion of automobile exhaust mixtures 2-15
2—9 Effect of 6 a.m.-9 a.m. hydrocarbon concentrations on maximum
daily oxidant concentrations during June, July, and August,
1965-1967 2-16
2—10 Effect of 6 a.m.-9 a.m. hydrocarbon concentrations on maximum
daily oxidant concentrations in Los Angeles, during April through
September, 1962 and 1963 2-16
2-11 Hourly variation of selected pollutants in Philadelphia on Tuesday,
July 18, 1967 ....2-17
2—12 Hourly variation of selected pollutants in Philadelphia on Saturday,
July 22, 1967 2-18
3—1 Monthly variation of mean hourly oxidant concentrations for three
selected cities 3—6
3—2 Monthly variation of mean daily maximum 1-hour average oxidant
concentrations for three selected cities 3_7
xx
-------
Figure Page
3—3 Diurnal variation of mean hourly average oxidant concentrations in
Los Angeles and St. Louis 3—8
3—4 Diurnal variation of mean hourly average oxidant concentrations in
Philadelphia, August 6-8, 1966 3-8
3—5 Comparison of the monthly variation in mean 1-hour average ozone
and oxidant concentrations in Los Angeles and Pasadena, 1964-1965 3—9
3—6 Comparison of the monthly variation of mean daily maximum 1-hour
average ozone and oxidant concentrations in Los Angeles and
Pasadena, 1964-1965 3-10
3—7 Comparison of the hourly variation of mean 1-hour average concen-
trations of ozone, oxidant, and oxidant adjusted for NO2 and SO2
response, Los Angeles and Pasadena, July 1964 3—10
3—8 Diurnal variation of hourly ozone concentrations in Philadelphia and
Denver 3-12
3—9 Variation of mean 1-hour average oxidant and PAN concentrations, by
hour of day, in downtown Los Angeles, 1965 3—13
3—10 Variation of mean 1-hour average oxidant and PAN concentrations, by
hour of day, at the Air Pollution Research Center, Riverside,
California, September 1966 3-14
3—11 Monthly variation of oxidant and PAN concentrations at the Air
Pollution Research Center, Riverside, California, June 1966-June 1967 3—15
3—12 Diurnal variation of mean 1-hour average oxidant concentrations at
selected California sites, October 1965 3—15
3—13 Diurnal variation of mean 1-hour average carbon monoxide concen-
trations at selected California sites, October 1965 3—16
4—1 Cumulative frequency distribution of average 15-minute ozone con-
centrations at Chalk River, Canada, June 1 to August 13, 1965 4—3
5—1 Schematic of dynamic calibration of ozone measuring techniques 5—3
8—1 Changes in lung water and tissue of rats exposed to 3,900 Mg/m3 (2
ppm) ozone for 3 hours 8—3
8—2 Average respiratory response of 75 rats exposed to 3,900 Mg/m3 (2
ppm) ozone for 3 hours 8—4
8—3 Average respiratory response of eight rabbits following first exposure
to 29,000 ng/m3 (15 ppm) ozone for 30 minutes 8—4
8—4 Effect of ozone exposure on respiration of guinea pigs 8—6
8—5 Respiratory response and recovery of guinea pigs exposed to ozone . . . 8—7
8—6 Cellular response to exposure to ozone for 3 hours 8—13
8—7 Increase in percent heterophiles following exposure to 9,800 ng/m3 (5
ppm) ozone for 3 hours 8—13
8—8 Effect of ozone exposure on histamine toxicity in guinea pigs 8—15
8—9 Effect of exposure to 390 and 980 Mg/m3 (0.2 and 0.5 ppm) ozone on
six subjects 8—21
8—10 Effect of ozone on airway resistance 8—24
8—11 Respiratory response of guinea pigs breathing auto exhaust 8—29
8—12 Effect of auto exhaust on expiratory flow resistance of guinea pigs . . . 8—30
8—13 Cumulative mortality of mice from exposure to PAN 8—37
8—14 Analytical data for auto exhaust chamber experiments 8—39
xxi
-------
Figure
9-1 Comparison of deaths of persons, 65 years of age and over, and
maximum daily temperatures, Los Angeles County, July 1 to
November 30, 1955 9~3
9-2 Comparison of nursing home deaths, maximum daily temperature, and
"smog alert" days in Los Angeles County, July through December
1955 9-4
9-3 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—5
9—4 Fourier curves fitted to data in Figure 9-3 9—6
9-5 Relationship between oxidant level in the hour before an athletic
event and percent of team members with decreased performance . ... 9— 12
9—6 Regression curves relating eye irritation and simultaneous oxidant
concentrations from a number of stations in the Los Angeles area .... 9—15
9—7 Variation of mean maximum eye irritation, as judged by a panel of
"experts" with maximum oxidant concentrations, Pasadena, August-
November, 1955 9-15
9—8 Relationship between oxidant concentrations and selected symptoms
in Los Angeles, October 29 through November 25, 1962 9—17
9—9 Mean index of eye irritation versus oxidant concentration 9—19
9—10 Relationship of high smog periods to incidence of illness and injury,
persons 65 years and over, August 2-November 28, 1954 9—24
9—11 Relationship of high smog periods to incidence of selected conditions
for persons of all ages, August 2-November 28, 1954 9-25
9-12 Air pollution responses for selected conditions obtained from volun-
teers in Los Angeles and San Francisco Bay areas 9—26
xxii
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AIR QUALITY CRITERIA
FOR
PHOTOCHEMICAL OXIDANTS
Chapter 1.
INTRODUCTION
Pursuant to authority delegated to the
Commissioner of the National Air Pollution
Control Administration, Air Quality Criteria
for PhoTochemical Oxidanrs is issued in accor-
dance 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 be-
tween 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 of the pollutants
and the techniques available for measuring
these characteristics must be considered,
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, visi-
bility, and climate. Further, 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 exposures or levels of
effect that a political jurisdiction determines
should not be exceeded in a specified geo-
graphic area, and are used as one of several
factors in designing legally enforceable pollu-
tant emission standards.
This document focuses on photochemical
oxidants as they are found in the ambient air.
In general, discussions in the earlier chapters
are oriented towards the physical and chemi-
cal nature of these oxidants, atmospheric
concentrations and measurement of these
oxidants, and possible natural sources of
ozone. The presence of photochemical oxi-
dants in the ambient air is then considered in
later chapters in relation to (1) effects on
vegetation. (2) effects on materials, (3) toxi-
cological studies of effects on animals and
man. and (4) epidemiological studies.
The National Air Pollution Control Admin-
istration is currently advocating the use of the
metric system to express atmospheric concen-
trations of air pollutants, e.g., micrograms per
cubic meter (/ig/'m3). In most instances, gas-
eous pollutants have hitherto been reported
on a volume ratio basis, i.e.. parts per million
(ppm). In this document, whenever possible,
both types of units are given. Conversion
from volume (ppm) to mass (jdg/m3) 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 temper-
ature and 760 mm Hg (atmospheric pressure
at sea level) as standard pressure. Since the
major oxidant in the atmosphere is ozone, the
methods of oxidant measurement are cali-
brated in ozone equivalents. Therefore, in
expressing ppm total oxidants in terms of
1-1
-------
Table 1-1. FACTORS TO BE CONSIDERED
IN DEVELOPING AIR QUALITY
CRITERIA3
Properties of pollution
Concentration
Chemical composition
Mineralogical structure
Adsorbed gases
Coexisting pollutants
Physical state of pollutant
Solid
Liquid
Gaseous
Kinetics of formation
Residence time
Measurement methods
Colorimetric
Coulometric
Spectroscopic
Chemical
Chromatographic
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
Corrosion of materials
Deterioration of materials
Effects on atmospheric properties
Effects on radiation and temperature
jug/m3, an ozone basis has also been used.
Throughout the document, wherever mass
concentrations of oxidants are mentioned, the
reference is to equivalent amounts of ozone.
It should be borne in mind that almost all
data for the photochemical oxidants have
originally been recorded in ppm. Factors for
converting O3 and PAN concentrations from
volume (ppm) to mass (Mg/m3) units are given
in Chapter 2. The determination of these
factors appears in the Appendix.
The terminology employed in this docu-
ment generally follows usage recommended in
the publications style guide of the American
Chemical Society.
The scientific literature has been reviewed
through January 1969, with additional
sources from publications as recent as Novem-
ber 1969. The results and conclusions of
foreign investigations have been evaluated for
their possible application to the air pollution
problem in the United States. This document
is not intended as a complete, detailed liter-
ature review, and it does not cite every
published article relating to the presence of
photochemical oxidants in the ambient atmo-
sphere. The literature has, however, been
reviewed thoroughly for information related
to the development of criteria, and the
document not only summarizes the current
scientific knowledge of photochemical air
pollution, but also attempts to point up the
major deficiencies in that knowledge and the
presently recognized needs for further re-
search.
Methods and techniques for controlling the
sources of photochemical oxidants as well a§
the costs of applying these techniques are
described in: AP-66, Control Techniques for
Carbon Monoxide, Nitrogen Oxide, and
Hydrocarbon Emissions from Mobile Sources;
AP-67, Control Techniques for Nitrogen Ox-
ide Emissions from Stationary Sources; and
AP-68, Control Techniques for Hydrocarbon
and Organic Solvent Emissions from Station-
ary Sources.
aAdapted from S. Calvert's 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 Subcommit-
tee on Air and Water Pollution of the Committee on Public
Works, United States Senate (Air Pollution-1968, Part 2)."
1-2
-------
Chapter 2.
PHYSICAL AND CHEMICAL NATURE
OF PHOTOCHEMICAL OXIDANTS
A. INTRODUCTION
As initiated by sunlight, the series of
atmospheric reactions between hydrocarbons
and oxides of nitrogen, which lead to the
formation of new products, is a most complex
system. Among these products are substances
termed "oxidants." Oxidants are chemical
entities detrimental to biological systems and
destructive to certain materials. The purpose
of this document is to examine and quantify
the deleterious effects of oxidants on man
and his environment. To accomplish this goal
it is necessary to delineate the atmospheric
physical and chemical parameters which cause
oxidant formation, a subject which is difficult
to discuss in a concise manner. Conciseness
frequently leads to unwarranted, if not false,
concepts and conclusions. The following dis-
cussion in the chapter is detailed, but it
cannot be condensed further without increas-
ing the chance of misinterpretations.
Because of the complexity of the subject
matter, this discussion of photochemical oxi-
dants has been divided into subsystems. The
interrelationship of these subsystems, how-
ever, and their relation to the total air
pollution system, should be kept clearly in
mind. Too sharp a focus on any one photo-
chemical subsystem can lead also to false
conclusions.
The purpose then of this chapter is to
detail the relationship of primary hydrocar-
bon emissions to oxidants, one of the second-
ary products. This involves the interaction of
certain hydrocarbons with light-absorbing
species, the subsequent oxidation of the
hydrocarbons, and the accompanying for-
mation of several new products, among which
are found the oxidants, ozone and peroxyacyl
nitrates. This subject is treated in greater
detail in AP-64, Air Quality Criteria for
Hydrocarbons.
B. GENERAL DISCUSSION
In the original sense, the term "oxidation"
describes chemical reactions in which certain
atoms combine with oxygen (O2) to form
compounds known as oxides. The complete
combustion of carbon in air to form carbon
dioxide (CO2) is a typical example of an
oxidation reaction.
Today, the term "oxidation" is more gen-
erally used to describe the loss of one or more
electrons by an atom, ion, or molecule.
Conversely, a gain of electrons is referred to
as "reduction." Oxidation-reduction reactions
cannot be separated since in any reaction, one
of the reactants is oxidized while the other is
reduced; for example, in the combustion of
carbon in air, carbon is oxidized while oxygen
is reduced.
The combustion of coal and petroleum
products such as natural gas, gasoline, and
fuel oil, termed "fossil fuels", is an oxida-
tion-reduction reaction which is responsible
for most of the air pollution in urban atmo-
spheres. Fossil fuels are composed principally
of hydrocarbons (RH or HC)* which, upon
complete combustion, produce two oxides,
carbon dioxide (CO2) and water (H2O).
A hydrocarbon is an organic compound containing
carbon and hydrogen only. The hydrocarbons are clas-
sified as alicyclic, aliphatic, and aromatic, according to
the arrangement of the atoms and the chemical proper-
ties of the compounds.
2-1
-------
These two oxides are not considered to be air
pollutants, since they are relatively non-toxic
and are normal constituents of the atmo-
sphere.
It is other by-products of combustion in
exhaust gases and the products of incomplete
combustion which lead to localized air pollut-
ion problems. Since combustion processes are
usually less than 100 percent efficient, the
exhaust gases contain minor amounts of the
original fuel as well as minor amounts of
partially oxidized fuel. Carbon monoxide
(CO), aldehydes, and unsaturated hydrocar-
bons (those which contain less than the
maximum number of hydrogen atoms as a
result of the presence of double or triple
bonds) are examples of partially oxidized
fuel. Small amounts of nitrogen, a major
constituent of air, are oxidized at the high
temperatures characteristic of combustion
processes, to nitric oxide (NO), and sulfur
compounds, also found in varying quantities
in fossil fuels, are oxidized to sulfur dioxide
(SO2). Therefore, the combusion processes
produce emissions which contaminate the air
with oxides of carbon, nitrogen, and sulfur, in
addition to a large variety of hydrocarbons
and partially oxidized hydrocarbon frag-
ments.
When these contaminants have been re-
leased into the atmosphere, they may react
chemically to produce other contaminants
quite different from those originally released.
Sunlight-induced oxidation processes, termed
photo-oxidation, are especially important in
some community air pollution problems. Dur-
ing daylight hours, for example, NO in pollut-
ed atmospheres is rapidly oxidized to nitrogen
dioxide (NO2). Similarly, the oxidation of
SO2 to sulfur trioxide (SO3) is accelerated
and olefins and alkylbenzenes are oxidized to
form aldehydes and ketones. Formation of
ozone (O3) is also observed, as well as
formation of a family of compounds identi-
fied as peroxyacyl nitrates [R?ooNo2].
Recent laboratory studies suggest the pre-
sence in such atmospheric mixtures of per-
oxybenzoyl nitrate, hydrogen peroxide, and
alkyl hydroperoxides.
Several of the pollutants formed during the
photochemical reaction process are termed
oxidants. These are defined as atmospheric
substances which will oxidize certain reagents
not readily oxidized by oxygen. Because they
are products of the photochemical air pollut-
ion process, these substances are often refer-
red to as photochemical oxidants.
The reagent most frequently employed to
measure the presence of photochemical oxi-
dants in polluted -atmospheres is a solution of
neutral-phosphate-buffered potassium iodide.
This reagent responds to ozone and, to some
extent, to nitrogen dioxide, and to the per-
oxyacyl nitrates. However, reducing agents
such as SO2 will negate the effect of oxidants
on the reagent solution. The potassium iodide
method may be used, therefore, to provide a
measure of the net oxidizing properties of
atmospheric pollutants without discrimin-
ation as to the species of the oxidants or
reducing agents. Details of this method and its
limitations are given in Chapter 5.
As has been noted, the recognized oxidants
which have been measured in the atmosphere
are ozone, the peroxyacyl nitrates, and nitro-
gen dioxide. Nitrogen dioxide will be consid-
ered here only in relation to its involvement
in the formation and the measurement of
other oxidants. Although they are not oxi-
dants but are involved in measurement and
formation of oxidants, sulfur dioxide and
hydrocarbons also will only be considered to
this extent in this report. The roles of
nitrogen dioxide and hydrocarbons in air
pollution are discussed in other air quality
criteria documents. The role of SO2 in air
pollution has been documented.1
C. PHYSICAL PROPERTIES
1. Ozone
Some physical properties of ozone are
listed in Table 2-1. The ultraviolet spectrum
of ozone has been studied extensively.2 The
strong absorption of ozone between 2,000
and 3,000 angstroms (A) is useful for analysis.
Ozone also exhibits strong infrared absorption
at about 1,050 cm" (wave number) or 9.5
microns. Detection of this band, with its
2-2
-------
characteristic shape, by long-path infrared
spectroscopy, provides the most unambiguous
demonstration of the presence of ozone in
polluted air.
TABLE 2-1. PHYSICAL PROPERTIES OF OZONE
Physical state
Chemical formula
Molecular weight
Melting point
Boiling point
Specific gravity relative to air
Vapor density
At 0°C, 760 mm Hg
At 25°C, 760 mm Hg
Solubility at 0° C
(Indicated volume of ozone at
0°C, 760mmHg)
Conversion factors
AtO°C,760mmHg
At 25°C, 760 mm Hg
Colorless gas
48.0
-192.7± 0.2° C
-111.9± 0.3°C
1.658
2.14 g/liter
1.96 g/ liter
0.494 ml/100 ml water
1 ppm=2141 Mg/m
lMg/m =4.670 x 10'4
lMg/m =5.097x 10-4
2. Peroxyacetyl Nitrate
Known physical properties of peroxyacetyl
nitrate (PAN) are listed in Table 2-2. In
addition, the infrared, ultraviolet, mass, and
nuclear magnetic resonance spectra of PAN
are available.3"7
Table 2-2. PHYSICAL PROPERTIES
OF PEROXYACETYL NITRATE
Physical state
Chemical formula
Molecular weight
Boiling point
Colorless liquid
CH38oONO2
121
No true boiling point, compound
decomposes before boiling
Vapor pressure
at room temperature
Conversion factors
At 0°C, 760 mm Hg
At 25°C, 760 mm Hg
About 15 mm Hg
lppm=5398Mg/m3
lMg/m3=1.85 2 x 10'4ppm
lppm=4945/jg/m3
lMg/mJ=2.022 x 10-4ppm
D. OXIDANT FORMATION PROCESSES
1. Nitrogen Dioxide Photolytic Cycle
The oxidant found in the largest quantity
in polluted atmospheres is ozone. In order to
photochemically generate these observed O3
concentrations, a process other than direct
light absorption by O2 must be involved.
Light absorption by O2 does occur in the
atmosphere several miles above earth. The
short ultraviolet wavelengths responsible for
this reaction do not reach the earth's surface,
however, and, therefore, could not produce
the amounts of ozone detected in the ambient
air. As will be indicated in Chapter 4, only a
small portion of the O3 observed near the
earth's surface could have been transported
from the stratosphere, where high concentra-
tions exist naturally. Consequently, some
other generation process must be involved.
Comparison of the absorption characteris-
tics of the major atmospheric pollutants
indicates that nitrogen dioxide is the most
efficient absorber of the portion of the sun's
ultraviolet light which reaches the earth's
surface. This absorption of ultraviolet light by
NO2 leads to a complex series of reactions.
NO2 is broken down (photolyzed) by
ultraviolet light energy into NO and O; ozone
is formed in the subsequent reactions of the O
atoms and O2 (stable oxygen molecules in the
air have two atoms); and new NO2 and O2 are
generated by the reaction of NO and O3.
Thus the balance is maintained and the cycle
is perpetuated. This cyclic set of reactions is
depicted in Figure 2-1.
As indicated, the absorption by NO2 of the
ultraviolet portions of sunlight (3,000 to
4,000 A) is followed by a set of three
reactions:
NO,
U.V.
light
O + O2 + M-
O3 + NO
NO + 0
(D
O3 + M (2)
NO2 + O2 (3)
2-3
-------
These reactions may be explained as fol-
lows. In reaction 1, the energy contained in
the ultraviolet light acting upon the NO2
molecule is sufficient to break its bond,
yielding two chemical substances, NO and O.
The most probable fate of the oxygen atom
thus formed is reaction with O2 in the
atmosphere to form O3.
Reaction 2 actually proceeds in two steps.
An O atom reacts with O2 to form an
energy-rich O3 molecule. In the absence of a
means to remove this excess energy, the O3
decomposes rapidly back to O2 and an O
atom. Collision with another molecule in the
system, however, will result in the transfer of
some of this excess energy, leading to forma-
tion of a stable O3 molecule. This colhsional
molecule is indicated by the symbol M in
reaction 2. It can be any molecule in the
system. In air, the collision will probably
occur with N2 or O2, since these account for
most of the molecules present.
Reaction 3 shows that the O3 reacts with
NO to reform NO2 and O2. Because reaction 1
is very efficient, in the absence of reactions 2
and 3, the half-life of NO2 in the atmosphere
during periods of intense sunlight would be
on the order of a few minutes. Reactions 2
and 3, which result in the reformation of NO2
in air, are also very fast, however, and tend to
maintain a constant level of NO2 . Reactions 1
to 3 can be visualized as a system (Figure 2-1)
in which the ultraviolet energy is acting as a
pump in the rapid destruction and reforma-
tion of NO2.
Analysis of reactions 1, 2, and 3 indicates
that ozone concentrations are constrained by
the steady state relationship:
NITROGEN
DIOXIDE
(N02)
Figure 2-1. Atmospheric nitrogen dioxide photolytic cycle.
2-4
-------
(03) =
(N02)
(NO)
(4)
In this equation, I represents the intensity
of light, and kj is a constant whose value is
determined by the absorption characteristics
of NO2 and by the rate constant for reaction
3. Parentheses are used to designate concen-
trations.
In the analysis of reactions 1 to 3, Leighton
concludes that equation 4 must play a
dominant role in determining ambient O3
concentrations.8 This conclusion is based on
the knowledge that reactions 1 to 3 are
proceeding at a rate which is one to two
orders of magnitude greater than any other
reactions known to be occurring in the
atmosphere. Thus, reactions 1 to 3 must play
a dominant role in any scheme which at-
tempts to account for ambient O3 concen-
trations. The upper limit on the numerical
value of the kt I term in equation 4 is fixed by
the maximum value of I. In the atmosphere,
measurements show that kxl can be no
greater than 13 to 26 jug/m3 (0.01 to 0.02
ppm). Therefore, to obtain O3 concentrations
of the order observed in the atmosphere, e.g.,
greater than 200 ng/m3 (0.1 ppm), the ratio
(NO2 )/(NO) must be 10 or greater. In general,
atmospheric measurements of O3, NO2, and
NO during hours of sunlight confirm this
prediction.
As indicated, nitric oxide and ozone cannot
coexist for long because of their very fast
interactions. Figure 2-2 shows, as an example
of this, concentrations of certain pollutants
measured in Los Angeles on July 19, 1965.
The concentrations of ozone and nitric oxide
0.16
NITRIC OXIDE
NITROGEN DIOXIDE
OZONE
HOUR OF DAY
Figure 2-2. Diurnal variation of NO, N02, and 63 concentrations in Los Angeles,
July 19, 1965.
2-5
-------
did not simultaneously exceed 0.01 ppm
except between 7:00 a.m. and 10:00 a.m.,
when concentrations of nitric oxide were
rapidly decreasing and ozone rapidly in-
creasing. It should be noted that the Los
Angeles Air Pollution Control District records
concentrations of 0 to 0.01 ppm as 0.01 ppm.
The noncoexistence of high concentrations of
both ozone and nitric oxide cannot always be
demonstrated when using 1-hour averages. It
is possible, for example, that during the first
half of an hour nitric oxide is present but
ozone is not, while during the last half of the
hour, ozone is present but nitric oxide is not.
On the average for the hour, the presence of
both will be indicated. Another factor is the
relatively long response time, 15 minutes or
more, which is characteristic of the nitric
oxide analyzer.
The changes which do occur in the atmos-
phere show that reactions other than 1 to 3
must also be occurring. As indicated in Figure
2-2, early in the morning nitric oxide is in
some instances the major oxide of nitrogen
present. Typical ratios of NO2 to NO usually
range between 0.25 and 0.50, but can reach 1
and above. As the ultraviolet light intensity
increases, a rapid and almost quantitative
oxidation of NO to NO2 is observed. This
photochemical oxidation is unusual since, as
Leighton8 points out, it is one of the few
known instances in which the concentration
of the light absorber, NO2, increases with
irradiation. In addition to the conversion of
NO to NO2, appreciable concentrations of O3
are found after the NO concentration has
been decreased as required by equation 4.
Additional reactions must occur, therefore,
which disrupt or modify the equilibrium
concentrations dictated by reactions 1 to 3.
At steady-state conditions, the circulation
scheme illustrated in Figure 2-1 indicates that
O3 and NO are formed and destroyed in equal
quantities. If the amount of O3 consumed
was slightly less than the amount of NO
converted to NO2, O3 and NO2 would
accumulate while NO would be depleted. A
process slower than that represented by re-
actions 1 to 3 can produce such an effect if it
2-6
converts NO to NO2 without destroying an
equivalent quantity of O3 .
2. Hydrocarbon Interaction with Nitrogen
Dioxide Photolysis
The NO2 photolytic cycle explains the
initial formation of ozone in polluted atmos-
pheres, but it does not explain how concen-
trations can develop as large as those which
have been measured. If no additional mech-
anism were involved, most of the O3 would
quickly break down as it reacted with the NO
created in NO2 photolysis. In other words, at
steady state conditions, O3 and NO would be
formed and destroyed in equal quantities.
Laboratory experimentation and atmos-
pheric measurements indicate that hydro-
carbons provide the necessary added
reactants. Certain types of hydrocarbons
which are also emitted into the atmosphere in
fossil fuel exhausts, notably olefins and sub-
stituted aromatics, enter the NO2 circulation
scheme. Studies suggest that oxygen atoms
attack the hydrocarbons and the resultant
oxidized compounds and free radicals react
with NO to form more NO2. Thus the balance
of O3 consumption by NO is upset so that O3
and NO2 levels build up while NO levels are
depleted.
Figure 2-3 shows schematically how hydro-
carbons are involved in photochemical oxi-
dation reactions. Both O atoms and O3
molecules have the ability to oxidize hydro-
carbons; but, by examining rates of reactions,
it has been deterimined that the more prob-
able initial reaction is O atom oxidation since
it is 108 times as fast as oxidation by O3.
Although very fast, O atom oxidation is still
one to two orders of magnitude slower than
reaction 2. As indicated, however, processes
very much slower than reaction 1 to 3 can
disturb the delicate balance of the NO2
circulation scheme illustrated in Figure 2-1.
Oxidation of hydrocarbons by O atoms is
not by itself an explanation of the O3
accumulation, nor the oxidation of NO. The
intermediate free radical formed from the O
atom attack on hydrocarbons is very reactive
and apparently undergoes a series of changes
-------
NITROGEN
DIOXIDE
(N02)
HYDROCARBON
FREE RADICAL
(R02)
Figure 2-3. Interaction of hydrocarbons with atmospheric nitrogen dioxide photolytic cycle.
2-7
-------
in which it readily reacts with O2 and
oxidizes NO to NO2. The effect of the
hydrocarbon involvement, which adds certain
postulated reactions to the NO2 circulation
scheme,is shown by the dashed lines in Figure
2-3. Reflection on the indicated alternate
path for oxidation of NO to NO2 shows that
the intermediates produced by the O + RH
reaction must oxidize more than one mole-
cule of NO to NO2. Figure 2-3 thus represents
schematically the manner in which hydro-
carbons enter the NO2 circulation scheme and
permit a rapid buildup of NO2 and the
accumulation of O3.
It is important to differentiate between
what is known and what is uncertain concern-
ing the mechanism outlined in Figure 2-3.
Reactions 1 to 3 have been investigated
extensively and are, therefore, reasonably
well understood.9 The importance of O atom
and O3 oxidation of RH also has been
investigated extensively and the rate constants
of these reactions are reasonably well-known
for a variety of hydrocarbons.8'1 °>11 How-
ever, the reactions of oxygen atoms and
ozone9' *2> 13 do not always account for the
observed disappearance of hydrocarbons.
Such discrepancies are probably due to the
additional reaction of free-radical inter-
mediates with the hydrocarbons.
The foregoing discussion of the interaction
of hydrocarbons with the NO2 photolytic
cycle should not be interpreted as invalidating
the applicability of equation 4. At atmos-
pheric O3 concentrations below 200 jug/m3
(0.1 ppm), however, the concurrent present
of nitric oxide and ozone occasionally can be
found.14 The time-averaging period for the
aerometric measurements, therefore, may be
significant with respect to the reaction on a
real-time basis.
In the atmosphere, the major component
of the peroxyacyl nitrate series is peroxy-
acetyl nitrate. A small amount of peroxy-
propionyl nitrate [CH3CH28oO NO2 ] has
also been observed. In the laboratory, these
compounds can be formed conveniently by
irradiation of the parent nitrite (RONO) in
oxygen or air.15 This has not been proven to
be a mode of formation in the atmosphere,
however, since the presence of the nitrites has
not been demonstrated conclusively either in
the atmosphere or in laboratory systems
designed to simulate photochemical air pollu-
tion systems. On the other hand, this lack of
direct evidence does not eliminate nitrites as a
potential source of peroxyacyl nitrates. Ni-
trites are rapidly photolized, and their con-
centrations as intermediates may not be
observable. An alternate possibility is that a
free radical arising from an O atom attack on
hydrocarbon reacts with O2 to form a
peroxyacyl radical [RCOO] • The peroxy-
acyl radical then reacts with NO2 to form
a peroxyacyl nitrate. This radical can be
formed also by the reaction of O atoms with
aldehydes.
3. Hydrocarbon Reactivity
"Hydrocarbon reactivity" is the term
used to denote the relative ability of a specific
hydrocarbon to exert particular effects on the
photochemical reaction process. For instance,
a specific hydrocarbon may be involved in
several reactions in the photochemical
process, depending on its concentration,
structure, and oxidation state. The end prod-
ucts of these reactions and the consequent
intensity of the symptoms generated, such as
eye irritation or plant damage, are largely
dependent on the nature of the hydrocarbon
involved. Any "rating of reactivity" for spe-
cific hydrocarbons will, of necessity, show
marked differences, depending on the effect
being measured. For example, a rating based
on the ability to react with O atoms will be
quite different from a rating based on the
capacity to generate eye irritation.
A number of schemes have been proposed
for rating the reactivity of hydro-
carbons.1 6~20 Some of these have been based
on the rate of oxidation of nitric oxide to
nitrogen dioxide, when the nitric oxide is
irradiated with a specific hydrocarbon; the
rate of disappearance of the hydrocarbon; the
yield of products or effects; and, most simply,
whether a hydrocarbon reacts or does not
2-8
-------
react. While there are differences in the
rankings, depending on which set of criteria is
used, there is general agreement that unsat-
urated hydrocarbons are of more importance
to photochemical air pollution symptoms
than are saturated hydrocarbons.
Unsaturated hydrocarbons are also of great
importance in the formation of oxidants.
Table 2-3 presents a partial list of yields of
ozone agd oxidant from the photooxidation
of various mixtures of organic substances and
nitrogen oxides, as reported by several in-
vestigators.
Haagen-Smit21 used the rubber cracking
method to measure the ozone produced by
organic compounds and nitrogen dioxide ir-
radiated during a 10-hour period. Schuck and
Doyle16 measured ozone with a long-path
infrared spectrophotometer. The initial con-
centrations of the reactants irradiated were
1230 Mg/m3 (1 ppm) of nitric oxide and 3
ppm of a selected hydrocarbon (except in the
case of ethylene, in which 6 ppm was irra-
diated). Soon after the start of irradiation,
ozone became detectable and continued to
increase until a stable level was reached at the
concentrations listed in Table 2-3. Altshuller
and Cohen22 and Altshuller et al.24 used the
colorimetric and coulometric potassium
iodide methods for measuring oxidants.
Because of the differences in methods,
concentrations of reactants, and physical
properties of the environmental test cham-
bers, the results obtained by one set of
authors are not quantitatively the sams as
those obtained by another, nor can they
necessarily be extrapolated to atmospheric
pollution conditions. They do have appli-
cability, however, on a relative basis. Thus, in
general, the internally double-bonded olefins,
the diolefins, and highly substituted aromatic
compounds produce the greatest yields of
oxidants or ozone. Acetylene, benzene, and
the paraffins having less than five carbon
atoms produce the least oxidant except at
very high hydrocarbon-to-NO reactant ra-
tios 16, 19,21-24
Several studies of peroxyacyl nitrate yields
have been reported.16'23'15-27 Table 24
tabulates the reported peroxyacetyl nitrate
yields from the photooxidation of various
mixtures of hydrocarbons and nitrogen
Table 2-3. OZONE OR OXIDANT YIELDS FROM PHOTOOXIDATIONS OF A MIXTURE
OF AN ORGANIC SUBSTANCE WITH NITROGEN OXIDES IN AIR
Organic substance
1,3-Butadiene
2-Alkenes
1,3,5-Tiimethylbenzene
Xylenes
1-Alkenes
Methanol, ethanol
Formaldehyde
Piopionaldehyde
3-Methylheptane
n-Nonane
Ethylene
Hexanes, heptanes,
iso-octane
Toluene
Acetylene
Cj - C$ paraffins
Static irradiation yields
Cracking depth,
mm
Haagen-Smit2 1
12
8
7
6-7
5
5
4
4
3
3
2
1
0.6
0.5
< 0.2
ppm by volume
Schuck and
Doyle16
0.65
0.55-0.73
0.18
0.58-1.00
—
—
1.1
0.2
—
0.0-0.2
Altshuller and
Cohen22
—
—
1.1
0.65-1.0
—
1.0
0.2
—
0.5
0.0
Heuss and Glasson23
0.48
0.44-0.60
0.46
0.26-0.39
0.41-0.54
—
—
0.28
0.2
0.30
=
Dynamic irradiation
yields
ppm by volume
Altshuller et al.24
0.72
—
0.37
0.4
—
1.05
0.80
0.69
0.0
0.36
=
2-9
-------
Table 2-4 PEROXYACETYL NITRATE YIELDS FROM PHOTOOXIDATION OF
HYDROCARBON-NITROGEN OXIDE MIXTURES IN AIR 6 • 1 6 y2 3 . 2 5
Hydrocarbon
n-Butane
Isopentane
n-Hexane
iso-octane
Ethylene
Propylene
1-Butene
iso-butene
1-Hexene
trans-2-Butene
cis-2-Butene
2-Methyl-2-butene
cis-3-Hexene
tians-3-Hexene
Tetramethylethylene
1,3-Butadiene
Benzene
Toluene
Cg+ Monoalkylbenzenes
o-Xylene
p-Xylene
w-Xylene
l,3>5-Trimethylbenzene
1,2,4,5-Tetramethylbenzene
Peroxyacetyl nitrate concentration,
ppm by volume
Stephens8
_
-
_
-
0
>0.55
0.55
0.15
-
_
0.7
-
0.8
1.0
-
-
_
-
-
0.4
0.4
0.55
0.8
0.7
Heuss and GIassonb
0
-
0
0
0.01
0.35
0.05
-
0.02
0.63
0.36
0.85
-
-
0.65
0.02
0.01
0.10
0.00 or 0.01
0.4
0.4
0.5
0.67
-
Schuck and Doylec
-
0
—
0.05
—
0.35
0.05
0.45
—
0.52
0.55
0.88
-
-
1.0
0.05
—
-
-
-
-
-
-
-
5 ppm hydrocarbon and 5 ppm NO or NO2 (References 6 and 25).
2 ppm hydrocarbon and 1 ppm NO (Reference 23).
3 ppm hydrocarbon and 1 ppm NO or NO2 (Reference 16).
oxides. Altshuller et al.19 • 2 8 have been able
to detect very low concentrations of peroxy-
acetyl nitrates in the 250- to 500-jug/m3 (0.05
to 0.10 ppm) range from the irradiation of
n-butane, iso-pentane, 2,4-dimethylhexane,
and toluene with nitrogen oxides. These
results indicate, as do ^he results of Heuss and
Glasson,23 that paraffinic hydrocarbons, to-
gether with benzene and monoalkylbenzenes,
contribute very little to PAN yields in atmos-
pheric reactions. The production of PAN-type
compounds is associated with the presence of
propylene and higher-molecular-weight
olefins, and with dialkyl- and trialkyl-
benzenes.
Heuss and Glasson have reported peroxy-
benzoyl nitrate as a minor product of the
irradiation of toluene and other benzyl-type
monoalkylbenzenes with nitric oxide.23 Sty-
rene and other aromatic olefins produce
somewhat greater yields of peroxybenzoyl
nitrate when irradiated with nitric oxide.
Peroxybenzoyl nitrate was found to be a very
potent eye irritant, since only 75 to 150
Mg/m3 (0.01 to 0.02 ppm) is capable of
causing from light to severe eye irritation.23
This lacrimator does not appear to be formed
from other types of hydrocarbons.
4. Nitric Oxide and Nitrogen Dioxide
One of the consequences of high-tempera-
ture combustion of fossil fuels in air is the
formation of NO by oxidation of a portion of
the N2 content of the air. As previously
2-10
-------
discussed, the major process by which atmos-
pheric nitric oxide is oxidized to nitrogen
dioxide is photochemical, involving hydro-
carbon interaction. There are, in addition,
two other reaction pathways which con-
tribute to atmospheric nitrogen dioxide con-
centrations.
The first of these, the reaction of ozone
with nitric oxide, has already been considered
briefly in the discussion of the nitrogen
dioxide photolytic cycle. At or near sunset,
when ozone photochemical formation ceases,
a polluted atmoshere will generally contain an
excess of ozone and a minimum of nitric
oxide. While ozone formation stops at sunset,
however, exhaust emissions of nitric oxide
usually do not. From a rate-of-reaction view-
point, the most probable fate of the remain-
ing ozone is reaction with the continuing
nitric oxide emissions. During the early even-
ing hours, therefore, some fraction of an
observed nitrogen dioxide concentration is,
and would be expected to be, contributed by
this reaction.
Nevertheless, a second reaction, the oxida-
tion of nitric oxide by oxygen in the air
during the early phases of atmospheric ex-
haust gas dilution, is the cause of some
fraction of the observed nighttime nitrogen
dioxide concentrations. The overall reaction,
as exhaust is diluted in air, is described by the
reaction:
2 NO + O,
2 NO,
(5)
The rate of formation of NO2 from reaction 5
is determined by:
(6)
When dilution is complete, that is, when the
NO concentration is in the ppm range, re-
action 5 will result in a small contribution to
the oxidation of nitric oxide. Since atmos-
pheric exhaust gas dilution is very rapid, the
amount of NO oxidized by this process is
usually less than 10 percent of the total NO
emissions from sunset to sunrise. Conse-
quently, it is not unusual to have the maxi-
mum daily NO concentration recorded early
in the morning.
E. METEOROLOGICAL EFFECTS
1. General
The diurnal urban emission pattern of
oxidant-forming pollutants is fairly uniform
from weekday to weekday. It is apparent,
therefore, that variations in the pattern of
oxidant concentrations must be due largely to
meteorological factors. Dilution of oxidants is
accomplished by the same process of atmos-
pheric turbulence and transport that affects
other gaseous contaminants. The large range
of values over which these parameters extend
often contributes significantly to the diurnal,
daily, and seasonal variations of observed
oxidant concentrations at a particular loca-
tion. Atmospheric concentrations of oxidant
are also dependent upon those meteorological
variables affecting oxidant formation. Some
of these factors are discussed in the following
sections.
2. "Sunlight
Light is measured in parameters of inten-
sity and wavelength. Intensity is the measure
in photons of the concentration of light,
while wavelength is the measure of how much
energy each photon contains. The longer the
wavelength, the less energy is contained in
each photon.
Interaction of light with an NO2 molecule to
form NO and an O atom (reaction 1) is a
reaction between a photon and the NO2
molecule. Thus, the rate of NO2 destruction,
or of 0 atom formation, is directly propor-
tional to the intensity of light and the
concentration of NO2. Since ozone concen-
tration is a function of 0 atom concentration
(reaction 2), the ozone concentration by
equation 4 is likewise directly proportional to
the light intensity.
NO2 efficiently absorbs most wavelengths
of light between 3,000 and 6,000 A.8'29
Efficient absorption alone, however, does not
guarantee that NO2 dissociation (reaction 1)
will take place. It has been determined that
2-11
-------
the dissociation of NO2. is a function of
wavelength.8'29 Over 90 percent of NO2
molecules are photolyzed when the light
wavelength is between 3,000 and 3,700 A.29
Above 3,700 A, the percentage drops off
rapidly; and above 4,200 A, dissociation does
not occur.
Disruption of the bond between O
and NO in NO2, as necessitated in reaction 1,
requires approximately 72 kilocalories of en-
ergy per mole at 25° C. This corresponds to
the energy available in light at a wavelength of
approximately 4,000 A. At longer wave-
lengths, light cannot break the NO2 bonds
because insufficient energy is available.
The wavelength at which NO2 dissociation
fails to occur is not precisely defined because
the individual molecules of NO2 do not all
possess the same ground state energy prior to
absorption. Figure 2-4 shows that the transi-
tion from 100 percent to 0 percent disso-
ciation occurs between 3,700 and 4,200 A.
This gradual transition indicates a variation in
ground state energy of about 10 kilocalories
per mole.
100
so
60
(J
O
1/5
—
O
CN 20
O
z
MAJOR REACTION!
DISSOCIATION N02" NO t.0
N02*
EXCITED INTERMEDIATE
FORMED BY LIGHT AB-
SORPTION
EXCITED SPECIES FORM-
ED BY COLLISION
MAJOR REACTIONS;
FLUORESCENCE N02' N02 <
DEACTI VAT ION N02* * M NO2 <
3,000 4,000
WAVELENGTH, angstroms
5,000
Figure 2-4. Nitrogen dioxide dissociation
as a functional wavelength of light absorbed.
The relative distribution of wavelengths
from sunlight reaching the earth's surface
does not vary appreciably except in the
presence of absorbing species or light scatter-
ing particles. Since polluted atmospheres
contain variable amounts of NO2, and since
the NO2 will absorb certain wavelengths of
sunlight, there can be some changes in both
the relative wavelength distribution and the
intensity of sunlight at the earth's surface.
Due to low ambient NO2 concentrations, any
such effects of NO2 absorption on wavelength
distribution and intensity are likely to be
small.
A reduction as high as 80 percent of
intensity near the region of 3,250 A has been
observed at the earth's surface during an
intense photochemical air pollution epi-
sode.30 Since most of the NO2 had disap-
peared from the atmosphere at this time, it
cannot be responsible for the observed de-
crease in light intensity. Rather, the reduction
has been generally attributed to the light-
scattering effect of atmospheric aerosols
formed as a by-product of the photochemical
interactions of RH, NOX and SO2 .
Light intensity reductions of the magnitude
observed would be expected to produce a
substantial decrease in the rate of photo-
chemical reactions. The actual effect, how-
ever, caused by aerosol diffusion is far more
complex. As pointed out by Leighton,8 the
available light energy is a function of the
height within a given polluted air mass.
Within the upper half of the air mass, the
available light energy will tend to be the result
of aerosol scattering, and this will be substan-
tially greater than that available from just
incident radiation. An opposite effect is ob-
served in the lower half of the air mass. Thus
the formation of photochemical aerosols has
the rather interesting effect of increasing the
rate of photochemical reactions in the upper
half of the polluted air mass and, at the same
time, decreasing these rates in the lower half
of the air mass. Thus, in areas where visibility
reduction are severe, a less direct correlation
between observed oxidant concentrations and
light intensity measured at ground level would
be expected. The total effect on oxidant
levels of such intensity effects cannot be
ascertained without quantitative data on verti-
cal mixing within a polluted air mass.
2-12
-------
Variations in sunlight intensity which most
affect development of oxidants are those
occurring as a function of time of day, time of
year, and geographical location. Maximum
intensities prevail around noon, with duration
times of near maximum intensities varying
according to season and latitude. Cloud cover
is, of course, another important factor, as well
as the atmospheric accumulation of light-
scattering and light-absorbing pollutants.
The combination of the factors of light
intensity and duration controls to some ex-
tent the amount of photooxidized materials
which can be formed. In the United States,
the maximum noonday intensity and the
duration of nearly maximum light intensity
do not vary appreciably with latitude during
the summer months. In the region of 3,000 to
4,000 A, the maximum total intensity is L x
1016 photons cm"2 sec"1, with the measure-
ment remaining near this value for 4 to 6
hours.9 By contrast, the winter values vary
from 0.7 x 1016 to 1.5 x 1016 photons cm'2
sec"1, depending on latitude, and time near
maximum light intensity in the winter is
reduced to 2 to 4 hours.9 These times and
intensities are important controlling factors in
determining the severity and duration of
photochemical air pollution symptoms.
3. Temperature
The temperature of a polluted air mass
determines the ground state energy of all
chemical species in the system. High tempera-
tures increase ground state energy. In Figure
2-4, for example, the transition curve can be
slightly shifted to longer wavelengths by
increasing the temperature and, thus, increas-
ing the ground state energy of the system.29
Since most chemical reactions require addi-
tion or subtraction of energy, a temperature
variation can also change the reaction rate.
Laboratory experiments have shown that a
40° F temperature rise increases the rate of
NO and hydrocarbon oxidations by a factor
of 2.31 There is also evidence in certain
systems that a temperature increase of this
magnitude results in a fourfold increase in
rate of oxidant production.32 These are
substantial changes which can affect the
concentrations of photochemical air pollution
products in the atmosphere.
Quantitative estimates of the effect of
ambient temperature variations upon these
manifestations cannot be made at this time.
The restrictive nature of the laboratory ex-
periments and the lack of knowledge concern-
ing the variables and reactions involved are
two of the factors which prohibit other than
qualitative estimates.
F. REACTANT CONCENTRATION
STUDIES
1. Environmental Chamber Studies
During the past 15 years, a number of
laboratory studies have investigated the for-
mation of photochemical air pollution. The
results of sucn studies are in agreement with
atmospheric measurements and present a con-
sistent picture. Ultraviolet irradiation of air
mixtures, containing concentrations in the
ppm range of certain hydrocarbons and NO or
NO2, leads to:
1. Oxidation of NO to NO2 and then to
nitric acid.
2. Reactions of NO2 to form products
such as peroxyacyl nitrates and in-
organic nitrates.
3. Oxidation of hydrocarbons to form
aldehydes and ketones.
4. Formation of 03.
5. Increase in the oxidation rate of SO2
to SO3 and sulfate.
Rather extensive data are available on the
consumption of reactant hydrocarbons and
nitrogen oxides and on the formation of
products from a number of irradiated hydro-
carbon-nitrogen oxide systems.1 3 Acceptable
carbon mass balances have been obtained for
the photooxidation of hydrocarbons such as
ethylene, propylene,12 1-butene,16 trans-2-
butene,33 n-butane,19 and pentanes.19 Major
products vary from system to system and
include formaldehyde, acetaldehyde, one or
more other aldehydes or ketones, carbon
monoxide, carbon dioxide, and peroxyacyl
nitrates;1 3 other important products include
2-13
-------
ozone, nitrogen dioxide, and inorganic ni-
trates. Acceptable nitrogen balances have
been obtained from irradiations of mixtures
containing hydrocarbons such as ethylene and
1,3-butadiene, which produce little if any
peroxyacyl nitrates. Acceptable carbon and
nitrogen balances have not been reported
from irradiation of nitrogen oxides with
higher-molecular-weight hydrocarbons, such
as the alkylbenzenes.
Several studies have been made of ultra-
violet-irradiated automobile-exhaust sys-
tems.34"39 Ozone, nitrogen dioxide, formal-
dehyde and other aldehydes, and peroxyacyl
nitrates have been identified and measured as
products. As would be expected, the same
types of products are found as in simpler
mixtures. From the results of one study, the
formation of aldehydes can be estimated to
account for about 30 percent of the carbon
atoms consumed from the hydrocarbons.
Hydrocarbon consumption and formaldehyde
and peroxyacetyl nitrate formation were de-
termined from a small series of experiments
on irradiated atmospheric samples collected
between 7 and 8 a.m. in downtown Los
Angeles.40 The formaldehyde accounted for
24 percent, and the peroxyacetyl nitrate 9
percent, of the carbon atoms consumed.
In addition to the product-yield-type stud-
ies discussed above, much attention has been
directed to the quantification of reaction
dynamics. It was realized at an early date,
however, that rates of reactions and concen-
trations of products are not strictly propor-
tional to concentration of reactants. Haagen-
Smit34 first noted this effect during
irradiation of flasks containing hydrocarbons
and NOX in air. In view of the previous
discussion concerning the complex hydro-
carbon interaction with NO2 photolysis, such
nonlinear effects are not unexpected. Since
concentration ratios, as well as absolute con-
centrations, of the primary reactants affect
oxidant concentrations and rates of forma-
tion, a summary of the available information
on these topics is required in order to
appreciate oxidant variations in polluted
atmospheres. Nevertheless, in discussing these
2-14
effects, it must be remembered that all of the
data on this subject have been generated in
experimental systems which only approxi-
mate the ambient atmospheres. Because of
the limitations of atmospheric data, re-
searchers have been unable to show as yet
that concentration ratio effects are unequi-
vocably operating in the real atmosphere.
Nevertheless, the implications demand an
examination of the experimental data.
Subsequent to the work of Haagen-Smit,
several investigators have attempted to quan-
tify the effect of changes in reactant con-
centrations and ratios.12• 16' 35- 37In one
sense, all the studies could be deemed success-
ful in that each laboratory was able to
confirm and quantify the effects. There ap-
pears to be only a qualitative agreement,
however, when comparing one study with
another, and there is no general agreement
concerning the meaning of the results when
extrapolated to the atmosphere. As indicated,
direct atmospheric data on this subject have
not as yet been obtained. A major stumbling
block is the lack of air monitoring data on
atmospheric concentrations of reactive hydro-
carbons. Such a lack means the applicable
concentrations or ratios in the real atmos-
phere cannot at this time be clearly specified.
Examples of the relationships observed
experimentally between reactant and oxidant
concentrations are shown in Figures 2-5
through 2-8. It should be noted that the
studies in Figures 2-5 and 2-7 refer to irradia-
tion of mixtures containing propylene as the
hydrocarbon, while the studies in Figures 2-6
and 2-8 refer to irradiated mixtures using auto
exhaust as the hydrocarbon source. In spite of
many differences in choice of initial reactants
and experimental design, the qualitative agree-
ment in these four studies is rather striking.
All studies show a similar dependence of
oxidant on hydrocarbon concentrations. All
studies further reveal a noticeable dependence
upon the NOX levels. From the previous
discussion, it is not unrealistic to envision the
complex NOX effect as the direct result of the
competition between the reactions resulting
in oxidant formation and destruction.
-------
12345
PROPYLENE CONCENTRATION,
ppm carbon
Figure 2-5. Maximum oxidant concentration
as a function of propylene and nitric oxide
reactant concentrations during 2-hour
dynamic irradiation."12
o °-5
I-
<
1- 0.4
(J
O 0.3
(J
K|
Z a
I 0.2
X
o
2 0.1
x
<
OXIDES OF NITROGEN, ppm
0 5
0 2 4 6 8 10 12
HYDROCARBON CONCENTRATION
REACTED, ppm carbon
Figure 2-6. Maximum oxidant concentration
as a function of hydrocarbon and nitrogen
oxide concentrations reacted during 1-hour
dynamic irradiation of automobile exhaust
mixtures. 41
2. Atmospheric Studies
As previously indicated, a severe handicap
exists when attempting tc demonstrate a
relationship between reactant concentrations
and oxidant concentrations in polluted atmo-
spheres. Theoretically, generation of an atmo-
spheric simulation model should be feasible,
o
I-
<
0.64
0.5
(J
z
o
"il
Z o-
0.4
X
o
X
<
0.3
0.2
0.1
NITRJC OXIDE, ppm
........ 1.0
- 0.5
--- 0.25
024 6 8 10 12
PROPYLENE CONCENTRATION,
ppm carbon
Figure 2-7. Maximum oxidant concentration
as a function of propylene and nitric oxide
reactant concentrations during static
irradiations. 37
<
Cf.
UJ
(J
.
o
u
Q
X
O
X
<
0.6
0.5
0.4
"0.3
0.2
0.1
OXIDES OF NITROGEN, ppm
__ °-5
1.0
0 2 4 6 8 10 12
HYDROCARBON CONCENTRATION,
ppm carbon
Figure 2-8. Maximum oxidant concentration
as a function of hydrocarbon and nitrogen
oxide reactant concentrations during 2-hour
dynamic irradiation of automobile exhaust
mixtures. 35
enabling the prediction of oxidant concentra-
tions from a knowledge of emission and
meteorological data. Unfortunately, such
models are in an early experimental stage.
Instead of such a model, however, it is still
possible to extract qualitative information
from monitoring data, but assumptions must
be made to accomplish this purpose. If these
2-15
-------
implications are kept in mind, there is little
danger of overestimating the value of informa-
tion generated in this manner.
One assumption is that observed concentra-
tions of reactants and products are largely a
function of meteorological factors. This as-
sumption implies that day-to-day emissions
are approximately constant, thus further im-
plying that the day-to-day human activities
leading to these emissions are relatively con-
stant. Since this latter assumption has been
shown to be approximately true for weekday
conditions only, the following study will be
confined to weekday data. Weekend emissions
show substantial changes attributable to
changes in human activities.
A necessary restriction in order to obtain
acceptable correlation between stations and
consequently between a single station and a
large area air mass, is that air quality values
are based on a large quantity of long-term
average data. In lieu of detailed meteorolog-
ical data, a further restriction is that data be
examined only for those portions of the year
which show the greatest atmospheric stability.
Adherence to this latter restriction produces
two desirable effects. First, it confines the
study to those portions of the year with the
greatest potential for oxidant formation. Sec-
ond, it restricts the examination of the data
to those days when there is the greatest
likelihood of a direct relationship between
morning and noontime meteorological fac-
tors.
Based on the discussed assumptions and
restrictions, the CAMP data for a 3-year
period during the months of June, July, and
August from six cities were examined. Figure
2-9 shows the resulting plot of early morning
hydrocarbon concentrations (6 to 9 a.m.) as a
function of average maximum daily oxidant
concentration (5-minute peak). A similar
treatment of the data from three stations in
Los Angeles is shown in Figure 2-10. Compar-
ison of the experimental data in Figures 2-5
through 2-8 with the atmospheric data in
Figures 2-9 and 2-10 shows that they are
similar. No additional statement or discussion
is justified in view of the gross techniques and
assumptions used to analyze the atmospheric
0.16
Q
X
o
0.14
dz°'12
< o
QH
§£0.10
0.08
LU O
o u
0.06 -
0.04
1 1
CHICAGO
• CINCINNATI
• DENVER
PHILADELPHIA
• ST. LOUIS
WASHINGTON
01 23456
HYDROCARBON CONCENTRATION, ppm carbon
Figure 2-9. Effect of 6 a.m.-9 a.m. hydro-
carbon concentrations on maximum daily
oxidant concentrations during June, July,
and August, 1965-1967.
0.20
x c
o |
_z
-------
TOTAL OXIDANT
CORRECTED FOR .
SOj AND N02
INTERFERENCES
2.0
u
o
o;
z
o
HOUR OF DAY
Figure 2-11. Hourly variation of selected
pollutants in Philadelphia on Tuesday,
July 18, 1967.
data. It should be apparent, however, that this
method of data treatment can be made
rigorous by application of statistical methods
and consideration of measured day-to-day
meteorological factors. Indeed, until such
time as simulation models are perfected, it
may be that this suggested approach is the
only means'of extracting ambient reactant-
product information from air monitoring
data.
The involvement of hydrocarbons in NO2
photolysis, with the resulting formation of
excess ozone, can also be demonstrated by
examination of the changes in pollutant con-
centrations occurring on any given day. For
this purose, 2 days in Philadelphia during July
1967, were chosen for examination. Phila-
delphia was chosen because, beginning in
1967, this city's CAMP station measured
nonmethane hydrocarbons and thus provided
data for a better measure of the hydrocarbons
involved in the formation of oxidants. Both
days, July 18 and 22, were chosen because an
appreciable oxidant formation occurred and
thus they were characteristic of stabilized
atmospheric conditions. Changes in pollutant
concentrations are, therefore, more likely to
be principally the result of emission variables
and sunlight-induced reactions. July 18th
(Figure 2-11) was a weekday; July 22nd
(Figure 2-12) was a Saturday. These days
were chosen to illustrate the effect of week-
end changes in human activities on emissions.
In most respects tne Philadelphia data
shown in Figure 2-11 are typical of a weekday
in Los Angeles. The only major difference is
that, in Philadelphia, the early morning NO
concentration is frequently less than the NO2
concentration, a contrast to Los Angeles
observations. Experimentally, it has been
shown that the only effect is a time delay
when irradiating hydrocarbons in the presence
of NO instead of NO. Hydrocarbon involve-
ment and formation of ozone occur earlier in
hydrocarbon-NO2 mixtures than in hydro-
carbon-NO mixtures, since the light absorber
(i.e., NO2) already is at an elevated concentra-
tion. It is evident, as shown in Figure 2-11,
that the advent of sunrise leads to the rapid
formation of oxidants. More complete analy-
sis of this data would indicate that NO is
being oxidized to NO2 and that hydrocarbons
are being destroyed. It is interesting to note
that secondary peaks near 11:30 a.m. in the
hydrocarbon and NO2 curves are followed 1
hour later by a secondary oxidant peak. At
the same time, and as expected, the NO
remains at a near zero value, as required by
the presence of elevated oxidant values. Satur-
day's changes, shown in Figure 2-12, indicate
that the major difference is one of time; the
peak hydrocarbon and NO2 values occur 2
hours later than on weekdays. As expected,
the oxidant peak is also 2 hours later.
A discussion of the relationship between
ambient concentrations of hydrocarbons and
photochemical oxidants may also be found in
Air Quality Criteria for Hydrocarbons,
NAPCA Publication No. AP-64.
G. FUTURE RESEARCH
In any evaluation of laboratory data on
photochemical air pollution, it should be
emphasized that environmental chamber ex-
periments are relatively simple when com-
pared to the highly complex and variable
situations occurring in the atmosphere. The
fact that various laboratory investigators have
2-17
-------
TOTAL OXIDANT
CORRECTED FOR
S02 AND N02
INTERFERENCES
NITROGEN DIOXIDE
4567891011121 2345
z
o
m
(J
O
HOUR OF DAY
Figure 2-12. Hourly variation of selected
pollutants in Philadelphia on Saturday,
July 22, 1967.
obtained significantly different quantitative
results illustrates this contrast. Such limited
findings can only be applied to the ambient
atmosphere in a suggestive and qualitative
manner. There is an apparent need for more
reliable and applicable quantitative informa-
tion derived from direct atmospheric obser-
vations, as well as for refinement in the results
obtained from irradiation chamber studies.
Relevant monitoring data in more detail are
needed on reactant concentrations and mete-
orological factors. Because these elements
control the size, ventilation rate, and mixing
characteristics of polluted air masses, they
determine to a large extent pollutant concen-
trations and photochemical reaction products.
The need for all types of basic irradiation
chamber experimentation remains acute. A
partial listing of such needed experiments is:
1. Kinetic measurements of the rates of
reaction of hydroxyl radicals with various
hydrocarbons. The observed overall rates of
hydrocarbon consumption are not explained
by reactions with atomic oxygen and ozone.
The most likely intermediate species contri-
buting to these reactions are hydroxyl radicals.
2. The relationship of oxidants, oxygen-
ated hydrocarbons, organic nitrates, and other
possible substances to such factors as reactant
concentrations, reactant concentration ratio,
temperature, light intensity, and water vapor.
While the products accounting for most of the
carbon atoms from lower molecular weight
paraffinic hydrocarbons and olefinic hydro-
carbons have been measured, the results of
carbon balances from the reactions of alkyl-
benzenes and higher molecular weight paraf-
fins are poor. Although the presence of
dicarbonyl compounds from alkylbenzenes
has been reported, quantitative measurements
are lacking. Peroxybenzoyl nitrate, a new and
minor product from the reaction of certain
alkylbenzenes, is a potent eye irritant which
has recently been identified in this type of
research.
3. The relationship of aerosol formation to
a variety of reaction parameters, including
water vapor content. Studies of the role of
sulfur dioxide, sulfuric acid, sulfates, nitric
acid, nitrates, and organics in aerosol for-
mation should also be extended. The compos-
ition of the organic fraction of aerosols is still
unknown.
4. More measurements on the yields of
organic and inorganic nitrates from a variety
of hydrocarbon-nitrogen oxide systems. Just
recently, the formation of inorganic nitrates
has been shown to occur at an appreciable
rate and as a direct result of photooxidation
of hydrocarbons in the presence of nitrogen
oxides.
5. Additional investigation of the impor-
tance of other primary absorbers or species
made reactive by energy transfer. Such species
include the products of aldehydes and
singlet oxygen.
Of even greater urgency, detailed investiga-
tions of the atmospheric reactions in several
representative urban atmospheres are needed.
Such studies have been in progress in Los
Angeles and have been initiated in the New
York-New Jersey area. The types of informa-
tion required includes:
1. Reactant and product composition ob-
tained from irradiation of atmospheric sam-
ples with solar radiation at atmospheric temp-
eratures. Such results can be used to verify
kinetic and product composition results in the
2-18
-------
laboratory. Such measurements have been
made in a limited group of experiments on
samples collected in Los Angeles.
2. Detailed results on the composition of
ground-level samples and samples obtained
aloft. Coordinated vertical distribution mea-
surements along trajectories are needed to
trace the reaction history of air masses.
Oxidant concentrations should be related to
hydrocarbon nitrogen oxide concentration
levels. Such measurements should also empha-
size clarification of the importance of various
species identified in laboratory irraditions but
not in the atmosphere, such as peroxybenzoyl
nitrate, hydrogen peroxide, alkyl hydroperox-
ides, and dicarbonyls.
3. Measurement techniques to estimate the
actual concentrations of radical intermediate
species in urban atmospheres.
4. Measuring techniques to obtain hourly
concentrations of total particulates, sub-
micron particulates, sulfate, nitrate, lead, and
other particulate species. Although a consider-
able body of measurements are now available
on the diurnal variations of gaseous pollut-
ants, comparable diurnal measurements of
particulates are not available.
H. SUMMARY
The atmospheric reactions leading to for-
mation of the photochemical oxidants, ozone
and peroxyacyl nitrates, are reasonably well
understood in a broad if not detailed sense. It
is known that certain hydrocarbon pollutants
interact with the photolytic cycle of nitrogen
dioxide and, as a result, the hydrocarbons are
oxidized to form various products. The pro-
duct mixtures contain substantial concentra-
tions of ozone, as well as such hydrocarbon
products as aldehydes, ketones, and perox-
yacyl nitrates.
Absorption of sunlight by nitrogen dioxide
in the region of 3,000 to 4,000 A results in
dissociation of the nitrogen dioxide into nitric
oxide and an oxygen atom. These oxygen
atoms react principally with the oxygen in au-
to form ozone. A small portion of the oxygen
atoms and ozone also react with certain
hydrocarbons to form free-radical intermedi-
ates, as well as various products. In some
unknown manner, these free radical inter-
mediates compete with ozone for nitric oxide.
One result is the very rapid oxidation of nitric
oxide to nitrogen dioxide and an increased
concentration of ozone.
Experimentally, this photochemical system
can be reproduced in the laboratory, and data
can be obtained relating oxidant concentra-
tions to the concentrations and types of both
hydrocarbons and oxides of nitrogen. For
various reasons, however, these results cannot
be extrapolated to the atmosphere in a
quantitative manner. Because of the complex-
ity of the atmospheric mixture and the
necessary use of non-specific monitoring tech-
niques, demonstration of the relationship of
hydrocarbon and oxidant concentrations in
the atmosphere is somewhat limited. A more
precise examination of the parameters affect-
ing atmospheric oxidant concentrations
awaits the application of statistical and mod-
eling techniques as well as improvements in
measuring methods.
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CPEHS, National Air Pollution Control Administration.
Publication Number AP-50. Washington, D.C. January
1969. 178 p.
2.Ozone Chemistry and Technology. In: Advances in
Chemistry Series. Vol. 21. Washington, D.C., American
Chemical Society, 1959. 465 p.
S.Nicksic, S.W., J. Harkins, and P.K. Mueller. Some Analy-
ses for PAN and Studies of its Structure. Atmos. Environ.
7:11-18, January 1967.
4.Stephens, E.R. Absorptivities for Infrared Determination
of Peroxyacyl Nitrates. Anal. Chem. .26:928-929, April
1964.
S.Stephens, E.R. et al. Photochemical Reaction Products in
Air Pollution. Intern. J. Air Water Pollution. 4(Vi):79-100,
June 1961.
6.Stephens, E.R. The Photochemical Olefin-Nitrogen Ox-
ides Reaction. In: Chemical Reactions in the Lower and
Upper Atmosphere. New York, Interscience Publishers,
1961. p. 51-69.
7.Stephens, E.R. ct al. Recent Developments in the Study
of the Organic Chemistry of the Atmosphere. J. Air
Pollution Control Assoc. 6(3): 159-164, November 1956.
S.Leighton, P.A. Photochemistry of Air Pollution. New
York, Academic Press, 1961. 300 p.
9.Bufalini, J.J. and A.P. Altshuller. Synergistic Effects in
the Photooxidation of Mixed Hydrocarbons. Environ. Sci.
Technol. 7:133-138, February 1967.
lO.Cvetanovic, R.J. Addition of Atoms to Olefms in the Gas
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-------
Phase. In: Advances in Photochemistry, Noyes, W.A., Jr.,
G.S. Hammond, and J.N. Pitts, Jr. (eds.), Vol. 1. New
York, Interscience Publishers, 1963. p. 115-182.
ll.Schuck, E.A. and E.R. Stephens. Advances in Environ-
mental Sciences and Technology, Vol. 1, Metcalf, R.L.
and J.N. Pitts (eds.). (In Press).
12.Altshuller, A.P. et al. Chemical Aspects of the Photooxi-
dation of the Propylene-Nitrogen Oxide System. Environ.
Sci. Technol. 7:899-914, November 1967.
13. Altshuller, A.P. and J.J. Bufalini. Photochemical Aspects
of Air Pollution: A Review. Photochem. Photobiol.
4(2):97-146, March 1965.
14.Richter, H.G., J.R. Smith, and L.A. Ripperton. Chem-
iluminescent Ozone Measurement Program-Ozone Total
Oxidant Relationship in Ambient Ak. Research Triangle
Inst., 1968.
15. Stephens, E.R., F.R. Burleson, and E.A. Cardiff. The
Production of Pure Peroxyacyl Nitrates. J. Air Pollution
Control Assoc. 57:87-89, March 1965.
16.Schuck, E.A. and G.J. Doyle. Photooxidation of Hydro-
carbons in Mixtures Containing Oxides of Nitrogen and
Sulfur Dioxide. Air Pollution Foundation. San Marino,
Calif. Report Number 29. 1959.
17.Altshuller, A.P. Reactivity of Organic Substances in
Atmospheric Photooxidation Reactions. Intern. J. Ak
Water Pollution. 70:713-733, October 1966.
IS.Glasson, W.A. and C.S. Tuesday. Hydrocarbon Reactiv-
ities in the Atmospheric Photooxidation in Nitric Oxide.
Presented at 150th National Meeting of the American
Chemical Society. Atlantic City. September 12-17, 1965.
19.Altshuller, A.P. et al. Photochemical Reactivities of
N-Butane and Other Paraffinic Hydrocarbons. J. Air
Pollution Control Assoc. 79:787-790, October 1969.
20.Altshuller, A.P. An Evaluation of Techniques for the
Determination of the Photochemical Reactivity of Organ-
ic Emissions. J. Air Pollution Control Assoc. 76:257-260,
May 1966.
21.Haagen-Smit, A.J. and M.M. Fox. Ozone Formation in
Photochemical Oxidation of Organic Substances. Ind.
Eng. Chem. 45:1484-1487, September 1956.
22.Altshuller, A.P. and I.R. Cohen. Structural Effects on the
Rate of Nitrogen Dioxide Formation in the Photooxida-
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Intern. J. Ak Water Pollution. 7(8):787-797, October
1963.
23.Heuss, J.M. and W.A. Glasson. Hydrocarbon Reactivity
and Eye Irritation. Environ. Sci. Technol. 2:1109-1116,
December 1968.
24.Altshuller, A.P. et al. Products and Biological Effects
from Irradiation of Nitrogen Oxides with Hydrocarbons
or Aldehydes Under Dynamic Conditions. Intern. J. Ak
Water Pollution. 70:81-98, February 1966.
25.Stephens, E.R. and W.E. Scott. Relative Reactivity of
Various Hydrocarbons in Polluted Atmospheres. Proc.
Amer. Petrol. Inst. 42:665-670, 1962.
26-Kopcznyski, S.L. Photooxidation of Alkylbenzene-Nitro-
gen Dioxide Mixtures in Ak. Intern. J. Ak Water
Pollution. 5:107-120, February 1964.
27.Tuesday, C.S. The Atmospheric Photooxidation of Ole-
fins: The Effect of Nitrogen Oxides. Arch. Environ.
Health. 7(2): 188-201, August 1963.
28.Altshuller A.P. et al. Photochemical Reactivities of
Paraffinic Hydrocarbon-Nitrogen Oxide Mixtures Upon
Addition of Propylene or Toluene. J. Ak Pollution
Control Assoc. 75:791-794, October 1969.
29.Pitts, J.N., Jr., J.H. Sharp, and S.I. Chan. Effects of
Wavelength and Temperature on Primary Processes in the
Photolysis of Nitrogen Dioxide and a Spectroscopic-
Photochemical Determination of the Dissassociation En-
ergy. J. Chem. Phys. 40(12):3655-3662, June 15, 1964.
30.Stair, R. In: Proceedings 3rd National Ak Pollution
Symposium. Pasadena. Stanford Research Institute, 1955.
31.Bufalini, J.J. and A.P. Altshuller. The Effect of Temper-
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Water Pollution. 7(8):769-771, October 1963.
32. Alley, F.C. and L.A. Ripperton. The Effect of Temper-
ature on Photochemical Oxidant Production in a Bench
Scale Reaction System. J. Ak Pollution Control Assoc.
77(19):581-584, December 1961.
33.Tuesday, C.S. The Atmospheric Photooxidation of Trans-
Butene-2 and Nitric Oxide. In: Chemical Reactions in the
Lower and Upper Atmosphere. New York, Interscience
Publishers, 1961. p. 15^9.
34.Haagen-Smit, A.J. and M.M. Fox. Photochemical Ozone
Formation with Hydrocarbons and Automobile Exhaust.
Ak Repair. 4(3): 105-108, November 1954.
35.Korth, M.W., A.H. Rose, and R.C. Stahman. Effects of
HC/NOX on Irradiated Auto Exhausts. Part I. J. Air
Pollution Control Assoc. 74:168-175, May 1964.
36.Leach, P.W. et al. Effects of HC/NOX Ratios on Irradiated
Auto Exhaust. Part II. J. Ak Pollution Control Assoc.
/4:176-183,May 1964
37.Romanovsky, J.C., R.M. Ingels, and R.J. Gordon. Esti-
mation of Smog Effects in the Hydiocarbon-Nitric Oxide
System. J. Ak Pollution Control Assoc. 7 7:454-459, July
1967.
38.Hamming, W.J. et al. Gasoline Composition and the
Control of Smog. Joint Study by Western Oil and Gas
Association and Los Angeles County Ak Pollution Con-
trol District. Los Angeles. 1961.
39.Shuck, E.A., H.W. Ford, and E.R. Stephens. Ak Pollution
Effects of Irradiated Auto Exhaust as Related to Fuel
Composition. Air Pollution Foundation. San Marino,
Calif. Report Number 26. October 1958. 91 p.
40. Altshuller, A.P. et al. A Technique for Measuring Photo-
chemical Reactions in Atmospheric Samples. (Submitted
for publication in Science, 1969).
41.Schuck, E.A. and G.J. Doyle. A Study of Irradiated Auto
Exhaust. Stanford Research Institute. Report No. 9,
Technical Report II. February 1958.
2-20
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Chapter 3.
ATMOSPHERIC PHOTOCHEMICAL
OXIDANT CONCENTRATIONS
A. INTRODUCTION
This chapter is concerned with the mea-
sured levels of oxidants in urban atmospheres
and some of the factors which affect these
levels. It is intended to be a straightforward
presentation of atmospheric measurements
and their interpretation. The only point likely
to cause confusion is the various terms used
to describe oxidant concentrations. Two of
these terms, "oxidant" and "total oxidant,"
are used to describe the "net" oxidizing
ability of the air sampled. Use of these
non-specific terms is required because the
most common method of measurement does
not differentiate between oxidizing or reduc-
ing agents in all cases. The terms "corrected
oxidant" or "adjusted oxidant" are used to
indicate that the measurements have been
corrected for certain known responses caused
by gases other than ozone or peroxyacetyl
nitrate. The terms "ozone" or "peroxyacetyl
nitrate" are used only when the method of
measurement is specific.
B. CONCENTRATIONS OF OXIDANTS
IN URBAN ATMOSPHERES
1. General Discussion
In the early 1950's, the Los Angeles
County Air Pollution Control District
(LACAPCD) established its first air monitor-
ing network (12 stations), using automatic
sampler-analyzers and thus enabling the Dis-
trict's staff to make detailed continuous
observations of gaseous pollutants. Network
equipment also included potassium iodide
(KI) oxidant recorders; ozone photometers
were added in 1958. In 1961, the State of
California Department of Public Health orga-
nized a 16-station Statewide Cooperative Air-
Monitoring Network (SCAN). Six of the
stations of SCAN were equipped and operated
entirely by the Department; seven were equip-
ped and operated jointly by the Department
and by LACAPCD.
The Public/ Health Service of the U.S.
Department of Health, Education, and Wel-
fare opened its Continuous Air Monitoring
Project (CAMP) in Cincinnati in October
1961. By early 1962, five additional CAMP
stations were operating in Chicago,
Philadelphia, San Francisco, New Orleans, and
Washington, in cooperation with local air
pollution control agencies. The station in New
Orleans was moved to St. Louis in 1964, and
in 1965, the San Francisco Station equipment
was moved to Denver.1 Air monitoring in San
Francisco was continued by the Bay Area Air
Pollution Control District as a new SCAN
station.
Today, data on oxidants are continuously
obtained in many U.S. cities by local, State,
and Federal agencies. In California alone,
oxidants are continuously measured at about
40 air monitoring stations. The oxidant data
presented in this report are from the CAMP
stations operated by the Public Health Ser-
vice,1 from a few stations in California,2 and
from the local agency in Phoenix.3 Two of
the California stations are in the Los Angeles
area, where the highest concentrations of
oxidants are found; two others are in large
coastal cities; and the remaining two are in
small cities, one on the coast and one in the
Central Valley of California.
3-1
-------
At the CAMP and LACAPCD stations,
oxidant concentrations are measured with
colorimetric analyzers using neutral-phos-
phate-buffered, 10 percent, KI reagent. At the
SCAN stations, 20 percent KI is used. All
stations of the networks, except those belong-
ing to CAMP, report the peak instantaneous
concentration of each day, the average con-
centration during each clock hour, and the
maximum hourly average concentration of
each day. CAMP reports the 5-minute peak
concentration rather than the instantaneous
peak, in addition to hourly averages and
maximum hourly averages.
The peak concentration for each day, or
the highest value for the day, may be of only
a few minutes duration. The hourly average
concentration is the average concentration
during any one of the twenty-four 60-minute
intervals beginning and ending on the hour,
such as 6:00 to 6:59 p.m. The maximum
hourly average is the highest hourly average
each day. From these basic data, other data
are obtainable, such as the monthly mean of
the hourly averages or of the maximum
hourly average concentrations.
In addition, as shown by Larsen,4 it is
possible to convert the maximum concentra-
tion for one averaging time to that for
another. He computes the expected maximum
concentration (C) for a given averaging time
by using the geometric mean (Mg), the stand-
ard geometric deviation (ag), and the "stand-
ard normal deviate" of no more than one
occurrence in 1.67N trials (z). His formula is
C=Mgagz
2. Oxidant Concentration Patterns
Table 3-1 shows the maximum hourly
average concentrations and peak concentra-
tions, as well as the number and percent of
days when the maximum hourly average
concentration exceeded 290, 200, and 100
Mg/m3 (0.15, 0.10, and 0.05 ppm) for 12
monitoring sites. These values vary greatly
from city to city. The percent of days that
oxidant concentrations exceed 290 jug/m3
(0.15 ppm) in Los Angeles and Pasadena are
of an order of magnitude greater than in other
cities. It is also interesting to note that peak
concentrations in St. Louis reached 1,670
Mg/m3 (0.85 ppm). The high peak concentra-
tion reported for the St. Louis air monitoring
station, however, is one of a series of extraor-
dinarily high readings which usually occur late
at night and are of short duration. It is
suspected that they result from emissions
from a nearby large chemical complex rather
than an atmospheric photochemical reaction.
The cumulative frequency distribution of
Table 3-1. SUMMARY OF MAXIMUM OXIDANT CONCENTRATIONS RECORDED
IN SELECTED CITIES, 1964-1967
Station
Los Angeles
San Diego
Denver3
St. Louis
Philadelphia
Sacramento
Cincinnati
Santa Barbara
Washington, D.C.
San Francisco
Chicago
Total days
of available
data
728
730
623
285
582
556
711
613
723
577
647
530
Number and percent of total days with
maximum hourly average equal to or
greater than concentration specified
0.15
Days
299
220
35
14
14
13
16
10
11
7
6
0
ppm
Percent
of days
41.1
30.1
5.6
4.9
2.4
2.3
2.3
1.6
1.5
1.2
0.9
0
0.10 ppm
Days
401
354
130
51
59
60
104
55
76
65
29
24
Percent
of days
55.1
48.5
20.9
17.9
10.1
10.9
14.6
9.0
10.5
11.3
4.5
4.5
0.05 ppm
Days
546
540
440
226
362
233
443
319
510
313
185
269
Percent
of days
75.0
74.0
70.6
79.3
62.2
41.9
62.3
52.0
70.5
54.2
28.6
50.8
Maximum
hourly
average,
ppm
0.46
0.58
0.38
0.25
0.35
0.21
0.26
0.26
0.25
0.21
0.18
Peak
concen-
tration,
ppm
0.67
0.65
0.46
0.31
0.85
0.25
0.45
0.32
0.28
0.24
0.22
3-2
-------
hourly average concentrations for these same
12 sites is presented in Table 3-2.
At most stations listed in Table 3-2, the
concentrations are equal to or greater than 80
Mg/m3 (0.04 ppm) 30 percent of the time.
Conversely, the concentrations are less than
80 Mg/m3 (0.04 ppm) 70 percent of the time.
The differences among stations are due almost
entirely to the high concentrations, which
occur less than about 10 percent of the time.
There does not appear to be a relationship
between the ranking of stations by yearly
average concentrations and the ranking by
peak or maximum concentrations. The yearly
average from Table 3-2 ranges from 37 to 82
Mg/m3 (0.019 to 0.042 ppm), which is
approximately in the range of ozone concen-
trations found in remote, unpopulated areas.
Caution, however, must be used in the
interpretation of this latter observation as
well as other conclusions which may be drawn
from the data presented in Table 3-2. For
example, one might, on the basis of yearly
average, conclude that Los Angeles, San
Diego, Denver, and Santa Barbara had similar
oxidant problems. Yet examination of the
data in Table 3-1 shows that the peak
concentration, maximum hourly average, and
percent of days with elevated oxidant concen-
trations are in fact quite different for these
four cities. The principal reason for this
apparent contradiction is associated with the
nature of oxidant formation. Since ozone, the
major oxidant, is a photochemical product
and not a direct emission, the conditions
necessary for its formation are restricted to
the hours of sunlight. During any one day,
therefore, the time when elevated oxidants
can occur is restricted to a 4- to 6-hour
period; at the most, this time interval repre-
sents 25 percent of the 24-hour period. On
this basis, 75 percent of the cumulative
hourly data in Table 3-2 represents values
which are close to zero. As a result, the
differences which do exist between cities tend
to disappear in the process of averaging. Thus
the usefulness and meaning of the yearly
averages presented in Table 3-2 have serious
limitations.
For similar reasons, the fact that yearly
oxidant averages in urban areas approach
atmospheric ozone background concentra-
tions has little or no significance. The very
rapid reaction between ozone and nitric oxide
precludes the possibility of the presence of
any nonurban-formed ozone in an urban
atmosphere. Nitric oxide, unlike oxidant, is a
direct emission and is being emitted in sub-
Table 3-2. CUMULATIVE FREQUENCY DISTRIBUTION OF HOURLY AVERAGE OXIDANT
CONCENTRATIONS IN SELECTED CITIES, 1964-1965
City
Pasadena
Los Angeles
San Diego
Denver3
St. Louis
Philadelphia
Sacramento
Cincinnati
Santa Barbara
Washington, D.C.
San Francisco
Chicago
Percent of hours with concentrations
equal to or greater than stated
concentrations, ppm
90
0.01
0.01
0.01
0.01
0.01
0.01
0.01
0.01
0.02
0.01
0.01
0.01
70
0.01
0.01
0.02
0.02
0.02
0.02
0.01
0.02
0.02
0.01
0.01
0.01
50
0.02
0.02
0.03
0.03
0.03
0.02
0.02
0.02
0.03
0.02
0.02
0.02
30
0.04
0.04
0.04
0.04
0.04
0.03
0.04
0.04
0.04
0.03
0.03
0.03
10
0.12
0.10
0.08
0.06
0.06
0.06
0.06
0.06
0.06
0.06
0.04
0.05
5
0.18
0.14
0.10
0.08
0.07
0.08
0.08
0.07
0.08
0.07
0.05
0.06
2
0.23
0.18
0.12
0.10
0.09
0.11
0.10
0.08
0.09
0.09
0.06
0.08
1
0.26
0.22
0.14
0.12
0.11
0.14
0.12
0.10
0.10
0.10
0.07
0.08
1964-1965
yearly
average,
ppm
0.042
0.036
0.036
0.036
0.031
0.026
0.030
0.030
0.036
0.029
0.019
0.028
all months of data beginning February 1965.
3-3
-------
stantial concentrations for most of the hours
in a day; the yearly average in most cities is in
the order of 50 Aig/m3 (0.04 ppm). Assuming
a background of 40 to 80 Mg/m3 (0.02 to
0.04 ppm) ozone permits calculation indicat-
ing an ozone destruction rate of 1,960 to
5,880 Mg/m3 (1 to 3 ppm) per hour. Thus any
nonurban-formed ozone would stand little
chance of existing in an urban atmosphere.
The yearly average oxidant values, therefore,
represent urban photochemically formed
oxidants. These yearly values are low because
75 percent of the averaged values are neces-
sarily near zero, as previously indicated.
Table 3-3 presents, on a yearly basis, the
maximum hourly average concentration and
the number of days when the maximum
hourly average exceeded specified values at
each of the CAMP sites, from 1964 through
1967.
3. Seasonal and Diurnal Variations
Seasonal and diurnal variations in oxidant
concentrations result largely from (1) varia-
tions in emissions of oxidant-forming pollu-
tants, (2) variations in the atmospheric trans-
port and dilution, and (3) variations in other
atmospheric variables invloved in the photo-
chemical formation of oxidant. Typically,
each of these factors varies significantly over
periods as short as a few hours; the latter two
also vary significantly seasonally. It is not
unexpected, therefore, to find considerable
variations in observed ambient oxidant con-
centrations.
At most of the stations, the highest
monthly mean concentrations occur during
the period from late spring to early fall.
Oxidant concentrations exhibit a daily as well
as a seasonal variation, and the maximum
Table 3-3. SUMMARY OF TOTAL OXIDANT CONCENTRATIONS RECORDED AT CAMP SITES,
1964-1967 2
City
Chicago
Cincinnati
Denver
Philadelphia
St. Louis
Washington, D.C.
Year
1964
1965
1966
1967
1964
1965
1966
1967
1965
1966
1967
1964
1965
1966
1967.
1964
1965
1966
1967
1964
1965
1966
1967
Days of
valid data
254
275
235
255
303
310
208
228
285
298
166
269
266
315
282
253
329
292
289
293
284
325
322
Number of days with at least 1 hourly
average equal to or exceeding
0.05 ppm
149
120
52
113
137
182
54
122
226
187
76
124
109
145
124
156
206
174
185
163
150
134
137
0.10 ppm
15
9
6
16
36
19
1
24
51
46
12
37
23
52
28
26
33
33
38
40
25
27
27
0.015 ppm
0
0
3
1
5
5
0
1
14
9
4
9
4
19
3
6
8
5
4
4
3
2
5
Maximum
hourly
average,
ppm
0.13
0.13
0.19
0.16
0.26
0.17
0.10
0.20
0.25
0.19
0.21
0.20
0.33
0.52
0.17
0.26
0.35
0.22
0.20
0.20
0.21
0.16
0.26
-------
generally occurs around the noon-hour, the
period when the shorter wavelength solar
radiation, which is photochemically impor-
tant, reaches the surface of the earth with
greatest intensity. Table 3-4 gives oxidant
concentrations recorded in selected cities
during the month having the highest mean
1-hour average concentration averaged for the
years 1964 and 1965. For these months, the
means of all hourly concentrations and the
means of the maximum daily 1-hour average
concentrations are also listed.
The seasonal variation of oxidant concen-
trations by month is illustrated for three of
the stations in Figures 3-1 and 3-2. Figure 3-1
illustrates the mean by month of all hourly
average concentrations for Los Angeles,
Denver, and Phoenix. Figure 3-2 shows the
mean by month of daily maximum 1-hour
average concentrations for the same cities. In
these figures, the importance of solar radi-
ation is readily apparent. Note that for
Denver, the liigh values occur around mid-
summer. For Los Angeles, the high values
shift toward late summer and autumn, appar-
ently due in part to slower windspeeds and
less cloudiness in these seasons. In addition,
the characteristics of atmospheric transport in
Los Angeles are more favorable to a day-to-
day carryover of precursor pollutants in
autumn than in midsummer, the result of the
greater balance between the sea and land
breezes.
In Figure 3-3, the diurnal variations of
mean 1-hour average oxidant concentrations
are shown for Los Angeles and St. Louis.
Selected for the Los Angeles presentation is
the calendar month which had the highest
monthly mean average for the years 1964 and
1965, while the St. Louis presentation illus-
trates the calendar month which had the
highest monthly mean average in 1966. Illus-
trated by Figure 3-4 is the diurnal variation of
mean 1-hour average oxidant concentrations
for a 3-day period, August 6-8, 1966, in
Philadelphia when unusually high concentra-
tions of oxidants were recorded. While there
are some differences, all curves of Figures 3-3
and 3-4 show a distinct peak around noon.
This peak results largely from the interaction
of diurnal variations in emissions, solar radi-
ation intensity, and atmospheric dilution.
Peak emissions occur with the morning
rush-hour traffic, at a time when solar radi-
ation and dilution are weak. As the emissions
drop off toward midmorning and midday,
Table 3-4. HIGHEST MONTHLY MEAN OF 1-HOUR AVERAGE OXIDANT CONCENTRATIONS
RECORDED IN SELECTED CITIES, 1964 AND 1965
Station
Pasadena
Los Angeles
San Diego
Denver3
St. Louis
Philadelphia
Sacramento
Cincinnati
Santa Barbara
Washington
San Francisco
Chicago
Month having
highest mean
1-hour average
oxidant concentration
July
August
October
July"
May
July
June
July
May and September5
May-
May
April
Monthly
mean of hourly
average concentrations.
ppm
0.075
0.056
0.050
0.050
0.042
0.054
0.040
0.048
0.042b
0.041
0.031
0.044
Monthly mean of
maximum daily
1-hour average
concentrations.
ppm
0.24
0.17
0.11
0.11
0.072
0.11
0.075
0.098
0.064 and 0.072
0.072
0.046
0.070
all months of data beginning February 1965.
b!964-1965 average for the months of May and September.
3-5
-------
radiation increases to a maximum around
noon; dilution increases rapidly in the fore-
noon to reach a maximum around midafter-
noon. Consequently, the diurnal variations of
oxidant concentration typically show a peak
around noon.
4. Oxidant Measurement Parameters
a. Sulfur Dioxide
Sulfur dioxide is a prevalent air pollutant in
many areas of the country. It causes a
negative response equal to its concentration
when oxidants are measured by the potassium
iodide method. If the atmospheric concentra-
tion of ozone and of sulfur dioxide were 0.5
ppm each, for example, the potassium iodide
method would indicate an oxidant-concen-
tration of zero, even though 0.5 ppm O3 was
present in the atmosphere.
To eliminate such sulfur dioxide interfer-
ence, chromium trioxide scrubbers were at-
tached to CAMP oxidant-analyzers at the
beginning of 1964.5 The scrubbers were
provided for all CAMP stations except the one
located in San Francisco. The post-1963
CAMP oxidant data presented, therefore,
were not affected by sulfur dioxide interfer-
ence. The extent of the interference at San
Francisco and at other stations in California is
generally very small because of the typically
low sulfur dioxide concentrations found
there.
b. Nitrogen Dioxide
The 1-hour-average concentrations of
oxidant adjusted for nitrogen dioxide during
selected summer and winter months for each
of four stations are shown in Tables 3-5 and
3-6. In these tables, the concentrations are
presented both adjusted and unadjusted for
nitrogen dioxide.
Table 3-5 lists the monthly mean hourly
average concentrations, while Table 3-6 lists
monthly means of daily maximum hourly
average concentrations. It was assumed in
calculating the adjustment that the nitrogen
0.06
LOS ANGELES
1964-1965
PHOENIX
JAN. 1967-JUNE 1969
JAN. FEB. MAR. APR. MAY JUN. JUL. AUG. SEP. OCT. NOV. DEC.
0.01
Figure 3-1. Monthly variation of mean hourly oxidant concentrations for three selected
cities.
3-6
-------
0.20
0.16
E
a.
o
I-
<
-------
0.14 -
0.12 -
Z
o
— 0.10
UJ
(J
Z
8 0.06
Z
<
LU .
0.02
/ \ \ ST. LOUIS _
LOS ANGELES,
AUGUST 1964 AND 1965
HOUR OF DAY
0.30
Figure 3-3. Diurnal variation of mean hourly
average oxidant concentrations in Los
Angeles and St. Louis.
HOUR OF DAY
Figure 3-4. Diurnal variation of mean hourly
average oxidant concentrations in Philadelphia,
August 6-8, 1966.
Table 3-5. MONTHLY MEAN HOURLY AVERAGE OXIDANT CONCENTRATIONS ADJUSTED
FOR NITROGEN DIOXIDE FOR SELECTED SUMMER AND WINTER MONTHS, IN FOUR CITIES
Station
Los Angeles
Sacramento
Denver
St. Louis
Los Angeles
Sacramento
Denver
St. Louis
Month
(Summer)
July 1964
July 1965
July 1965
July 1964
(Winter )
Jan 1965
Jan 1965
Feb 1965a
Jan 1965
Mean concentration, ppm
Unadjusted
0.055
0.042
0.048
0.035
0.021
0.020
0.029
0.024
Adjusted
0.044
0.036
0.041
0.029
0.005
0.015
0.019
0.020
Calculated N02
interference,
%
20
14
15
17
76
25
35
17
a!2 days of data only.
similar to oxidant concentrations measured
by oxidant recorders.
In Figure 3-5, the monthly variation in
means of hourly average concentrations of
ozone are compared to analogous concentra-
tions of oxidants in Pasadena and in Los
Angeles. In Figure 3-6, the monthly variation
in means of the daily maximum hourly
averages are compared.
In Figure 3-7, hour-by-hour comparisons of
1-hour average ozone and oxidant concentra-
tions for Los Angeles and Pasadena are shown
for the month of July 1964. The line termed
"adjusted oxidant" shown in Figure 3-7 is
calculated from the following:
Adjusted oxidant = Ox - 0.2 NO2 + SO2
3-8
-------
Table 3-6. MONTHLY MEAN DAILY MAXIMUM 1-HOUR AVERAGE OXIDANT CONCENTRATIONS
ADJUSTED FOR NITROGEN DIOXIDE FOR SELECTED SUMMER AND WINTER MONTHS,
IN FOUR CITIES
Station
Los Angeles
Sacramento
Denver
St. Louis
Los Angeles3
Sacramento
Denver
St. Louis
Month
(Summer)
July 1964
Julyl965
July 1965
July 1964
(Winter)
Jan 1965
Jan 1965
Febl965b
Jan 1965
Mean concentration, ppm
Unadjusted
0.166
0.085
0.110
0.078
0.037
0.035
0.073
0.046
Adjusted
0.154
0.075
0.098
0.071
0.020
0.028
0.060
0.040
Calculated NO2
interference,
%
7
12
11
9
46
20
18
13
a9 days of data when NO2 measured at time of maximum hourly average oxidant
concentration.
b!2 days of data only.
a
0.09
0.08
^ 0.07
— 0.06
£; 0.05
z
u °-04
I 0.03
Z
< 0.02
LLJ
s
0.01
i r
lOXIDANT I
OZONE* I
OXIDANT t PASADENA
OZONE* ) ""AiAUtiNA
\
*OZONE DATA FOR SEPTEMBER-DECEMBER IS FROM 1964 ONLY
JAN. FEB. MAR. APR. MAY JUN. JUU. AUG. SEP. OCT. NOV. DEC.
MONTH
Figure 3-5. Comparison of the monthly variation in mean 1-hour average ozone and
oxidant concentrations in Los Angeles and Pasadena, 1964-1965.
where:
Ox = measured oxidant concentration
NO2 = measured nitrogen dioxide con-
centration
SO2 = measured sulfur dioxide concen-
tration
The specific equation required to calculate
this "adjusted oxidant" value will depend on
whether the KI instrument is equipped with
chromium trioxide scrubbers. In the case of
the California data shown in Figure 3-7, no
such scrubbers were used and both the posi-
tive effect of NO2 and the negative effect of
SO2 were considered in the calculation of
adjusted oxidant.
3-9
-------
l-
z
LU
u
o
u
0.24
0.22
0.20
0.18
0.16
0.14
0.12
0.10
0.08
0.06
0.04
0.02
I I I
2 and SC-2 response, Los Angeles and Pasadena,
July 1964.
3-10
-------
As previously noted, chromium trioxide
SO2 scrubbers have been used at CAMP
stations since 1964. Adjusted oxidant values
for the CAMP network, therefore, can be
calculated by subtracting solely the effect of
NO2. Thus, adjusted oxidant from the raw
CAMP data is calculated:
Adjusted oxidant =
where: Ox - 0.2 NO2 - 0.11 NO
Ox = measured oxidant concentration
NO2 = measured nitrogen dioxide con-
centration
NO = measured nitric oxide concentra-
tion
Specific values for the constants in the
above equation are dependent upon individual
instrument response. Therefore, calibration
with known quantities of interfering com-
pounds is suggested.
The close agreement between adjusted
oxidant and ozone concentrations indicates
that the contribution to oxidant measurement
by peroxyacetyl nitrate (PAN) or other oxi-
dants is very low. As will be discussed later,
PAN concentrations are usually much lower
than ozone concentrations.
The agreement between the unadjusted
oxidant and ozone concentrations is also
good. Adjusting for SO2 and NO2 did not
cause much change in the agreement between
the oxidant and ozone concentrations because
the response of the oxidant-recorder to NO2
was largely compensated by the opposite
response to SO2. If SO2 is not present, or if
scrubbers are used, the measured oxidant
concentrations will be higher than the ozone
concentrations by the amount of the response
toNO2-
2. Ozone Concentration Patterns
In a recent study made by the Research
Triangle Institute under contract to the Public
Health Service, the daily maximum 1-hour
average ozone concentration was recorded for
certain cities, and the number of days when
this daily maximum exceeded 100, 200, and
290 Mg/m3 (0.05, 0.10, and 0.15 ppm) is
reported in Table 3-7.6- 7 Table 3-8 lists the
mean 1 -hour average ozone concentrations by
hour for each city involved in the 1967
portion of the same study. Figure 3-8 shows
the diurnal patterns of 1-hour average ozone
concentrations experienced on 2 selected days
at the Denver and Philadelphia CAMP sites.
This graph illustrates the high levels of ozone
concentrations that have been reached.
D. CONCENTRATIONS OF
PEROXYACETYL NITRATE IN
THE URBAN ATMOSPHERE
Utilizing gas chromatographic techniques
with an electron-capture detector, PAN con-
Table 3-7. SUMMARY OF MAXIMUM DAILY 1-HOUR AVERAGE
OZONE CONCENTRATIONS FOR SELECTED CITIES 6
City
Cincinnati
Washington, D.C.
Denver
Los Angeles
Philadelphia
Time
period
9/15/67 to
9/29/67
10/3/67 to
10/16/67
10/1 7/67 to
11/1/67
8/10/68 to
10/11/68
11/2/67 to
11/19/67
6/1/68 to
7/31/68
Number
of days
of valid data
15
15
15
58
18
59
Number of days with at
least one hourly average
equal to or exceeding
0.05 ppm
7
3
7
51
16
47
0.10 ppm
2
0
1
11
14
21
0.15 ppm
0
0
1
1
5
3
Maximum
hourly average,
ppm
0.11
0.07
0.19
0.16
0.26
0.18
3-11
-------
Table 3-8. AVERAGE HOURLY OZONE CONCENTRATIONS IN SELECTED CITIES, 1967
(ppm)
Hour
0000
0100
0200
0300
0400
0500
0600
0700
0800
0900
1000
1100
1200
1300
1400
1500
1600
1700
1800
1900
2000
2100
2200
2300
Washington, D.C.
10/2-10/16
0.0032
0.0035
0.0036
0.0038
0.0031
0.0021
0.0010
0.0012
0.0032
0.0075
0.0142
0.0178
0.0274
0.0282
0.0277
0.0197
0.0130
0.0055
0.0019
0.0019
0.0021
0.0023
0.0024
0.0028
Denver
10/17-11/1
0.0055
0.0065
0.0077
0.0061
0.0053
0.0040
0.0018
0.0038
0.0108
0.0226
0.0292
0.0416
0.0444
0.0440
0.0369
0.0261
0.0178
0.0061
0.0043
0.0041
0.0039
0.0037
0.0037
0.0045
Cincinnati
9/15 - 9/29
0.0119
0.0096
0.0103
0.0091
0.0108
0.0066
0.0033
0.0041
0.0044
0.0078
0.0163
0.0270
0.0279
0.0338
0.0280
0.0271
0.0271
0.0232
0.0178
0.0162
0.0105
0.0110
0.0124
0.0122
Los Angeles
11/2-11/19
0.0052
0.0078
0.0079
0.0074
0.0075
0.0060
0.0051
0.0044
0.0067
0.0121
0.0383
0.0928
0.1204
0.1132
0.0872
0.0662
0.0238
0.0093
0.0048
0.0047
0.0046
0.0028
0.0021
0.0058
centrations were measured in Los Angeles
during September and October of 1965, by
the California Department of Public Health.7
Seven measurements per day were made for
each of 16 weekdays in September and 19
weekdays in October. The mean 1-hour aver-
age concentrations of PAN and oxidant by
hour of day for these periods are shown in
Figure 3-9. The measurements were made
near the downtown Los Angeles air-monitor-
ing station.
PHILADELPHIA 6-15-68
/DENVER 10-20-67
2-3 4-5 6-7 8-9 10-11 12-1 2-3 4-5 6-7
HOUR OF DAY
Figure 3-8. Diurnal variation of hourly ozone concentrations in Philadelphia and Denver.
3-12
-------
0.2C
0.18
AVERAGES:
19 WEEKDAYS, OCTOBER
16 WEEKDAYS, SEPTEMBER
HOUR OF DAY, PST
Figure 3-9. Variation of mean 1-hour average oxidant and PAN concentrations, by hour
of day, in downtown Los Angeles, 1965.
3-13
-------
Beginning in June 1966, measurements of
PAN have been made on the campus of the
University of California at Riverside using the
gas-chromatograph-with-electron-capture
method mentioned. Samples are usually col-
lected once each hour between 7:00 a.m. and
4:00 p.m., Pacific standard time. Other pollu-
tants are also measured at this station which is
operated by the Riverside Air Pollution Re-
search Center and supported by the Public
Health Service. In Figure 3-10, the mean
1-hour-average oxidant concentrations, as
measured with a Mast analyzer, and the mean
1-hour-average PAN concentrations are shown
by the hour of the day for the month of
September 1966. The monthly mean hourly
oxidant and PAN concentrations and the
monthly mean of the daily maximum hourly
average of 1 year's data are shown by month
in Figure 3-11.
The comparison shown in Figure 3-11 is a
good illustration of how specific averaging
processes affect results. The considerable
0 . 1 8 r
— 0.008 -,-
0.006 <
-0.004
- 0.002
HOUR OF DAY, PST
Figure 3-10. Variation of mean 1-hour
average oxidant and PAN concentrations,
by hour of day, at the Air Pollution Re-
search Center, Riverside, California,
September 1966.
variations in daily maximum hourly concen-
trations as a function of time of year become
much less obvious if the data include all
hours. As stated previously, the latter damp-
ing effect is the result of including in the data
those hours for which oxidant is necessarily at
or near zero. Since these near-zero hours
account for approximately 75 percent of the
time of sampling, they have the effect of
averaging out the elevated daytime values.
Each method of averaging has its purpose,
however, and subsequent interpretations of
the results require careful consideration.
In Figure 3-10, there are two daily maxima
for the oxidant and PAN concentrations. As
will be discussed, the second maximum is
probably due to the transport of pollutants
from Los Angeles to Riverside. The PAN
concentrations in Riverside are an order of
magnitude lower than those in Los Angeles,
while the concentrations of oxidants are of
the same order of magnitude.
E. METEOROLOGICAL FACTORS
1. General Discussion
In any given area, the concentration of
oxidant is dependent on many factors. Some
of these, such as the concentration ratio of
oxides of nitrogen to hydrocarbons, light
intensity, and the reactivity of hydrocarbons,
have been mentioned earlier. Other important
factors are the size of the area, the meteorol-
ogy, the topography, the number and distri-
bution of sources, and the rates of emis-
sions.8-1 °
These latter factors are important because
they affect the distribution of pollution over
a city. Concentrations of oxidant on the
upwind side of an area are substantially
different from concentrations downwind.
Oxidants may be transported many miles
beyond the source area under certain meteor-
ological and topographical conditions.10"12
These spatial variations in concentrations
make the location of air monitoring stations
of great importance if representative air pol-
lution data are to be collected for an area or
city.
3-14
-------
Q.
a
z*
o
z
UJ
o
z
o
u
X
o
z
<
UJ
MONTHLY MEANS OF DAILY MAXIMUM
1-hour AVERAGE CONCENTRATIONS
MONTHLY MEANS OF
CONCENTRATIONS
hour AVERAGE
*OXIDANT BY MAST, CONTINUOUS
24 hours; PAN BY PANALYZER,
SEQUENTIAL, 6 a.m. TO
4 OR 5 p.m. ONLY.
OXIDANT*
O —
JUN. JUL. AUG. SEP. OCT. NOV. DEC. JAN. FEB. MAR. APR. MAY JUN.
Figure 3-11. Monthly variation of oxidant and PAN concentrations at the Air
Pollution Research Center, Riverside, California, June 1-966-June 1967.
2. Transport
The transport of pollutants by wind in the
Los Angeles Basin has been the subject of
several studies.10> 13> 14 Most of the trajec-
tories enter the basin from the west and, in
general, surface winds are predominately from
the ocean to the land during the spring,
summer, and fall months.
To illustrate the eastward transport of
oxidant, the diurnal variation of mean hourly
average concentrations during October 1965,
in West Los Angeles, Los Angeles, Azusa, and
Riverside are shown in Figure 3-12. Data from
the first three stations are from the Los
Angeles County Air Pollution Control Dis-
trict, while data for the city of Riverside are
from the Riverside County Air Pollution
Control District.
The station at West Los Angeles is about 10
miles west, and Azusa is about 20 miles east,
of downtown Los Angeles. Riverside is about
30 miles east of Azusa. As shown, the time of
the peak oxidant concentrations follows those
in West Los Angeles by about 1 hour in Los
Angeles, 2 hours in Azusa, and 4 hours in
Riverside.
z
o
0.12
0.08
0.04
I I I I
1
WEST /
_LOS ANGELES .
—I— I -7-1
r
\.
I I I 1
•"•>»
\
\
\
1 1 1, 1
1 I
-
—
*T T ""
0.16
0.12
0.08
0.04
1 1 1 1 1 \f
DOWNTOWN /
_ LOS ANGELES *
/
— /
-f.r"r*t i i
-i i i
\
\
\
s
1 1 L
1 1
-
—
—
"~i "7~
UJ
( 1
z
o
(J
z
UJ
•s.
0.16
0.12
0.08
0.04
I 1 I I
~ AZUSA
— J
"i '\"T\
i i
/
/
/
/
i i
U. ' '
' \
\
\
\
i i i
i i
-
—
i ~"7 ""
0.16
0.12
0.08
0.04
1 1 1 1 1 1 1
RIVERSIDE *>*S
"")~"f1^l 1 1 1
rV ' '
\
\
X,^
1 1 1
1
—
-
-]^
HOUR OF DAY, PST
Figure 3-12. Diurnal variation of mean 1-hour
average oxidant concentrations at selected
California sites, October 1965.
3-15
-------
Oxidant concentrations at Riverside exhib-
ited a double peak, as did the data on PAN
and oxidant measured at the University of
California at Riverside (Figure 3-10). The first
peak at about 11:00 a.m. is attributed to
pollutants generated at or near Riverside,
while the peak at 4:00 p.m. is attributed to
pollutants transported from the large and
more densely populated Los Angeles metro-
politan area.
As shown in Figure 3-13, which is a plot
for carbon monoxide analogous to Figure
3-12, the afternoon peak concentration of
carbon monoxide in Riverside is much smaller
than the morning peak in Los Angeles. This
suggests that the polluted air mass was diluted
as it moved eastward to Riverside. On the
other hand, the afternoon oxidant peak con-
centrations in Riverside were about as high as
the peak concentrations in Los Angeles. It is
possible, therefore, that, as the polluted air
mass moved eastward, the oxidants continued
to be formed at a rate about as great as the
rate of dilution. It is also just as probable that
the second peak at Riverside represents oxi-
dant contributions from local as well as
distant sources.
On the average, the direction of flow of
surface wind and of pollutant transport
appear to coincide, but they are not the only
meteorological factors responsible for the
transport of pollutants. Bell's appraisal of
hour-by-hour development of oxidant con-
centrations indicates that other mechanisms,
such as turbulence and downward motions
created mechanically by airflow through
mountain gaps, were also responsible for
pollutant transport.11
On some days, as observed by Stephens,
the polluted air mass from the Los Angeles
metropolitan area is defined by a sharp
boundary which may not extend as far as
Riverside.15 The reason for this sharp bound-
ary, Stephens postulates, is that the tempera-
ture profile at the front of the air mass
increased to the adiabatic lapse rate. At this
point, rapid vertical ventilation had begun.
24.0
20.0
16.0
12.0
/*
Q.
°- 20.0
Z 16.0
0
H 12.0
2 ~
h- 0
Z
u 12'°
O 8.0
U
z 4-°
1 1 1 I 1 1 1 1 1 1 1
A WEST -. _
^LOS ANGELES > X
- ( 1 1 1 1 1 1 1 1 1 1 7
1 1 ^^ 1 1 1 1 1 1 !
DOWNTOWN
— LOS ANGELES —
" i i i i i i i i i i i 7
•.' 1 1 | 1 1 1 1 — L —i —1 _,
_ AZUSA _
1 1 1 1 1 1 1 1 1 1 |
z.u
8.0
4.0
1 1
_
_ **-
1 I
1 1 1 1 1 1 1 1 1
^"V *••• """"" "—" "^ ^s>~
N-— ' RIVERSIDE
1 1 1 1 1 1 1 1 1
12 2
8 10 12
K-
6 8 10 12 2 4
a.m »^4
HOUR OF DAY, PST
Figure 3-13. Diurnal variation of mean 1-hour
average carbon monoxide concentrations at
selected California sites, October 1965.
The prevailing winds are not always west-
erly. Under some meteorological conditions
described by Bell,11 pollutants from Los
Angeles have been transported out to sea and
then southward to Oceanside14 and even to
San Diego, a distance of over 100 miles.
Under other conditions, pollutants have been
transported from the sea northward to Ven-
tura and Santa Barbara Counties.16> 17
Preliminary data from a SCAN station
recently established in Santa Cruz, California,
indicate that a similar phenomenon may
occur in the region of the San Francisco -
Oakland metropolitan area. Under certain
conditions, pollutants from the metropolitan
area are transported out to sea and then
brought back to shore by the local sea breeze
to Santa Cruz, about 50 miles south. On these
occasions, the hourly average oxidant con-
centrations have been as high as from 240 to
3-16
-------
350 jug/m3 (0.12 to 0.18 ppm) in Santa Cruz.
The very low concentrations of oxides of
nitrogen and hydrocarbons measured during
these occasions again suggest substantial oxi-
dant formation in spite of high dilution.
3. Monitoring Station Location
Of the many air monitoring programs that
measure oxidant values, the network opera-
tion of the Los Angeles County Air Pollution
Control District has provided the most exten-
sive experience. Determination of the number
of sites and selection of the locations was
regarded by its designers as one of the most
important factors in planning a continuing air
quality survey.1 8 From the early 1950's until
July 1955, 14 stations were maintained. The
locations of the 14 stations were selected on
the basis of surface wind trajectories, popula-
tion, and industrial concentrations. On the
average, each station covered an area of about
70 square miles.
After evaluation of the data obtained
during 1957 and 1965, it became apparent
that fewer permanent stations strategically
located in the most frequent pattern of the
smog masses could achieve adequate warning
of hazardous pollution levels. Subsequently,
the number of stations for this purpose was
reduced to six.
The Bay Area Pollution Control District
also has a network of air monitoring stations.
Examination of their data and data of the Los
Angeles County Air Pollution Control District
shows that average oxidant concentrations are
not uniform throughout a metropolitan area.
In the Los Angeles Metropolitan Area
during July 1965, for example, the mean of
the daily maximum 1-hour average oxidant
concentrations was 430 jug/m3 (0.22 ppm) at
Burbank, 470 Mg/m3 (0.24 ppm) at Pasadena,
and 510 jug/m3 (0.26 ppm) at Azusa. On the
other hand, in the city of Los Angeles, which
is southerly and adjacent to both the Burbank
and Pasadena stations, this mean was 270
Mg/m3 (0.14 ppm). At North Long Beach,
south of and adjacent to Los Angeles, it was
120ng/m3 (0.06 ppm).
Thus, the data from a single CAMP or
SCAN station may be indicative only of the
concentrations in the immediate area where it
is located. In order to determine the local
variation in air quality throughout an urban
area, a complete air sampling network is
necessary.
F. SUMMARY
Examination of the aerometric data from
several major U.S. cities indicates in all cases
the presence of photochemically formed oxi-
dants. This is not an unexpected finding since
the precursor reactants, hydrocarbons and
oxides of nitrogen, are inevitable by-products
of current technology.
On a concentration basis, ozone has been
identified as the major observed component
of elevated oxidant levels. Demonstration of
this fact, however, can be a most difficult
task. One of the difficulties arises because the
oxidant measuring method in common use is
nonspecific and subject to several interfer-
ences, although it is true that the major
atmospheric components which cause these
interferences have been identified and thus
can be given appropriate consideration. Never-
theless, the inherent danger of oxidant con-
centration artifacts must be borne in mind.
A complicating feature of oxidants is the
fact that their appearance in the atmosphere
is dependent on chemical reactions, and they
occur, therefore, later in time than their
precursor reactants. These chemical reactions
are dependent on such variables as sunlight
intensity, duration of sunlight, and tempera-
ture, in addition to variables affecting atmo-
spheric dilution and dispersion. As a result,
relationship between precursor emissions and
atmospheric oxidant concentrations is much
less direct and more difficult to quantify than
is the case in the study of primary pollutants.
The second class of photochemical oxi-
dants, peroxyacyl nitrates, has not been rou-
tinely measured, although they have been
identified in the atmosphere of several cities.
These hydrocarbon peroxy derivatives have
been shown to be intimately related to
atomospheric photochemical ozone formation
3-17
-------
and therefore can be assumed to be present
whenever oxidant levels are elevated.
By analysis of oxidant concentration data
for 4 years at 12 stations, the daily maximum
1-hour-average concentration was shown to be
equal to or exceeded 290 Mg/m3 (0.15 ppm)
up to 41 percent of the time; the maximum
1-hour-average concentrations ranged from
250 to 1,140 Mg/m3 (0.13 to 0.58 ppm), with
short-term peaks as high as 1,310 jug/m3 (0.67
ppm); yearly averages for a 2-year period
ranged from 370 to 820 jug/m3 (0.19 to 0.42
ppm). Yearly averages are not representative
of air quality with respect to oxidant pollu-
tion, however, because the 1-hour-average
ozone concentration will necessarily be at or
about zero for approximately 75 percent of
the time, when photochemical reactions are
minimal.
At four stations, maximum 1-hour-average
ozone concentrations ranged from 140 to 510
Mg/m3 (0.07 to 0.26 ppm) in various studies.
Adjusted oxidant and ozone concentration
values are usually relatively the same.
G. REFERENCES
1. Ak Quality Data from the National Air Sampling
Network and Contributing State and Local Networks,
1966. Division of Air Pollution. Cincinnati, Ohio. 1967.
2. Data obtained from appropriate local agencies in Cali-
fornia.
3. Data obtained from Maricopa County Health Dept.
Phoenix, Arizona.
4. Larsen, R. I. A New Mathematical Model of Air
Pollutant Concentration Averaging Time and Frequency.
J. Ak Pollution Control Assoc. 79:24-30, January 1969.
5. Station Operator's Bulletin. Public Health Service.
Memorandum 2-65. April 23, 1965.
6. Richter, H. G., J. R. Smith, and L. A. Ripperton.
Chemiluminescent Ozone Measurement Program - Ozone
Total Oxidant Relationship in Ambient Ak. Research
Triangle Institute. 1968.
7. Mayisohn, H. and C. Brooks. The Analysis of PAN by
Electron Capture Gas Chromatography. Presented at
Western Regional Meeting of the American Chemical
Society. Los Angeles. November 18, 1965.
8. Schuck, E. A., J. N. Pitts, and J. K. Swan. Relationships
between Certain Meteorological Factors and Photochem-
ical Smog. Int. J. Ak Water Pollution. 70:689-711,1966.
9. Smith, M. E. The Concentrations and Residence Times
of Pollutants in the Atmosphere. In: Chemical Reactions
in the Lower and Upper Atmosphere. New York,
Interscience Publishers, 1961. p. 155-166.
10. Neiburger, M. What Factors Determine the Optimum
Size Area for an Ak Pollution Control Program. In:
Proceedings of the 3rd National Conference on Air
Pollution, December 12-14, 1966. Washington, D. C.
PHS Publication Number 1649. 1967. p. 442449.
11. Bell, G. B. A Study of Polluted Transport Due to Surface
Winds in Los Angeles, Orange, Riverside and San
Bernardino Counties. California Dept. of Public Health.
Berkeley. December 1959.
12. Middleton, J. T. and A. J. Haagen-Smit. The Occurrence,
Distribution and Significance of Photochemical Ak
Pollution in the United States, Canada and Mexico. J.
Ak Pollution Control Assoc. 77:129-134, March 1961.
13. Neiburger, M. and J. G. Edinger. Summary Report on
Meteorology of The Los Angeles Basin with Particular
Respect to the "Smog" Problem. Vol. I. Ak Pollution
Foundation. Los Angeles, Calif. Report Number I. April
1954.54 p.
14. Neiburger, M., N. A. Renzetti, and R. Tice. Wind
Trajectory Studies of the Movement of Polluted Ak in
the Los Angeles Basin. Vol. 2. Air Pollution Foundation.
Los Angeles, Calif. Report Number 13. April 1956. 74 p.
15. Stephens, E. R. Temperature Inversions and the Trap-
ping of Ak Pollutants. Weatherwise. 7 5(4): 172-175,
August 1965.
16. Meteorological Conditions During Oxidant Episodes in
Coastal San Diego County in October and November,
1959. California Dept. of Public Health. Berkeley. May
22,1960.
1,7. Faith, W. L., G. S. Taylor, and H. W. Linnard. Ak
Pollution in Ventura County. California Dept. of Public
Health. Berkeley. June 1966.
18. Ak Quality of Los Angeles County. Volume II. Los
Angeles County Ak Pollution Control District. Los
Angeles. Technical Progress Report. February 1966.
3-18
-------
Chapter 4.
NATURAL SOURCES OF OZONE
A. INTRODUCTION
In order to make full use of aerometric
data, it is necessary to know the relative
magnitude of that portion of a pollutant's
concentration which arises from nontechno-
logical sources, often termed "background
concentration." Such background concentra-
tion of an air pollutant represents an impor-
tant factor in air pollution control, since it is
a concentration which will persist even if all
technological sources are eliminated. It is
necessary to emphasize, however, that even in
those cases where measurable natural emis-
sions are considered relatively substantial,
their contribution to current urban back-
ground concentrations is only a very small
percentage of the total measure of ambient air
quality. This is particularly the case with
ozone, as indicated in this chapter. The largest
natural source of ozone is the upper atmo-
sphere, and a process of migration is therefore
necessary in order to affect ground level air
quality.
B. NATURAL SOURCES OF OZONE
Ozone can be formed naturally by electri-
cal discharge. The electrical energy available
from the atmosphere, however, is inadequate
to form significant ozone concentrations over
a large metropolitan area. Calculations reveal
that in urban atmospheres the concentrations
of ozone available from power-loss energy are
several orders of magnitude less than 20
Mg/m3 (0.01 ppm).1 Such a natural source of
ozone, therefore, does not account for the
high concentrations found in urban atmo-
spheres.
Ozone is also formed naturally by the
action of solar radiation in the stratosphere at
altitudes of from 15,000 to 37,000 meters
(50,000 to 120,000 feet). At these altitudes,
ultraviolet radiation of wavelengths less than
2,450 A causes oxygen molecules to photo-
lyze to atomic oxygen. The oxygen atoms
then combine with oxygen molecules in the
air to form ozone.
The total amount of ozone in the upper
atmosphere, as measured spectrographically,
has been found to vary between 2 and 4
millimeters.2 The unit "millimeter of ozone"
is the thickness the ozone layer would have if
it were compressed at 1 atmosphere of pres-
sure; 2 to 4 millimeters is equivalent, there-
fore, to between 490 and 980 Mg/m3 (0.25 to
0.50 ppm) for uniform distribution through a
constant density atmosphere. Maximum
ozone concentrations occur at altitudes of
about 20 kilometers (12 miles)
The unit "centimeter of ozone per kilo-
meter" (cm/km) also is used to express ozone
concentrations determined spectrographically.
Maximum ozone concentrations as high as
0.02 cm/km occur at altitudes of about 20
kilometers (12 miles).2 At this altitude, the
pressure is about 44 mm Hg. The concentra-
tion of 0.02 cm/km in terms of ppm is:
0.02 cm/km x 1CT5 km/cm x 106 =0.20 ppm
If compressed with ozone-free air to sea level
pressure, this concentration would be 390
Mg/m3 (0.20 ppm).
C. OZONE TRANSFER
Several explanations have been offered for
the manner in which ozone is transferred
from the upper atmosphere to the lower
troposphere.2 • 3 The transfer apparently
occurs in the vicinity of the jet stream and in
weather-frontal zones. It is also postulated
that such a transfer occurs directly across the
tropopause region. The concentrations trans-
ferred to ground level, however, are not
4-1
-------
believed to be high. Stable air systems, includ-
ing temperature inversions, serve as barriers to
the descent of stratospheric ozone. In the
troposphere, ozone is destroyed by chemical,
photochemical, and catalytic reactions; clouds
and combustion gases rapidly dissociate
ozone.
In the early 1950's, it was believed that
stratospheric ozone was a significant source of
surface ozone.4' s Several investigators have
reported concentrations of ozone or of oxi-
dant up to a few-tenths of a ppm in nonurban
areas.5'7
It is now considered, however, that it is not
possible to attribute high concentrations sole-
ly to natural sources with certainty, and that
limitations in methodology may have contri-
buted to the high readings.7 In agreement
with those who postulate that high concentra-
tions of stratospheric ozone do not reach
ground level, certain researchers have found
very little ozone at some remote sites. In
general, it can be said that oxidant concentra-
tions in remote areas range from less than 20
to about 100 Mg/m3 (0.01 to 0.05 ppm), with
most of the measurements falling between 20
and 60 Mg/m3 (0.01 and 0.03 ppm). The
proportion of these ozone concentrations
which is due to transport from the strato-
sphere and the proportion which is due to
transport from urban areas is uncertain. But,
in any case, stratospheric ozone alone cannot
account for the high concentrations found in
urban atmospheres.
Ozone and oxidant concentrations have
been measured in a variety of nonurban
locations. The reported results of a number of
these studies are discussed in this section.
In Greenland in July 1960, a maximum
concentration of 25 Mg/m3 (0.013 ppm) was
reported.8 In the Antarctic, the mean
monthly surface ozone values from April
1957 to May 1958 ranged from 20 to 67
Mg/m3 (0.01 to 0.034 ppm).9 Measurements
obtained at a French station in the Antarctic,
from February 14, 1958 to January 15, 1959,
indicated that daily mean concentrations dur-
ing the months of September and October
4-2
were almost tenfold higher than those of
April and May.10 At the Amundsen-Scott
station located at the geographical South
Pole, ozone was measured using the chemi-
luminescent method of Regener from 1961
through 1964, and using the Mast method
during 1963 and 1964. The monthly mean
averages were from about 40 to 80 Mg/m3
(0.02 to 0.04 ppm) by the former method,
and from 20 to 60 Mg/m3 (0.01 to 0.03 ppm)
by the latter.11 Haagen-Smit, using the rub-
ber-cracking method, reported concentrations
of from 0 to 60 Mg/m3 (up to 0.03 ppm) in
the beach and desert regions of California.12
From December 1962 to August 1964,
ozone concentrations were measured using
balloonborne chemiluminescent ozonesondes
at network stations of the Air Force Cam-
bridge Research Laboratories.13 Of 867
soundings .up to pressure levels of 500 milli-
bars (18,280 feet or 5,570 meters at standard
atmospheric conditions), 14 percent had max-
imum ozone concentrations greater than
about 100 Mg/m3 (0.05 ppm) and 0.7 percent
had maximum ozone concentrations greater
than about 200 Mg/m3 (0.10 ppm). The
concentration of 100 Mg/m3 (0.05 ppm) was
exceeded most frequently at stations near
large cities. The 200 Mg/m3 (0.10 ppm)
concentration was exceeded at two stations
only, near Bedford, Massachusetts, and
Seattle, Washington.
When oxidants were measured at the
Petawawa Forest, Chalk River, Ontario, the
daily average concentration varied from slight-
ly under 20 Mg/m3 (0.01 ppm) to slightly over
80 Mg/m3 (0.04 ppm).14 Measurements were
made over a period of years using both the
rubber-cracking method and a Mast meter,
and the highest concentration encountered
was 120 Mg/m3 (0.06 ppm) for 4 hours.
Observed diurnal fluctuations revealed that
oxidant values at night were usually less than
20 Mg/m3 (0.01 ppm), increasing in the
morning hours to a peak around noon of 60
Mg/m3 (0.03 ppm), and then again dropping
in the evening hours. From June 1, 1965,
through August 13, 1965, measurements of
-------
a 15-minute duration were made 24 hours a
day. A total of 6,865 measurements were
made. The mean concentration was 22 Mg/m3
(0.011 ppm), and the maximum instantaneous
reading was 120 Mg/m3 (0.06 ppm). The
cumulative frequency distribution of the con-
centrations measured in this study is shown in
Figure 4-1.14
Using Mast analyzers, Berry determined the
oxidant concentrations in valleys and on
mountain tops in the Southern Appala-
chians.1 5 At one valley location, there was a
strong diurnal variation, with a highest con-
centration of 80 Mg/m3 (0.04 ppm) at about 2
p.m. Minimum concentrations, about 29
Mg/m3 (0.015 ppm), occurred during the late
evening and early morning hours. At other
locations, the average oxidant concentrations
generally ranged between 20 and 60 Mg/m3
(0.01 and 0.03 ppm).15 At Green Knob,
North Carolina, 2,394 instantaneous readings
were made every 15 minutes from June 15,
1952, through July 11, 1962. The mean
concentration was 33 Mg/m3 (0.017 ppm), the
maximum instantaneous reading was 140
Mg/m3 (0.07 ppm), and the standard deviation
was 16 Mg/m3 (0.00790 ppm). At Pocahontas
County in West Virginia, similar measure-
ments were made from June 6 through July 6,
1961. Of 2,880 instantaneous measurements,
the mean was 49 Mg/m3 (0.025 ppm), the
maximum was 125 Mg/m3 (0.064 ppm), and
the standard deviation was 28 Mg/m3 (0.01475
ppm).16
In the summary of data by Junge, most of
the ground-level concentrations reported were
also in the range of about 20 to 60 Mg/m3
(0.01 to 0.03 ppm).17 Spectrographic deter-
minations indicate that, at surface level, the
ozone concentrations range from 0 to 0.0004
cm/km (80 Mg/m3, or 0.04 ppm).2
D. SUMMARY
Ozone can be formed naturally in the
atmosphere by electrical discharge. Ozone is
also formed in the stratosphere by the action
of solar radiation, with maximum concentra-
tions occurring at altitudes of about 20
kilometers (12 miles). These processes are not
capable of forming significant concentrations
at ground level over a large metropolitan area
and thus do not account for the high con-
centrations of ozone found in some urban
atmospheres. Maximum instantaneous ozone
levels of from 20 to 100 Mg/m3 (0.01 to 0.05
ppm) have been recorded in nonurban areas.
0.06
o.os
b
Q.
0.04
< 0.03
z
LU
u
-z.
o
(J
0.02
0.01
N = 6868
MEAN =0.0114
STD DEV =0.0102
MEDIAN =0.0125
0
0.01
0.1
1 5 10 20 30 40 50 60 70 80 90 95
PERCENT LESS THAN STATED CONCENTRATION
99
99.9
99.99
Figure 4-1. Cumulative frequency distribution of average 15-minute ozone concentrations
at Chalk River, Canada, June 1 to August 13, 1965.14
4-3
-------
E. REFERENCES
1. Ozone in the Lower Atmosphere. Stanford Research
Institute. American Petroleum Institute. New York.
Technical Report Number 1. September 8, 1953. 24 p.
2. Gotz, F. W. P. Ozone in the Atmosphere. In: Com-
pendium of Meteorology, Malone, T. F. (ed.). Boston,
American Meteorology Association, 1951. p. 275-291.
3. Paetzold, H. K. The Photochemistry of the Atmospheric
Ozone Layer. In: Chemical Reactions in the Lower and
Upper Atmosphere. New York, Interscience Publishers,
1961. p. 181-195.
4. Volz, F. On the Destruction of Ozone in the Tropo-
sphere [Uber die Zersfrorung des Ozons in der Tropo-
share]. Zericte, 55:257, 1952.
5. Bartel, A. W. and J. W. Temple. Ozone in the Los
Angeles and Surrounding Areas. Ind. Eng. Chem.
44:857-861, April 1952.
6. Leighton, P. A. Photochemistry of Air Pollution. New
York, Academic Press, 1961. 300 p.
7. Harrison, W. K. and J. P. Lodge. Some Measurements of
Oxidant Levels of Remote California Sites. Ind. and Eng.
Chem., 44:857,1952.
8. McKee, H. C. Atmospheric Ozone in Northern
Greenland. J. Air Pollution Control Assoc. 77:562-565,
December 1961.
9. Odishaw, H. International Geophysical Year. Science.
129 (3340): 14-25, January 2, 1959.
10. Vassy, A. and A. Rouhani. Concentration of Ozone at
the Soil Level of Adelie Coast [Concentration de 1'Ozone
au Niveau du Sol a la Terre Adelie]. C. R. Acad. Sci.
(Paris). 250(2): 380-382, January 11,1960.
11. Aldaz, L. Surface Air Radioactivity and Ozone at
Amundsen-Scott Station (90 ), Antarctica. Nature.
275(5102):722-723, August 12,1967.
12. Haagen-Smit, A. J. Chemistry and Physiology of Los
Angeles Smog. Ind. Eng. Chem. 44:1342-1346, June
1952.
13. Lea, D. A. Vertical Ozone Distribution in the Lower
Troposphere Near an Urban Pollution Complex. J.
Applied Met. 7:252-267,1968.
14. Data obtained from Canada Department of Forestry and
Rural Development, Ottawa, Summer 1967.
15. Berry, C. R. Differences in Concentrations of Surface
Oxidant Between Valley and Mountaintop Conditions in
the Southern Appalachians. J. Air Pollution Control
Assoc. 74:238-239, June 1964.
16. Data obtained from Southeastern Forest Experiment
Station. AsheviUe, N.C. September 1967.
17. Junge, C. E. Air Chemistry and Radioactivity. Vol. 4.
International Geophysics Series, Mieghem, J. (ed.). New
York, Academic Press, 1963. 382 p.
4-4
-------
Chapter 5.
MEASUREMENT OF OXIDANTS, OZONE, AND
PEROXYACETYL NITRATE IN AMBIENT AIR
A. INTRODUCTION
Total oxidants in the air may be defined as
those compounds that will oxidize a reference
material which is not capable of being oxi-
dized by atmospheric oxygen. Methods for
measuring oxidants, therefore, involve expos-
ing an oxidizable substance to a sample of
ambient air and determining the degree of
oxidation which has occurred. There are
many such methods, each one being depen-
dent upon the reference substance chosen.
Two widely used methods of determining
the degree of oxidation are colorimetric and
coulometric analysis of the iodine released by
atmospheric oxidants from a potassium iodide
(KI) solution. Since these methods are the
most widely used, they will be discussed in
greater detail.
It should be recalled that:
1. Ambient air contains a mixture of
oxidizing and reducing compounds-
ozone, nitrogen dioxide, peroxyacetyl
nitrate (PAN), sulfur dioxide, hydro-
gen sulfide, aldehydes, unsaturated
hydrocarbons, and others.
2. The concentrations of these com-
pounds may be constantly varying
within relatively wide limits-from 0
to 1 ppm.
Since reducing compounds in air have an
opposite effect on the reference material
that is, cause a decrease in the degree of
oxidation observed the result obtained by
these KI methods is a "net" oxidant value
rather than a total one unless empirical
corrections are made.1 Thus the net value
describes a condition of the air, rather than a
specific compound concentration. For this
reason, concentrated efforts are being made
by researchers to obtain measurements for
each specific oxidant present. Hopefully these
efforts will enable air pollution scientists to
better define this atmospheric "condition."
Most oxidant data which have been col-
lected are net determinations, and a high
correlation between these values and other
pollutant levels has been observed.2 Conse-
quently until the more promising methods
become routinely available net determina-
tion must serve as indicators of total oxidant
levels. Oxidant measurement parameters are
discussed in detail in Chapter 3.
It snould be emphasized that in studies
seeking a better evaluation of health effects, it
is essential that data be obtained for indi-
vidual oxidants, such as nitrogen dioxide,
ozone, PAN, formaldehyde, acrolein, and
organic peroxides, rather than data on total
oxidants. Instrumentation currently available
permits the accurate measurement of atmo-
spheric ozone, nitrogen dioxide, and PAN. A
further essential need exists to develop instru-
mentation capable of measuring the other
individual gaseous pollutants which have the
properties of oxidants.
Photochemical reactions and other prob-
lems derived from oxidants can be much
better defined using specific methods for
measurement of nitrogen dioxide and ozone,
in preference to the traditional methods for
determination of total oxidants.
B. REFERENCE METHOD FOR MEASURE-
MENT OF TOTAL OXIDANTS
Because of the complexity and variety of
the methodology involved in oxidants deter-
mination, it has become necessary to adopt
5-1
-------
one reference method for use in comparisons
between techniques. The most widely used
method for this purpose is the neutral-
phosphate-buffered KI colorimetric technique
described by Saltzman.3 In this method,
oxidants are absorbed in neutral buffered 1
percent KI aqueous solution and the liberated
tri-iodine ion is measured colorimetrically at
3,520 A. Since one mole of ozone theoreti-
cally liberates one mole of iodine from this
solution, the iodine measured is directly
related to the concentration of ozone present
in the air sample. Results may thus be
expressed directly as equivalent volumes of
ozone.
At present, there is no satisfactory means
of testing this theoretical reaction. There is
evidence that the amount of tri-iodine ions
liberated by ozone is dependent on the design
of the gas bubbler and on the phosphate
concentration at neutral pH. Nevertheless, the
error of measurement produced as a result of
neglecting to account for the above variables
is estimated to be no larger than ± 10 percent
of the true value. Since ozone is believed to
be the principal oxidant present in the atmo-
sphere, this reference method has been adop-
ted by NAPCA. A reference method in which
the stoichiometry depends on fewer variables
is, however, needed.
In addition to serving as a manual pro-
cedure for determining oxidants, the refer-
ence method may be used in conjunction with
a "dynamic calibration" technique for instru-
mental methods, as follows: By passing
scrubbed clean air over an ultraviolet lamp at
a constant rate, ozone is generated at a
constant rate. Analysis of the effluent with
both the bubbler reference method and the
particular system to be tested makes it pos-
sible to calibrate the various methods against
this constant ozone source, and to express the
results obtained as "ozone concentrations."
Since some instruments use different color-
imetric techniques which require static liquid
calibrations, comparisons of these liquid
standards may be made using such a dynamic
system. A diagram of the procedure is shown
in Figure 5-1.
5-2
As a manual procedure for the determina-
tion of oxidants in the atmosphere, the
neutral-buffered KI technique is useful if
analysis is completed immediately after sam-
pling. Rapid analysis is necessary because the
iodine-color deteriorates with time. Concen-
trations of oxidant in a range from about 20
to 19,600 Mg/m3 (0.01 to 10 ppm) can be
determined using this method, although the
accuracy for concentrations below 100 ng/m3
(0.05 ppm) is compromised because of the
cumulative errors of sampling and analysis.
C. METHODS FOR MEASUREMENT OF
TOTAL OXIDANTS
1. Continuous Methods Utilizing Potassium
Iodide
a. Colorimetric
Continuous analysis of total oxidants is
most commonly accomplished with instru-
mentation using a 10 to 20 percent solution
of neutral—buffered potassium iodide as the
absorbing medium. In devices using a color-
imetric method sample air is passed at a
known rate through a liquid absorbing reagent
with a vacuum-pump arrangement. Oxidants
in contact with the KI react to free iodine and
the tri-iodine ion. These are determined color-
imetrically in a continuous flow colorimeter
at 3,520 A. The continuous instrumental
method is extremely sensitive to oxidizing
substances and is suitable for determinations
from 0 to 1,000 Aig/m3 (0 to 0.5 ppm) ozone
with an accuracy similar to the KI reference
method. The negative interference caused by
sulfur dioxide is often reduced by passing the
air sample over chromium trioxide (CrO3)
scrubbers, but this technique has not been
entirely successful, primarily because the
effects of humidity on scrubber systems often
render them ineffective.3 As discussed in
Chapter 3, these scrubber systems also con-
vert a portion of the ambient NO to NO2,
thus necessitating an additional correction
factor. Despite these drawbacks, CrO3 scrub-
bers remain the most generally used technique
for removing SO2 interferences; they are
particularly useful for this purpose during
periods of high SO2 concentrations. Never-
-------
ROTAMETER
(20 liter/min.)
rf
TANK AIR
SOURCE CHARCOAL
FILTER
OZONE
GENERATOR
TO INSTRUMENT OR
METHOD TO BE USED
TO Kl BUBBLERS
WITH VACUUM
ROTAMETER
(1 liter/min.)
Figure 5-1. Schematic of dynamic calibration of ozone measuring techniques.
theless, better methods for eliminating SO2
interference are critically needed.
b. Coulometric
A coulometric method, commonly referred
to as Mast-analysis, is also widely used for
measurement of oxidants. In devices using
this technique, sample air is passed in a
manner similar to the colorimetric type of
instrument into an electrolytic detector-cell
containing KI.4 The free iodine liberated by
the oxidants is reduced at the cathode of the
cell, causing a current flow through an exter-
nal circuit. The current flow is proportional
to the amount of iodine liberated, and. in
turn, to the oxidants entering the solutions.
The current is measured with a microammeter
which is usually calibrated directly in pphm
of ozone.
A method utilizing this technique for the
continuous measurement of total oxidants has
been prepared for collaborative testing by the
Intersociety Committee on Manual of Air
Sampling and Analysis.5
c. Colorimetric versus Coulometric Methods
Since these are the types of instruments
which are the most widely used for oxidant
measurements, there have been studies con-
ducted comparing the results obtained with
the colorimetric and coulometric approaches.
Field comparisons of measurements from
colorimetric and coulometric oxidant
analyzers, where readings did not exceed 390
/jg/m3 (0.20 ppm) and corrections were made
for NO2 interferences, indicate that differ-
ences are no greater than would be expected
if two colorimetric-type instruments were
working side-by-side.6 Comparative data,
including readings greater than 390 jug/m3
(0.20 ppm), show a correlation coefficient of
0.87 between readings of the two different
instruments, both calibrated with respect to
5-3
-------
known ozone-streams.7 In spite of the rela-
tively good correlation obtained in this study,
there were some instances when the agree-
ment between the two methods was poor. To
resolve some of these discrepancies, more
comparative studies of this type are needed.
Perhaps the largest variations between the
two methods are related to the differences in
reagent formulation. Generally, 10 to 20
percent KI solutions are used in colorimetric
instruments; at these concentrations, response
to nitrogen dioxide is higher than at the 2
percent level used with coulometric instru-
ments. Results of several studies are shown in
Table 5-1. Analyzers utilizing other principles
of detection vary in their sensitivity to nitro-
gen dioxide. As shown in Table 5-1, the
coulometric cell analyzers register about 10
percent of the nitrogen dioxide concentration
as ozone, and the U. V. photometer device
shows the least interference from nitrogen
dioxide.
Studies comparing the two methods indi-
cate that both instruments must be checked
and calibrated frequently and that variations
are usually caused by changes occurring in the
airflow or reagent flow and by interfering
compounds. Table 5-2 gives some indication
of the reliability of the continuous color-
imetric oxidant analyzers used at seven Cali-
fornia stations. These analyzers are dynami-
cally and statically calibrated about twice a
Table 5-1. EFFECT OF NITROGEN DIOXIDE ON OXIDANT DETERMINATION IN
THE ABSENCE OF OZONE
Range of NO2
concentration in aii,a
ppm
> 0 to 36
1.5 to 5.5
2.0
> Otol
0.24 to 0.43
2.0
2.0
Method
1% KI, pH 7
bubbler
2% KI, pH 7
bubbler
10% KI, pH 7
contact column
20% KI, pH 7
contact column
20% KI, pH 7
contact column
coulombic cell
U.V. photometer
N02
concentration
(as ozone),
%
8 to 11
6.4
21
30
12 to 47
(average: 25)
10
2
Reference
8
9
7
8
10
7
7
aBased on 4-liter sample.
Table 5-2. CALIBRATION STABILITY OF COLORIMETRIC OXIDANT MONITORING STATIONS,
STATEWIDE CONTINUOUS AIR-MONITORING NETWORK, CALIFORNIA,
SEVEN STATIONS, 1963 to 1965
Change from previous
calibration, %
± 0 to 10
±11 to 20
±21 to 30
±31 to 40
Number of
stations
7
4
2
2
Occurrences
Number
20
7
3
2
% of total
62.3
22.0
9.4
6.3
-------
year. The percentage of change from the
previous calibration indicates the uncertainty
in measurements obtained during the time
between calibrations. Table 5-2 shows that 62
percent of the time there was less than a 10
percent change, and 78 percent of the time
there was less than a 20 percent change.
Changes greater than 20 percent occurred at
three of the seven stations, which indicates
that some stations provide more reliable data
than others.
2. Other Methods - Intermittent Sampling
a. Ferrous Ammonium Sulfate
The ferrous ammonium sulfate measure-
ment technique is in use on an experimental
basis by NAPCA because of its possible
application to intermittent sampling by the
gas sampling network. This method is based
on the conversion of the ferrous ion by
oxidation to the ferric ion. Samples of ambi-
ent air are drawn through an acidified ferrous
ammonium sulfate solution. The ferric ion
formed in the collection solution is com-
plexed in the laboratory with ammonium
thiocyanate, and the resultant color is mea-
sured on a spectrophotometer. The oxidized
solution is stable after sampling and can be
analyzed later. Depending on the sample flow
rate and interval of collection, this method is
useful in the range of 1 to 2,400 jug/m3
(0.0005 to 1.2 ppm). As with the KI method,
this method suffers from the drawback of
interferences from reducing compounds in the
atmosphere. Another weakness is the lack of
agreement with results obtained by other
methods.
b. Alkaline Potassium Iodide
This method3 is intended for the manual
determination of oxidants in a range from a
few Mg/m3 to about 39,000 Mg/m3 (20 ppm).
The advantage of this procedure over the
neutral iodide, or reference, technique is that
a delay between sampling and completion of
analysis is allowed. Sampling is conducted in
midget impingers containing 1 percent KI in a
1-normal sodium hydroxide solution. Because
of the simplicity of the preferred reference
neutral-buffered KI method, however, the
alkaline procedure is not widely used.
c. Phenolphthalin
The phenolphthalin method is based on the
oxidation of phenolpthalin to phenolphtha-
lein by the oxidant present in the atmosphere.
Phanolphthalein is pink in alkaline solution.
Because the technique responds to pH and
temperature changes, it also is not widely
used at present, although it was used exten-
sively to obtain oxidant data in the past.
Measurement results obtained by this method
are approximately twice those obtained by
the KI method. Consequently, when data
obtained by the two methods are compared,
it is necessary to adjust for this difference.
D. METHODS SPECIFICALLY FOR MEA-
SUREMENT OF OZONE
1. Chemiluminescence
The chemiluminescent method of measur-
ing ozone was developed by Regener.11'12 If
air containing ozone is passed in the dark
across the surface of a chemiluminescent or
fluorescent substance such as Rhodamine B
adsorbed on silica gel, light is emitted. The
intensity of emitted light can be measured
with a photomultiplier tube. The chemilumi-
nescent reaction between the ozone and
Rhodamine B is highly specific to ozone and
concentrations less than 2 /ug/m3 (0.001 ppm)
can be measured. Nitrogen dioxide, sulfur
dioxide, and peroxyacyl nitrate give negli-
gible, if any, interference. The sensitivity for
ozone detection of the chemiluminescent
surface gradually decays with time, and daily
calibration with a constant ozone source is
required. Although the method has not been
widely used for routine ambient air monitor-
ing, it shows considerable promise and poten-
tial for this application and represents a
needed attempt to obtain ozone specificity in
measurement. Devices of this type are cur-
rently being thoroughly evaluated in the field
and are available commercially.
5-5
-------
2. Ultraviolet Photometry
Two instruments have been developed
based on ozone's absorption of ultraviolet
radiation. Ozone is unique in having a high
optical opacity within the wavelength band
centered at 2,500 to 2,600 A.13 The first
instrument, based on the researches of
Stairs,14 required an optical path-length of
250 feet between source and receiver units,
which was a major difficulty.15
The second instrument designed to monitor
ozone is one developed and previously manu-
factured by the Harold Kruger Instrument
Company. It was of a more conventional
design, using 10-inch cells, a single source of
radiation, and a double path of fixed wave-
length at 3,537 A. One cell had ambient air
passing through it, while the other cell sam-
pled air with the ozone removed by catalytic
decomposition.15
The Kruger photometer was available com-
mercially for several years but, because of
electronic instability and temperature depen-
dence, it required frequent attention. As a
result, it was not used extensively. It is not
available presently.
3. Trans-butene-2 Gas Phase Titration
This method, which has been only recently
described,16 involves a periodic gas-phase
titration of the air sample with trans-butene-2
prior to analysis for total oxidants. This
reactive olefin selectively removes the ozone
present in the air stream and provides a
specific ozone concentration by difference.
The technique is applicable to coulometric
and colorimetric methods of iodine measure-
ment but has been evaluated more fully with
a colorimetric instrument.1 7
4. Rubber Cracking
One of the earliest techniques used to
identify ozone in ambient air was based on
the rapid cracking of stressed rubber strips. A
strip of a suitable rubber is bent double,
stretched, and exposed to the air. Either the
time until the rubber begins to crack or the
depth of crack after a specified time can be
related to the ozone concentration. Although
it does not provide a direct quantitative
measurement, this technique is useful for
survey work, as it involves inexpensive equip-
ment and is a simple operation. It cannot,
however, be automated to obtain continuous
data and, although presumed specific for
ozone, other reactive species such as free
radicals may contribute to rubber cracking
over extended periods.1 8
5. Other Chemical Methods
Hauser and Bradley19 have described a
specific ozone technique using l,2-Di-(4
pyridyl) ethylene as the absorbing medium
and colorimetric analysis of the resulting
aldehyde by the 3-methyl-2-benzothiazolone
hydrazone method.3 This method can be
applied in field analysis of atmospheric ozone
because sampling and analysis need not be
performed on the same day.
1-hexene, hydrogen peroxide, and PAN
were found to interfere when a 24-hour
sampling period was used. Glacial acetic acid,
which is used in the collection solution, also
presents a problem since it cannot be sent
through the mails. Furthermore, the absorb-
ing solution used freezes at 16° C and must be
artificially warmed if used below this temper-
ature. For a 30-minute sample collected in a
bubbler at 0.5 liters/minute, the range of
measurement for this technique is 100 to
2,300 ;ug/m3 (0.05 to 1.2 ppm) ozone.
E. METHODS FOR DETERMINATION OF
PEROXYACETYL NITRATE
1. Long-path Infrared Spectroscopy
Peroxyacyl nitrates were discovered using
long-path infrared spectroscopy. Although
water vapor interferes with the principal
absorption band used in this determination, an
alternate band may be used to avoid this
effect. Strong bands are located at 5.75 and
8.62 n and weaker bands at 7.3, 9.5, 10.0,
10.8, and 12.2 ju. A 500-meter-long-path
infrared cell is used to detect PAN in polluted
ambient air.20
5-6
-------
2. Gas Chromatography
Increased sensitivity for the detection of
PAN is provided by gas chromatography using
an electron-capture detector.21 The advan-
tage of this detector is its relative insensitivity
to other compounds which might interfere.
Short columns (9 to 18 inches in length by
1/8 inch in diameter) packed with carbowax
coated on an inert substance are used for the
separation. Retention time for PAN is 1 to 2
minutes. Two-milliliter samples containing 5
Mg/m3 (0.001 ppm) PAN give detectable
peaks. This method has been automated, but
currently it is used primarily as part of a
manual sampling program.
F. SUMMARY
The most widely used method for the
analysis of atmospheric total oxidants is the
neutral-buffered KI technique. This technique
is currently recommended by NAPCA as the
reference method. Oxidizing species in the
atmosphere react with potassium iodide to
release iodine. The iodine may then be mea-
sured either spectrophotometrically or
coulometrically. Both of these principles have
been used in instruments which are suitable
for continuous determinations from 0 to
1,000 Mg/m3 (0 to 0.5 ppm) ozone with a
sensitivity of about 10 Mg/m3 (0.005 ppm).
The spectrophotometric technique also may
be used on an intermittent basis provided that
analysis is completed within 5 minutes after
sampling. This limit is necessary because of
the iodine color deterioration with time.
Although currently there is no widely used
method for the specific measurement of
ozone in the atmosphere, there are several
promising instruments being evaluated for this
purpose. These include a device employing
the chemiluminescent reaction between ozone
and Rhodamine B and measurement of the
emitted light; concentrations less than 2
Mg/m3 (0.001 ppm) can be measured by this
technique. Another method uses a gas phase
titration of the air sample with trans-butene-2
to selectively remove the ozone present. This
technique is applicable to coulometric or
colorimetric methods of iodine measurement,
the concentration of ozone in the sample
being obtained by difference. Chemical meth-
ods for the specific manual determination of
ozone include the 1,2-Di-(4 pyridyl) ethylene
method which may be used for 30-minute or
24-hour sampling periods. Though this tech-
nique suffers from several operational draw-
backs, it is capable of measuring ozone
concentrations from 100 to 2,300 /xg/m3
(0.05 to 1.2 ppm) for a 30-minute sample.
The methods generally used for the mea-
surement of PAN include long-path infrared
spectroscopy and, more commonly, gas chro-
matography using an electron-capture detec-
tor. Sensitivity is in the Mg/m3 (ppb) range
and the latter procedure has been automated
by some researchers.
There is a further need for the development
of instruments capable of continuously mea-
suring other individual oxidants such as for-
maldehyde, acrolein, and organic peroxides.
Acquisition of data on ambient levels of
individual oxidants will facilitate interpreta-
tion of the results of studies on the effects of
photochemical oxidants.
G. REFERENCES
1. Renzetti, N. A. and J. C. Romanovsky. A Comparative
Study of Oxidants and Ozone in the Los Angeles
Atmosphere. Arch. Ind. Health. 74(5):458-467, Novem-
ber 1956.
2. Renzetti, N. A. An Aerometric Survey of the Los
Angeles Basin August-November 1954. Vol. 1. Air
Pollution Foundation. Los Angeles, Calif. Report Num-
ber 9. July 1, 1955. 333 p.
3. Selected Methods for the Measurement of Air Pollutants.
Division of Air Pollution. Cincinnati, Ohio. PHS Publica-
tion Number 999-AP-ll. May 1965.
4. Mast, G. M. and H. E. Saunders. Research and Develop-
ment of Instrumentation of Ozone Testing. Instr. Soc.
Amer. Trans. 1(4):325-328, October 1962.
5. Analytical Methods of the Intersociety Committee on
Methods for Ambient Air Sampling and Analysis. Health
Lab. Sci. In press, 1970.
6. Potter, L. and S. Duckworth. Field Experience with the
Mast Ozone Recorder. J. Air Pollution Control Assoc.
15:207-209, May 1965.
7. Cherniack, I. and R. J. Bryan. A Comparison Study of
Various Types of Ozone and Oxidant Detectors which
are Used for Atmospheric Air Sampling. J. Air Pollution
Control Assoc. 75:351-354, August 1965.
8. Byers, D. H. and B. E. Saltzman. Determination of
Ozone in Air by Neutral and Alkaline Iodide Procedures.
Amer. Ind. Hyg. Assoc. J. 7P(3):251-257, June 1958.
5-7
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9. Information obtained from California Dept. of Public
Health. June 1965.
10. Cholak, J. et al. Air Pollution in a Number of American
Cities. Arch. Ind. Health. 11:280-289, April 1955.
11. Regener, V. H. On a Sensitive Method for the Recording
of Atmospheric Ozone. J. Geophys. Res. 65:3975-3977,
December 1960
12. Regener, V. H. Measurement of Atmospheric Ozone with
the Chemiluminescence Method. J. Geophys. Res.
<5P(18):3795-3800, September 15,1964.
13. Stair, R. Measurement of Ozone in Terms of its Optical
Absorption. Ozone Chemistry and Technology, Ameri-
can Chemical Society, Advances in Chemistry Series, No.
21, March, 1959pp. 269-285.
14. Stair, R. G., T. C. Bagg, and R. G. Johnston, Continuous
Measurement of Atmospheric Ozone by an Automatic
Photoelectric Method. Journal of Research of the Na-
tional Bureau of Standards, 52(133), March, 1954.
15. Romanovsky, J. C... et al., Air Monitoring of the Los
Angeles Atmosphere with Automatic Instruments. Paper
No. 49-22, presented at the 49th Annual Meeting of the
Air Pollution Control Association. Buffalo. May 21,
1956.
16. Bufalini, J. J. Gas Phase Titration of Atmospheric
Ozone. Environ. Sci. Technol. 2:703-704, September
1968.
17. Dudley, J. E. et al. Continuous Monitoring for Atmo-
spheric Total Oxidant and Simultaneous Determination
of Ozone by Gas Phase Titration. Presented at Air
Pollution Control Association Meeting. New York. June
24,1969.
18. Vega, T. and C. Seymour. A Simplified Method for
Determining Ozone Levels in Community Air Pollution
Surveys. J. Air Pollution Control Assoc. 11:28-33,
January 1961.
19. Hauser, T. R. and D. W. Bradley. Effects of Interfering
Substances and Prolonged Sampling on the 1, 2-Di-
(4-Pyridyl)Ethylene Method for Determination of Ozone
in Air. Anal. Chem. 59(10):! 184-1186, August 1967.
20. Darley, E. F., K. A. Kettner, and E. R. Stephens.
Analysis of Peroxyacyl Nitrates by Gas Chromatography
with Electron Capture Detection. Anal. Chem.
55:589-591, April 1963.
21. Stephens, E. R. Absorptivities for Infrared Determina-
tion of Peroxyacyl Nitrates. Anal. Chem. 56:928-929,
April 1964.
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Chapter 6.
EFFECTS OF PHOTOCHEMICAL OXIDANTS ON
VEGETATION AND CERTAIN MICROORGANISMS
A. INTRODUCTION
Injury to vegetation was one of the earliest
manifestations of photochemical air pollu-
tion.1"19 A peculiar type of injury to leafy
vegetables, ornamentals, and field crops, now
characterized by banding, silvering, and stip-
pling of the leaves, was first investigated by
Middle ton et al.12 in 1944 in a small area of
Los Angeles County. By 1950, such injury
had spread over a large segment of southern
California and the San Francisco Bay Area.1 °
Plant injury of this kind has since spread to
many widely separated areas of the United
States, with increasing severity and with
associated economic losses to both farmers
and nurserymen.2 °"2 7
Three specific phytotoxic materials have
been isolated from the photochemical com-
plex: ozone, nitrogen dioxide, and the per-
oxyacyl nitrates. The latter homologous series
of compounds includes peroxyacetyl nitrate
(PAN), peroxypropionyl nitrate (PPN), per-
oxybutyryl nitrate (PEN), and peroxyiso-
butyryl nitrate (PisoBN). Preliminary work
has shown that PPN is several times as toxic
to vegetation as PAN,2 5 '2 8'3 ° while PEN and
PisoBN are more toxic than PPN.28 Since
PAN is the only member of the series which
has received much study, and also since PPN
and PEN are usually present but below
detectable limits, discussion will be restricted
to the effects of PAN. Discussion of the
quantitative effects of ozone and PAN has to
be limited to laboratory and controlled field
exposures since, under ambient conditions,
the effects of these compounds cannot be
easily differentiated. The term "oxidant" will
be used when discussing the toxic materials to
which the plants are exposed under ambient
conditions. Research in several laboratories
using a variety of reaction systems suggests
that additional phytotoxicants may be pres-
ent in the photochemical complex.5' 16> 31> 32
Synergistic effects between the toxicants dis-
cussed and other atmospheric contaminants
may also produce injury to sensitive plant
species.25' 33~37 Available information sug-
gests that ozone is the most important phyto-
toxicant of the photochemical complex.
Sensitive plants are useful biological indi-
cators of photochemical air pollu-
tion_2,3,9,11,13,14,16,21,31,38-46 The moSt
detailed study of this phenomenon was made
in Los Angeles, with annual bluegrass and
petunia as monitoring species.3'40'44 This
study was designed to use plants to determine
relative concentrations of photochemical pol-
lution by attempting to establish a relation-
ship between oxidant concentrations and
plant injury. A similar survey42 used pinto
beans, grown under greenhouse conditions.
The injured leaf area in both studies was
measured and showed poor correlation with
oxidant levels, suggesting that unknown fac-
tors were affecting sensitivity, or that the
oxidant index did not accurately measure the
phytotoxic substances in the air. Tobacco has
also been widely used as a monitor for
photochemical pollutants. It was first sug-
gested because its injury pattern seemed
specific for the PAN-type of injury.47 The
injury pattern and sensitivity of tobacco to
ozone4 8 makes it a useful monitor in study-
ing the extent, severity, and frequency of
ambient oxidant.39
6-1
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B. SYMPTOMS OF THE EFFECTS OF
PHOTOCHEMICAL AIR POLLUTANTS
ON VEGETATION
The visible symptoms of injury to plants
attributable to oxidant air pollution can be
classified into three general categories: acute
injury, severe injury occurring within several
hours after exposure, identified by cell col-
lapse with subsequent development of identi-
fiable necrotic patterns; chronic injury, light
to severe injury developing over an extended
time period, identified by necrotic patterns
with or without chlorotic or other pigmented
patterns found in sensitive leaf tissues and not
easily attributable to other than oxidant air
pollutants; and physiological effects, includ-
ing growth alterations, reduced yields, and
changes in the quality of plant products. The
acute symptoms are generally characteristic of
a specific pollutant. Chronic injury patterns
are often highly characteristic but by no
means specific for the toxic agents. Disease,
insects, nutrition, and other factors can pro-
duce leaf patterns similar to those induced by
air pollution.
The most easily recognized effect of air
pollutants is the necrotic patterns which
develop after the occurrence of injury to cells
and final collapse of the tissue. The initial
plasmolysis is due to changes in cell-wall
permeability and then to changes in structural
integrity; a slightly water-soaked or bruised-
looking area appears in the intact leaf. These
areas generally dry out, leaving necrotic pat-
terns characteristic of the toxicant.
Ozone-type injury to field crops was first
observed as a "stippling" on grape leaves in
California.49'50 Heggestad and Middleton51
found that the tobacco "weather fleck"
symptoms found along the eastern seaboard
could be reproduced by exposing tobacco to
ozone fumigations. Daines et al.52'53 report-
ed ozone-type injury to several crop plants in
New Jersey, and indicated that continued
production of these crops was seriously
threatened. Since these early reports, ozone-
type injury to sensitive crop plants has been
reported from Florida to southern On-
tario.54'62 The conifer "x-disease"6 3 and the
citrus decline in California26 have also been
related to ozone injury.
The initial effect of ozone is in the palisade
cell layer and involves scattered groups of
cells. In acute injury, the cells plasmolyze and
the cell contents become disrupted and disin-
tegrate with or without the production of a
dark pigment, called "stipple" in the former
case and "fleck" in the latter. With continuing
exposure or with a high-level exposure, these
upper-surface necrotic areas will enlarge,
coalesce, and eventually injure the spongy
cells and form necrotic lesions through the
leaf. Ozone enters the leaf through the sttf-
mata, but the gas preferentially attacks the
palisade cells. A detailed discussion of ozone
symptoms with illustrations of several plants
has recently been published.6 4
PAN-type injury, characterized by under-
surface glazing or bronzing of the leaves of
many plant species, has been observed prima-
rily in California and in the states along the
eastern seaboard.22'25'52'65 This type of
injury has also been reported in other parts of
the United States and in several metropolitan
areas of foreign countries.2 *>66 Injury occur-
ring in the field has been identified in spinach,
beets, celery, tobacco, endive, romaine let-
tuce, Swiss chard, pepper, alfalfa, petunias,
snapdragon, primrose, asters, and other
plants.13'14'25'53
PAN has been accepted as the primary
phytotoxicant which causes the oxidant-type
injury initially described by Middleton et
al.12 and more completely by Bobrov et al.3
and Glater et al.47 The initial collapse is in
the spongy cells surrounding the air space into
which a stoma opens. The effect in some cases
is limited for the most part to cells nearest the
lower epidermis. This results in a slight
separation of the lower leaf epidermis, which
produces a characteristic under-surface silver-
ing, glazing, or bronzing. More acute injury
causes the necrosis to extend through the
entire leaf. Injury to the leaves of grasses,
petunia, and tobacco causes a crossleaf band-
ing associated with the sequential maturation
6-2
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of cells from the tip to the base of the leaf. A
detailed discussion of PAN symptoms with
illustrations has recently been published.6 7
Chronic injury may be characterized by
chlorosis or other color changes, in addition
to several necrotic patterns. Chlorosis, the loss
or reduction of chlorophyll, is a very common
and nonspecific symptom in plants. Its ap-
pearance generally signifies either a deficiency
of some nutrient required by the plant or a
general metabolic disturbance. The loss of
chlorophyll results in leaves with a pale-green
or yellow color pattern. There are other color
changes in leaves, often with general chlorosis,
which are associated with maturity or senes-
cence, e.g., the color change in the autumn.
There are cases where the photochemical
complex or its specific components will pro-
duce chlorosis in leaves which have been
exposed to the pollutant at low levels over a
long period of time. The pattern, however, is
usually not distinctive, appearing only as an
early senescence. The pigmentation of small
areas of the palisade cells (stipple) seems to be
characteristic of ozone injury in some plants,
as a silvering or bronzing of the undersurface
of some leaves is associated with PAN injury.
Physiological effects causing growth- and
yield-reductions have been experienced in
several areas of the United States.2 5 A serious
decline in citrus, manifested by early loss of
leaves, changes in water relationships, smaller
fruit, and poor growth,24'26 is currently
being experienced in the Los Angeles area.
Similar effects are detected in vegetable and
other horticultural crops of the area. Photo-
chemical pollutants such as ozone and PAN
have been suggested as responsible.26 Feder
and Campbell6 8 exposed carnations continu-
ously over a 2-month period to low levels of
ozone [100 to 200 jug/m3 (0.05 to 0.10
ppm)] and reported a significant reduction in
the number of flowers as well as a reduction
in height and flower-stock length. Time to
produce flowers was also lengthened. Experi-
mentation has shown that some of these
effects, such as early leaf drop, changes in
water relationships, increased respiration, sub-
normal growth of vegetables, and effects on
flower development, can be alleviated by
exposure to air filtered through activated
carbon to remove photochemical oxi-
dants.7'69 It should be noted that reduced
growth and yields can occur without visible
injury to the leaves.35'36
Taylor7 ° has reported on observed physio-
logical upsets in trees due to oxidants. Others
have reported on generally poor growth and
early senescence due to oxidants.7 Hill and
Littlefield71 have reported a reduction in
photosynthesis at ozone concentrations which
caused only slight visible injury. At the
present time, there is no sound basis for
accurately evaluating the significance of these
observations and results. Additional work of
this type, together with basic work such as
that reviewed by Dugger et al.,72 will be
required before an evaluation can be made of
the physiological and biochemical effects of
photochemical oxidants on the intact plant.
C. FACTORS AFFECTING RESPONSE OF
VEGETATION TO PHOTOCHEMICAL
AIR POLLUTANTS73
The response of a given species or variety
of plant to a specific air pollutant cannot be
predetermined on the basis of the known
response of related plants to the same pollu-
tant. Neither can the response be predeter-
mined by the given known response of the
plant to similar doses of a different pollutant.
Genetic susceptibility and environmental in-
fluences must, therefore, be determined for
each plant and pollutant.
1. Genetic Factors
Variability in response to pollutants is
known to exist between species of a given
genus and between varieties within a given
species. Species variability has been well-
documented in numerous genera, and major
varietal or strain differences have been shown
in such species as petunia, tobacco, white
pine, soybean, tomato, and radish.59'74"78
Varietal variations have been studied most
extensively in the species Nicotiana tabacum.
Heggestad and Menser48 isolated and devel-
6-3
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oped a sensitive tobacco strain (Bel-W3) and
have compared its sensitivity to a number of
other varieties. Macdowall et al.59 tested 32
varieties of tobacco and found the White Gold
variety to be most susceptible. Menser76 and
Reinert et al.77 have also studied and report-
ed on varietal response differences in the field
and laboratory associated with oxidant or
ozone exposures. Injury to susceptible vari-
eties of tobacco in the Connecticut River
Valley fields and elsewhere has led to the
development of more resistant varieties for
commercial use. The more sensitive varieties
are being used in monitoring programs and as
biological material for studying the effects of
air pollutants on plants.
A study was conducted in Wisconsin on
varietal ozone susceptibility.79'80 Ozone-
resistance in onions was found to be related
to a dominant gene which controlled the
response of the guard cells to ozone. This
single-factor inheritance of sensitivity of
onion to ozone is perhaps unique, but it
deserves further investigation.
Feder81 reported a 40 percent reduction in
pollen germination and a 50 percent reduc-
tion in pollen tube growth following a 5- to
24-hour exposure of tobacco to 200 ng/m3
(0.10 ppm) of ozone. This could represent a
major loss in reproductive capacity.
2. Environmental Factors
Field and laboratory observations and
experiments have shown that the environ-
mental conditions under which plants are
grown and/or exposed have a major influence
on their sensitivity to phytotoxic air pollu-
tants. Macdowall et al.58 correlated the sensi-
tivity of tobacco with oxidant levels and
found that sensitivity is related to general soil
conditions and to the interaction of several
meteorological factors such as temperature,
wind speed and direction, humidity, and light.
By using these factors and an empirical factor
(the coefficient of evaporation) and relating
them to oxidant dose, the authors had some
success in forecasting tobacco-fleck attacks.
During growth, the influence of light
intensity on the sensitivity of plants is depen-
dent on the phytotoxicant. Plants are more
sensitive to PAN when grown under high light
intensities,82 but are more sensitive to ozone
when grown under low light intensities.82'84
Sensitivity of Poa annua during exposure to
oxidant shows a positive correlation with
increasing light intensity to at least 3,000
foot-candles.4 ° A similar response of plants to
ozone has been reported.8 s For some pollu-
tants and with specific plants, sensitivity may
increase with increasing light intensity up to
full sunlight.
In a study on the standardization of Poa
annua response as an index of smog concen-
trations, it was found that sensitivity in-
creased as temperatures increased from 40° to
85° F.40 When plants are exposed under
greenhouse conditions, it is almost impossible
to separate the effect of temperature at the
time of exposure from the effect of light
intensity since a positive correlation exists
between these two factors. Reported findings
are in general agreement that sensitivity of
plants to oxidants increases with temperature
from 40° to 100°F. However, when plants
were exposed to ozone under controlled
lighting conditions,85 there was an inverse
relationship between temperature and sensi-
tivity as the temperature was raised from 65°
to 85°F. This suggests that the positive
correlation between sensitivity and tempera-
ture found under ambient conditions is due to
the overriding influence of light intensity.
The effects of humidity during growth and
exposure have not been well documented.
Early work suggests that plants grown and/or
exposed under high humidities are more
sensitive than those grown at low humidities.
The results of Menser86 on exposure of
sensitive tobacco to ozone suggests the same
trend; however, his results are not conclusive.
Otto and Daines8 7 found a marked reduction
in sensitivity of pinto bean and tobacco to
ozone when they were exposed at 26 percent
relative humidity as opposed to 51 percent
relative humidity. However, they found varied
plant responses to higher humidities. These
6-4
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findings are in general agreement with earlier
work. The overall importance of humidity is
still poorly understood.73 Heggestad et
al.88 noted that tobacco plants grown out-of-
doors and in greenhouses in Utah and Cali-
fornia were not as sensitive to either ambient
oxidant or ozone as similar plants grown in
eastern states where the relative humidity is
higher.
The increased use of carbon dioxide as an
additive for increased production in green-
houses may act to reduce the sensitivity to
photochemical pollutants of plants grown
under these conditions.8 3
The relative importance of some meteoro-
logical factors, such as wind speed and baro-
metric pressure, has seemed insignificant in
relation to the primary factors already dis-
cussed. Plants appear to be more sensitive
when high pollution levels occur from mid-
morning to early afternoon than at other
times during the day or night.
Research has largely neglected the influ-
ence of soil factors on the sensitivity of plants
to phytotoxic air pollutants. There are numer-
ous reports that plants grown under drought
conditions are less susceptible to air pollu-
tants than those grown under moist condi-
tions. Field observations61 have shown that
tobacco plants irrigated just prior to a natural
fumigation are more sensitive than unirrigated
plants, even when the unirrigated plants have
a sufficient water supply to prevent wilting.
Withholding of water from greenhouse and
irrigated crops during times of high pollution
potential has been recommended by several
researchers as a preventive measure against
pollution injury.
Various studies have shown that plant
sensitivity to phytotoxic air pollutants in-
creases when they are grown under low
total-soil-fertility. This has been found under
both natural and laboratory conditions. Other
studies have shown that an increased nitrogen
supply makes plants more sensitive, although
differing results have been reported. General
observation suggests that the healthier the
plant, the greater its sensitivity toward air
pollutants.73
Plants are not as sensitive when grown in
heavy soils. The effects of soil temperature,
aeration (both oxygen and carbon dioxide),
texture, compaction, and composition have
not been studied. This is partly due to their
seeming unimportance in relation to many
other factors, but their effects need to be
explored.
3. Other Factors
The growth stage of a plant is important in
determining its sensitivity to air pollutants.
The age of the leaf under exposure is of more
specific importance than the age of the plant.
Components of the photochemical complex
cause different responses in sensitive plants.
In annual bluegrass and tobacco, the youngest
mature cells are the most sensitive.3'47 Since
these cells develop progressively from the tip
to the base of the leaf, the injury occurs as a
band on the sensitive area of the leaf. This
pattern is the generally accepted pattern for
PAN injury. In other plants, where the cells
mature rather uniformly within a given leaf,
PAN injury affects the young leaves before
they are fully expanded. Ozone injury gener-
ally does not develop until the leaves are
mature, although Ting and Dugger,84 in
studying cotton, report greatest sensitivity in
leaves about 75 percent expanded.
There is some evidence that oxidant or
ozone injury may be reduced by pretreatment
with the toxicant.7'79 In the sensitive onion
variety, pretreatment was linked to stomatal
action which prevented further entrance of
ozone. Stomatal closure as related to pollu-
tants has not been studied extensively; avail-
able information suggests, however, that the
stomata of many species are affected by
ozone.
Essentially no evidence is available on the
possible synergistic or antagonistic effects of
two or more pollutants in combination.
Ethylene, propylene, acetylene, and nitrogen
dioxide show no synergistic or antagonistic
6-5
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action; neither do the photochemical phyto-
toxicants produced by irradiation of nitrogen
dioxide propylene mixtures when ethylene
and/or acetylene are mixed with the reaction
systems.89 However, subthreshold levels of
sulfur dioxide combined with subthreshold
levels of ozone were reported to cause an
ozone-like fleck on sensitive tobacco.34 This
interaction has since been reported by several
other investigators with positive results on
most of the species studied. The response, in
general, does not appear to be truly synergis-
tic_33-37
4. Discussion
The various factors affecting the response
of vegetation to air pollution must be medi-
ated through control of the stoma, other
internal factors that affect cellular responses,
or a combination of these. Although stomatal
opening is an accepted prerequisite for the
entrance of pollutants, there are certain plant
tissues that are sensitive to a specific pollutant
and not sensitive to another, even when
stomatal function is not a factor. Work with
irradiated auto exhaust best exemplifies this
premise, since three toxicants were identified
from the mixture by the differential responses
of tobacco leaf tissue. Biochemical control of
sensitivity to ozone and PAN is also sug-
gested, since ozone first affects the mature
tobacco leaves and PAN affects the younger
leaves even though stomatal openings are
present in leaves of both ages. Thus, although
stomatal opening is a prerequisite for pollu-
tant entrance, the injurious reaction of the
pollutant within the leaf tissue is a biochemi-
cally mediated response, dependent upon
unknown factors within the cells.
D. PROBLEMS IN DIAGNOSIS AND AS-
SESSMENT OF THE ECONOMIC IM-
PACT OF PHOTOCHEMICAL AIR POL-
LUTION ON VEGETATION
The plant is a product of its environment,
responding in many ways to the stresses and
support afforded by that environment. Air
pollution must be considered as simply
another quality of the environment, together
with climate, soil, insects, disease, as well as
genetic history and patterns of care or abuse
by man. The injury created by an air pollu-
tant may not only be modified or obscured
by other environmental factors but, from
these other factors, the plant may develop
injuries which are difficult or impossible to
distinguish from those caused by air pollu-
tion. Ornamental and agronomic crops grown
under special management practices must be
carefully examined before attributing poor
growth to air pollution. Many bacterial, viral,
and fungal diseases, as well as insects, can
produce injury symptoms in plants which are
quite similar to the symptoms produced by
air pollutants. To properly diagnose air pollu-
tion effects on vegetation, therefore, the
injuries must be observed in the field and
supported by both measurements of the
concentration in the ambient air and by
laboratory fumigation studies, using different
levels of the suspect pollutant. Furthermore,
the observer must have a thorough knowledge
of local cultural conditions.
While the markings on the leaves of a plant
may be identified with an air pollutant, it is
often quite difficult to evaluate these mark-
ings in relation to their effects on the intact
plant. The question which must be answered
is whether or not the plant has been so altered
by the air pollutant as to significantly alter its
growth, survival, yield, or use. In evaluating
some of the leaf injuries the problem is
relatively straightforward. This is especially
true in cases where the appearance of the
plant is paramount, or where there is a loss or
a failure to develop a desired product. Other
cases, however, require some assessment of
the extent to which the leaf injury has
affected the essential processes of the plant.
Whether the air pollutants directly or indirect-
ly upset the basic plant processes through
injury to the leaf, however, is really immate-
rial to the question of an evaluation of
economic loss.
A German report by Guderian et al.90
expresses a philosophy on the general prob-
lem of the effect of air pollutants on vegeta-
6-6
-------
tion. The authors make a useful distinction
between "injury" and "damage". They define
injury due to air pollution as any identifiable
and measurable response of a plant to air
pollution. They define damage which results
from an air pollution injury as any identifi-
able and measurable adverse effect upon the
desired or intended use or derived product of
the plant. Thus, necrotic lesions on the leaves
of lettuce when identifiable as due to an air
pollutant are injury. Any assessment of dam-
age requires a judgment that this injury
affects the yield or use of the vegetation. The
initial identification of injury also requires an
informed judgment.
The appearance of romaine lettuce, as the
appearance of many other truck crops, affects
sales on the market. If the outer leaves have been
marked by oxidant, the crop may not be mar-
ketable. The labor of stripping the outer leaves,
with a resultant loss of shape, may not be justi-
fied. The yield in crates per acre may be unaf-
fected, but the crop may still be a total loss.
Thus both injury and damage have occurred.
In other crops, where the marketable pro-
duct is not the leaves, the case is somewhat
more complicated. Hill and Thomas91
showed that the yield of alfalfa was reduced
in proportion to the area of the leaf destroy-
ed. This offers a method of evaluating the
damage sustained by such crops.
Leaf injury to a fruit tree becomes far more
difficult to assess as "damage". The effect of
a given percentage of leaf destruction on total
fruit yield or on the distribution of grades in
the crop is not known. It is known that in
severe cases, the growth of the tree will be
affected, yet it is very difficult to evaluate the
injury in terms of the value of subsequent
crops. To properly evaluate such evidence in
relation to a crop which is to be harvested 10
to 20 years from now requires more than the
knowledge now available. In forest trees, the
problem is similar; there is evidence of re-
duced growth-rings which can be attributed to
prior leaf injury.
The problem of leaf injury to ornamentals
is equally difficult to assess. If the injury is
severe, the stock in a nursery may not be
salable. If it is less severe, pruning may make
the stock salable but at a reduced price. The
damage in these cases usually can be esti-
mated; however, the problem of injured stock
held over for subsequent seasons is more
difficult. Often such injured stock may repre-
sent a sizeable portion of the entire inventory.
Then again, individual plants may appear fully
recovered by the following season. In some
cases, if growth of the plant is somewhat
stunted, this can be a benefit to the grower.
After the stock has been sold and planted
in a yard, park, or cemetery, the concept of
damage becomes broader in scope. Damage
may not be so much to the leaves of a plant as
to the feelings of people concerned.
E. DOSE-INJURY RELATIONSHIPS OF
PHOTOCHEMICAL AIR POLLUTION
AND VEGETATION
The interrelations of time and concentra-
tion (dose) as they affect injury to plants are
essential elements of air quality criteria. They
have been inadequately studied and are there-
fore poorly understood. Discussion of time-
concentration relationships is simplified by
considering them in terms of three types of
injury to plants: acute, chronic, and growth.
There is little data in the literature relative to
the effect of time-concentration relationships
on the production of chronic injury, or in the
reduction of growth, yield, or quality of plant
material. There is also a dearth of information
concerning the relationship of time and con-
centration on acute injury by PAN and
mixtures of pollutants in the photochemical
oxidant complex. There is more information
in this area on the acute effects of ozone, but
it is far from complete.
At the present time, it is impossible to cite
more than cursory results on the effects of
time-concentration relationships on plant
growth. Table 6-1 summarizes the available
information for PAN, ozone, and the photo-
chemical complex as they affect the growth
and biochemistry of plants.
No attempt has been made to tabulate the
slight amount of information available on
6-7
-------
chronic effects, since it cannot be separated
easily from the results on growth or acute
effects.
The acute effects of the photochemical
toxicants have been the most widely studied.
The fragmentary reports which are available
for PAN and the photochemical complex are
tabulated in Table 6-2. Relative phytotoxicity
of four members of the peroxyacyl nitrates
are shown in Table 6-3.28 Threshold levels of
injury for ozone are tabulated in Table 6-4.
The acute effects of ozone at various
concentrations and times has received suffi-
cient study to permit preliminary time-
concentration curves to be constructed for
several sensitivity groupings. One of the first
time-concentration relations was reported by
O'Gara.94 He was concerned only with an
acute type of injury which develops over a
relatively short period of time. He related
concentration (c) and time of exposure (t) as:
t(c-a) = b
The parameters "a" and "b" are dependent
upon the species and variety of plant and the
Table 6-1. EFFECTS OF PAN, OZONE, -AND THE PHOTOCHEMICAL
COMPLEX ON THE GROWTH AND BIOCHEMISTRY OF PLANTS
Species
PAN10
Bean
(Phaseolus vulgaris,L.)
Ozone
Peanut
(Arachis hypogaea)
Radish
(Raphanus sativus,L.)
Carnation
Concentration,3
ppm
1.0
1.0
0.02
0.05
(Dianthus caryophyllus,L.) 0.07
Tobacco
(Nicotiana tabacum,L.)
Bel-W3
Bel-W3
Photochemical complex
Tobacco
(Nicotiana tabacum,L.)
Bel-W3
Bel-B
0.10
0.05
0.03-0.22
0.03-0.22
Time
0.5 hr
0.5 hi
24-28 hi
8.0 hi/day
(20 days)
60 days
5.5 hr
8.0 hr/day
(20 days)
700 hi
700 hi
Effects
Reduction in photosynthesis
Changes in chloroplasts
Chlorosis-leaves
may abscise
50 percent reduction
in yield
50 percent reduction
in floral developmen*
50 percent reduction in
pollen germination and
pollen tube growth
Reduction in
growth
Severe leaf
injury
70 percent reduction
in growth
Reference
92
93
33
36
68
81
35
69
69
Concentrations reported for the photochemical complex and ozone have been
corrected to neutral KI values. Reported Mast oxidant values have been
multiplied by a factor of 1.5.
bResults of laboratory exposures.
6-8
-------
Table 6-2. SUSCEPTIBILITY OF PLANTS TO CONCENTRATIONS OF PAN,
THE PHOTOCHEMICAL COMPLEX, AND MIXTURES OF SULFUR DIOXIDE
AND OZONE PRODUCING ACUTE INJURY SYMPTOMS
Species
PAN
Petunia
{Petunia hybrida, Vilm)
Sensitive species
Sensitive species
Bean
(Phaseolus vulgaris,L.)
Photochemical complex
Tobacco
(Nicotiana tabacum,L.)
Bel-W3
White Gold
Bean
(Phaseolus vulgaris,L.)
White Pine
(Pinus strobus,L.)
Sulfur dioxide/ozone
Tobacco
(Nicotiana tabacum,L.)
Bel-W3
Bel-W3
Bel-W3
Peanut
(Araches hypogaea)
Tomato
(Lycopersicon esculentum,
Mill)
Radish
(Raphanus sativus,L.)
Pine
(Pinus strobus,L.)
Concentration,1
ppm
0.1
0.01
0.002 (PPN)
1.0
0.1
0.06
0.07
0.05
0.10
0.15 (max)
0.10
0.25/0.03
0.10/0.03
0.05/0.05
0.03/0.02
0.25/0.05
0.25/0.05
0.05/0.05
0.05/0.05
Time
5.0 hr
6.0 hi
6.0 hi
0.5 hr
5.0 hi
1.0 hi
2.0 hi
3.0 hr
3.0 hr
1.0 day
4.0 hr
2.0 hr
4.0 hr
8.0 hr/day
(20 days)
6.0 hr
4.0 hr
4.0 hr
8.0 hr/day
(20 days)
8.0 hr/day
(20 days)
Effects'3
3
2
2
3
3
1
2
1
2
2
1
2
2
1
1
1
1
1
1-2
Reference
16
29
29
82
16
123
95
58
58
42
54
34
25
35
33
25
25
36
37
Concentrations reported for the photochemical complex and ozone have
been corrected to neutral KI values. Reported Mast oxidant values
were multiplied by a factor of 1.5.
bSeverity of injury: 1 = slight, 2 = moderate, 3 = severe.
6-9
-------
Table 6-3. RELATIVE PHYTOTOXICITY OF FOUR MEMBERS OF THE PEROXYACYL
NITRATES, INDICATED BY PRELIMINARY FUMIGATION ON TWO
SPECIES OF PLANTS 28
Bean,
var-.
Pinto
Petunia,
vai. Rosy
morn
Fumigation
time,
hr
0.5
1.0
4.0
8.0
0.5
1.0
Toxicant
PAN
Cone.,
ppb
_
140
40
20
-
140
Injury,
%
55
90
44
-
33
PPN
Cone.,
ppb
100
24
10
5
50
24
Injury,
%
90
7
86
100
7
35
PEN
Cone.,
ppb
100
30
-
—
100
12
Injury,
%
80
59
-
—
90
45
PisoBN
Cone.,
ppb
100
—
—
~
25
—
Injury,
%
80
-
-
18
—
Table 6-4. THRESHOLD SUSCEPTIBILITY OF PLANTS TO ACUTE INJURY FROM OZONE
Species
Tobacco
(Nicotians tabacum, L.)
Bel-W3
White Gold
Bean
(Phaseolus vulgaris,L.)
Oat
(Avena sativa)
White Pine
(Firms strobus,L.)
Alfalfa
(Medicago sativa,}^.)
Tomato
(Lycopersicon esculentum,
Mill.)
Radish
(Raphanus sativus, L.)
Onion
(Allium cepa,L.)
Peanut
(Arachis hypogaea)
Concentration,3
ppm
0.15
0.75
0.15
0.08
0.03
0.15
0.05
0.15
0.40
0.08
0.12
0.10
0.20
0.08
0.08
0.40
0.02
Time,
hr
0.5
0.2
1.0
2.0
8.0
2.0
3.0
0.5
0.33
4.0
2.0
4.0
2.0
1.0
2.0
2.0
24-48
Effects13
1
1
1
2
1
2
1
1
1
1
1
1
2
1
1
3
1
Reference
96
123
96
95
83
97
58
96
41
25
60
54
98
124
f 124
79
33
Concentrations have been corrected to neutral KI values. Reported
Mast oxidant values were multiplied by a factor of 1.5.
bSeverity of Injury: 1 = slight, 2 = moderate, 3 = severe
6-10
-------
degree of injury. Concentration is measured in
parts per million and time in hours. O'Gara's
equation can be rearranged to:
c = b/t + a
The plot of "c" versus "1/t" is a straight line.
The parameter "a" is the intercept for 1/t = 0
or when "t" is infinitely large. This intercept
could be considered the threshold concentra-
tion for injury. The O'Gara equation is a
mathematical form which fits experimental
data obtained from exposures limited in time.
Guderian et al.90 do not believe that the
O'Gara equation fits their observations and
suggest an exponential relationship to best
describe their data:
t =
-a (c'r)
where K, a, and r are parameters varying with
species and degree of injury. In the middle
time range, both forms of equations reason-
ably fit available data. The exponential form
probably fits better over a wider range of
time.
An expression of the degree of injury
produced as time and concentration vary is
needed in describing injury. Heck et al.96
presented this information graphically for
pinto bean and Bel-W3 tobacco exposed to
ozone. Mathematical surfaces of this type
can make apparent the frequently steep slope
in the injury-versus-concentration or injury-
versus-time planes. The steepness in these
slopes gives a relative measure of the degree of
variability to be expected in data collected
under practical control conditions. Similar
reports, stressing the importance of consider-
ing both time and concentration, have recent-
ly appeared in the literature.84'99
Such relationships give an insight into what
may happen under a given set of circum-
stances. These relationships are probably uni-
versal and could be derived for any toxicant
producing a definite acute-type of tissue
collapse. Relationships of this type permit the
assumption with reasonable assurance that as
long as a certain concentration is not ex-
ceeded for a given period of time, no acute
injury will occur. They do not indicate the
severity of injury at higher concentrations for
longer time periods. To extend any of these
relationships beyond the available experi-
mental data upon which they are based is
questionable.
None of the experimental data presented
provide any more than suggestions of what
takes place in the field. They cover only single
time-concentration relationships under stan-
dard conditions. They do not consider fluc-
tuations in concentration in a given time
interval or the effect of repeated fumigations
over either several days or even several hours
in one day. Further, most of the available
data are from rather short-time exposures,
that is, short as related to a growing season.
To extrapolate any of the presentations to
long time periods would give results of very
questionable validity.
A number of investigators have reported
the time-concentration effects of ozone on
various species of plants. Table 6-4 summa-
rizes some of the threshold-level (5 percent)
time-concentration results with ozone. From
these results, Tables 6-5 and 6-6 have been
developed. These tables suggest the times and
concentrations necessary to produce injury in
sensitive, intermediate, and resistant plants at
the threshold (5 percent) and 20 percent
injury levels, respectively. The lower levels
shown in Table 6-5 for the sensitive plants
were taken essentially from Table 6-4. The
remaining values in Tables 6-5 and 6-6 were
developed from the threshold values by exten-
sive study of ozone effects on a group of
economically important plants. Table 6-7
gives a complete list of the plants which have
been studied, places them in three sensitivity
classes, and lists them alphabetically by fami-
ly.
The sensitive range for 1/2, 1, 2, and 4
hours from Table 6-5 was analyzed using the
O'Gara equation. This equation gives a good
fit at the shorter time periods but gives a
threshold concentration above experimental
6-11
-------
values for infinite time. These results suggest
that the O'Gara equation does not give an
exact fit to experimental data with ozone, but
that the approximate fit obtained can be used
with a fair degree of confidence with the
fragmentary data presently available for anal-
ysis.
F. EFFECTS OF PHOTOCHEMICAL
OXIDANTS ON MICROORGANISMS
The bacteriocidal action of ambient photo-
chemical oxidant has been demonstrated by
Goetz and Tsuneishi.1 °4 In fact, the BIA test,
where bacteria of uniform density are ex-
posed to a concentration of oxidant, was
developed as a bacteriological analog for the
measure of eye irritation from photochemical
oxidant aerosols. Photochemical oxidant con-
centrations from irradiated auto exhaust con-
taining as little as 0.125 ppm hydrocarbons
proved bacteriostatic for common bacteria
such as Eschericha coll
G. EFFECTS OF OZONE ON
MICROORGANISMS
The growth suppression of microorganisms
by ozone is a well-known phenome-
non.105"113 Ozone at higher concentrations
readily oxidizes organic matter and is used in
a variety of applications, such as in cold
storage plants for the control and suppression
of fungi and bacteria associated with food
spoilage,114 drinking water purifica-
tion,115"117 and the treatment of sew-
age.1 18 The value of ozone in preventing the
spoilage of fruit and vegetables, however, is in
question. The use of ozone with food and
drinking water is permitted because safe-
guards can protect personnel from excessive
exposures, but these same safeguards cannot
be applied so as to permit the use of ozone
for air sterilization in the general ventilation
of homes and public buildings.
It is now recognized that ozone is not an
Table 6-5. PROJECTED OZONE CONCENTRATIONS WHICH WILL PRODUCE, FOR
SHORT-TERM EXPOSURES, 5 PERCENT INJURY TO ECONOMICALLY IMPORTANT
VEGETATION GROWN UNDER SENSITIVE CONDITIONS
Concentrations producing injury in three types of plants, ppm
Time,
hr
0.2
0.5
1.0
2.0
4.0
8.0
Sensitive3
0.35-0.75
0.15-0.30
0.10-0.25
0.07-0.20
0.05-0.15
0.03-0.10
Intermediate
0.70-1.00
0.25-0.60
0.20-0.40
0.15-0.30
0.10-0.25
0.08-0.20
Resistant
0.90 and up
0.50 and up
0.35 and up
0.25 and up
0.20 and up
0.15 and up
aThe lower levels obtained from data presented in Table 6-4.
Table 6-6. PROJECTED OZONE CONCENTRATIONS WHICH WILL PRODUCE, FOR
SHORT-TERM EXPOSURES, 20 PERCENT INJURY TO ECONOMICALLY IMPORTANT
VEGETATION GROWN UNDER SENSITIVE CONDITIONS
Concentrations producing injury in three types of plants, ppm
Time,
hr
0.2
0.5
1.0
2.0
4.0
8.0
Sensitive
0.40-0.90
0.20-0.40
0.15-0.30
0.10-0.25
0.07-0.20
0.05-0.15
Intermediate
0.80-1.10
0.35-0.70
0.25-0.55
0.20-0.45
0.15-0.40
0.10-0.35
Resistant
1 .00 and up
0.60 and up
0.50 and up
0.40 and up
0.35 and up
0.30 and up
6-12
-------
Table 6-7. LISTS OF PLANTS IN THREE SENSITIVITY GROUPS BY SENSITIVITY
TO OZONE
Species
Sensitive
CHENOPODIACEAE
Spinach (Spinacia oleracaae, L.)
CRUCIFERAE
Radish (Raphanus sativus,L.)
CURCURBITACEAE
Muskmelon (Cucumis melo,L.)
GRAMINEAE
Bromegrass (Bromus inermis,L.)
Oat (Avena sativa) Hexaploid
Oat (Avena strigosa) Diploid
Rye (Secale cereals)
LEGUMINOSAE
Bean (Phaseolus vulgaris,L.)
Peanut (Arachis hypogaea)
PINACEAE
Pine (Pinus strobus,L.)
POLYGONACEAE
Buckwheat (Fagopyrum sagittatum)
Smartweed, perennial (Polygonum. sp.)
SOLANACEAE
Potato (Solarium tuberosum,L.)
Tobacco (Nicotiana tabacum,L.)
Tomato (Lycopersicon exculentum, Mill)
Intermediate
AMARYLLIDACEAE
Onion (Allium cepa,L.)
BEGONIACEAE
Begonia (Begonia semperflorens)
CHENOPODIACEAE
Spinach (Spinacia oleracea,L.)
Beet (Beta vulgaris,L.)
Variety
Early Hybrid 7
Early Scarlet Red
Sac Smooth
Black Valentine
Pinto
Sanilac
Maryland Mammoth
Bel-W3
White Gold
Bonny Best
Roma
Old Dominion
Virginia Savoy
Bloomsdale Long Standing
Hybrid 7
Northland
Early Hybrid
Unknown
Reference
100
124
124
124
60
60
60
124
42,100,124
62
33
54
124
100
100
100
95,124
58
100
124
79
124
98
98
98
98
124
124
124
101
6-13
-------
Table 6-7 (continued). LISTS OF PLANTS IN THREE SENSITIVITY GROUPS BY SENSITIVITY
TO OZONE
Species
COMPOSITAE
Chrysanthemum (Chrysamnemum sp.)
Endive (Cichorium endivia,L.)
Stevia (Piqueria trinervia, Cav.)
CORNACEAE
Dogwood (Cornusflorida,L.)
CRUCIFERAE
Broccoli (Brassica oleracea
botrytis.L.)
Cabbage (Brassica oleracea,L.)
GRAMINEAE
Annual Bluegrass (Poa anrlua,L.)
Barley (Hordeum vulgare,L.)
Sweet Corn (Zea mays,L.)
Field Corn (Zea mays,L.)
Oat (Avena sativa,L.)
Rye (Secale cereale,L.)
Sorghum (Sorghum vulgare)
Timothy (Phelum partense,L.)
Wheat (Triticum aestivum, L.)
Wheat (Triticum vulgare)
HYPERICACEAE
Hypercium (Hypercium sp.)
LABIATAE
Coleus (Coleus blumei,L.)
LEGUMINOSAE
Alfalfa (Medicago sativa,L.)
Bean (Phaseolus vulgaris,L.)
Cowpea ( Vigna catjana, Walp)
Lima (Phaseolus lunatus,L.)
Peanut (Arachis hypogaea,L.)
Pea (Pisum sativum)
Soybean (Glycine max)
MALVACEAE
Cotton (Gossypium sp.)
OLEACEAE
Forsythia (Forsythia suspensa,
Vahl.)
PINACEAE
Pine (Pinus ponderosum)
Variety
Pippin
Variegated
Calabrese
Italian Green Sprouting
All Season
Bonneville
lochief
Portwalco
Overland
Unknown
Martin
Lemhi
Wells
Benth
Ranger
Vernal
Unknown
Black Valentine
Mexican Pinto
Early Ramshorn
Thaxter
Starr
Unknown
Scott
Unknown
Arnold
Reference
100
101
100
124
124
98
124
101
60,98
98
98
98,100
124
98
124
124
98
124
60
100
100
98
124
100,124
98
98
124
124
124
100
101
124
124
124
124
102
6-14
-------
Table 6-7 (continued). LISTS OF PLANTS IN THREE SENSITIVITY GROUPS BY SENSITIVITY
TO OZONE
Species
Variety
Reference
ROSACEAE
Peach (Primus persica,L.)
SOLANACEAE
Pepper (Capsicum fmtescens,L.)
Petunia (Petunia hybrida)
Tobacco (Nicotiana tabacum, L.)
UMBELLIFERAE
Paisley (Petroselinum hortense,
Hoffm.)
Elbcrta
Celestial Rose
"C"
White Gold
Turkish
Bel B
Vamorr 48
Moss Curled
98
101
124
98
124
100
99,124
100
98
Resistant
ACERACEAE
Red Maple (Acer rubrum)
AMARYLLIDACEAE
Onion (Allium cepa,L.)
BALSAMINACEAE
Impatiens (Impatiens sp.)
(Impatiens sultani. Hook)
BEGONIACEAE
Begonia (Begonia sp.)
CELASTRACEAE
Euonymous (Euonymous sp.)
CHENOPODIACEAE
Beet (Beta vulgaris.L.)
COMPOSITAE
Chrysanthemum (Chrysanthemum sp.)
Endive (Cichorium endivia,L.)
Lettuce (Lactuca sativa,L.)
Marigold (Tagetes sp.)
Zinnia (Zinnia sp.)
CONVOLVULACEAE
Sweet Potato (Ipomea batatas,
Lam)
CRASSULACEAE
Kalanchoe (Kalanchoe diagremontiaiw, Hamet &
Pierrier)
Yellow Sweet Spanish
Unknown
Detroit Dark Red
Unknown
Green Curled
Unknown
Romaine
Unknown
Porto Rico
124
98
79,124
98
124
98,124
124
98
100,101,124
98,100,124
98
124
98
101
124
124
100
100
6-15
-------
Table 6-7 (continued). LISTS OF PLANTS IN THREE SENSITIVITY GROUPS BY SENSITIVITY
TO OZONE
Species
Variety
Reference
CRUCIFERAE
Turnip (Brassica rapa,L.)
Radish (Raphanus sativus,L.)
CURCURBITACEAE
Cucumber (Cucumis sativus,L.)
EUPHORBIACEAE
Poinsettia (Euphorbia pulcherrima)
GERANIACEAE
Geranium (Geranium sp.)
GRAMINEAE
Annual Bluegrass (Poa annua,L.)
Orchard grass (Dactylis giomerata,L.)
Rice (Oryza sativa, Linn)
Sudangrass (Sorghum vulgare)
HAMAMELIDACEAE
Sweetgum (Liquidambar styraciflua,L.)
IRIDACEAE
Gladiolus (Gladiolus sp.)
JUGLANDACEAE
Black Walnut (Jugians nigra,L.)
LABIATAE
Coleus (Coleus blumei,L.)
Mint (Mentha piperita,L.)
Salvia (Salvia sp.)
LAURACEAE
Avacado (Persea sp.)
LEGUMINOSAE
Bean (Phaseolus vulgaris,L.)
Red Clover (Trifolium pratense,L.)
(Trifolium sp.)
Sensitive Plant (Mimosa pudica,L.)
MALVACEAE
Cotton (Gossypium hirsutum,L.)
OLEACEAE
Lilac (Syringa sp.)
White Ash (Fraximus americana)
ONAGRACEAE
Fuchsia (Fuchsia sp.)
Purple-Top White Globe
Sparkler, White Tip
Marketer
Unknown
Sudanese
Snow Princess
Tendergreen
Upland 1517
Unknown
Acala SJ-1
98
98
98
124
124
98,100,124
98
98
124
124
124
100
124
98,124
100
124
100
100
98
124
100
98
103
84
124
124
98,124
6-16
-------
Table 6-7 (continued). LISTS OF PLANTS IN THREE SENSITIVITY GROUPS BY SENSITIVITY
TO OZONE
Species
Variety
Reference
PINACEAE
Spruce (Picea sp.)
ROSACEAE
Spirea (Spirea sp.)
Strawberry (Fragaria sp.)
RUTACEAE
Lemon (Citrus limon)
SAXIFRAGACEAE
Piggy-back plant (Tolmiea menziesii, Ton & Gray)
SOLANACEAE
Jerusalem Cherry (Solanum pseudo-capsicum,]^.)
Pepper (Capsicum frutenscens,L.)
Petunia (Petunia hybrida, Vilm.)
Potato (Solanum tuberosum,^.)
UMBELLIFERAE
Carrot (Daucus carota,L.)
Parsnip (Pastinaca sativa,L.)
VERBENACEAE
Verbena (Verbena sp.)
VITACEAE
Grape (Vitis vinifera,L.)
SCROPHULARIACEAE
Snapdragon (Antirrhinum ma/us)
Empire
Grossum Bailey
Unknown
Rose Charm
Irish
Imperator
White Model
L.A.
Mission
Zing
Tokay
Concord
Unknown
124
124
100,124
101
100
100
100
124
98
124
98
98
100
98
100
100
100
50
124
effective germicide at concentrations below
the level of human sensitivity (80 jug/m3, or
0.04 ppm).119 The germicidal effectiveness
of ozone varies with its concentration, the
relative humidity, and the species of
bacteria.105'107'120 Jordan and Carlson1 20
were unable to obtain any positive germicidal
action for ozone against bacteria (Staphylo-
coccus pyrogenes, Staphylococcus aureus and
Bacillus pyocyaneus) grown on agar plates
and exposed to 5,880 to 9,016 Aig/m3 (3.0 to
4.6 ppm). Concentrations which killed dry
typhus bacilli, staphylococci, or streptococci
in the course of several hours, were found by
Sawyer et al. to kill guinea pigs sooner.1 °6
Hibben found ozone toxic to the exposed
moist fungus spores of some species, even at
the 200 Mg/m3 (0.1 ppm) level.108 Exposure
to 980 and 1,960 Mg/m3 (0.5 and 1.0 ppm)
reduced or prevented germination of spores of
all species tested. Ozone at 200 /ug/m3 (0.1
ppm) for 4 hours or at 1,960 /ug/m3 (1.0
ppm) for 2 hours stopped apical cell division
of conidiophores of Alternaria solani and
caused collapse of the apical cell wall.1 °9
Giese and Christensen found that protozoa
6-17
-------
in hanging drop suspensions exposed to
approximately 8 percent ozone in ozonized
water were killed in from 4 minutes (col-
pidium) to a maximum of 64 minutes (Til-
lina).121
Scott and Lesher, in studies of the effects
of ozone on Escherichia coli, found that
ozone caused leakage of the cell contents into
the medium, with lysis of some cells.11 *
They postulated that the primary effect of
ozone was on the cell wall or membrane of
the bacteria, probably by reaction with the
double bonds of lipids, and that the leakage
depended on the extent of the reaction. The
bactericidal action of ozone on E. coli has
been considered by Fetner and Ingols to be an
all-or-none effect.112 Haines found that E.
coli growth in a culture medium was retarded
by 7,840 Aig/m3 (4 ppm) ozone in the
atmosphere and that 19,600 Mg/m3 (10 ppm)
ozone prevented bacterial growth.1 J 3
Elford and van den Ende found that 390
/ug/m3 (0.2 ppm) ozone in a moderately
humid atmosphere exercises a very definite
lethal effect against certain bacteria deposited
from aerosol mists or suspensoids on various
surfaces.122 The effectiveness depends on:
(1) the type of surface on which the bacteria
are deposited, (2) the medium in which the
organisms are contained before being sprayed
(a higher protein content favoring protection
of the bacterium in the ultimate particle), and
(3) the different resistances to ozone of the
different types of organism. Relative humidi-
ty plays a dominant role in influencing the
action of ozone, particularly when the gas is
present in low concentrations. In relatively
dry air, at relative humidities lower than 45
percent, there was no appreciable killing
action on the bacterial aerosols studied, even
when the ozone concentration was in excess
of 1,960 Mg/m3 (1.0 ppm). In contrast, when
Streptococcus salivarius, in a fine aerosol-
broth suspension, was exposed at a relative
humidity of 60 to 80 percent to 50 Mg/m3
(0.025 ppm) ozone for 30 minutes and
deposited from the aerosol on glass plate
surfaces, a kill of more than 90 percent
resulted.
6-18
The effects exerted by humidity on fine
suspensoid systems of bacteria depend on: (1)
its purely physical effect on limiting particle
size and settling rate, (2) its effect on the
normal viability, and (3) the interaction be-
tween ozone and the organisms, as reflected
in the increased death-rate of the latter when
influenced by high humidity. When bacteria
are covered with a protective coating of
organic matter, as in coarse aerosols from
suspensions containing appreciable amounts
of serum protein such as in sneezes and
coughs, ozone toxicity rapidly diminishes and
much greater concentrations are necessary to
achieve any appreciable killing effect on the
organisms. Elford and van den Ende's evi-
dence1 22 leads to the conclusion that ozone,
at low concentrations which do not otherwise
cause irritation of the human respiratory
tract, cannot be expected to provide any
effective protection against airborne bacterial
infection through direct inactivation of the
infectious carrier particulates. A summary of
the effects of ozone on certain microorga-
nisms is given in Table 6-8.
H. SUMMARY
Injury to vegetation was one of the earliest
manifestations of photochemical air pollu-
tion. Due to this fact, sensitive plants have
been useful biological indicators of this type
of pollution. The visible symptoms of photo-
chemical-oxidant-produced injury to plants
may be classified as: 1) acute injury, identi-
fied by cell collapse with subsequent develop-
ment of necrotic patterns; 2) chronic injury,
identified by necrotic patterns with or with-
out chlorotic or other pigmented patterns;
and, 3) physiological effects, including growth
alterations, reduced yields, and changes in the
quality of plant products. The acute symp-
toms are generally characteristic of a specific
pollutant while, though highly characteristic,
chronic injury patterns are not. Injury to
leaves by ozone is identified as a stippling or
flecking. Such injury has occurred experi-
mentally in the most sensitive species after
exposure to 60 Mg/m3 (0.03 ppm) ozone for 8
hours. Injury will occur in shorter time
-------
periods when low levels of sulfur dioxide are
present. PAN-produced injury is characterized
by an under-surface glazing or bronzing of the
leaf. Such injury has occurred experimentally
in the most sensitive species after exposure to
50 Mg/m3 (0.01 ppm) PAN for 5 hours. Leaf
injury has occurred in certain sensitive species
after a 4-hour exposure to 100 jug/m3 (0.05
ppm) of total oxidant. Ozone appears to be
the most important phytotoxicant in the
photochemical complex.
There are a number of factors affecting the
response of vegetation to photochemical air
pollutants. Variability in response is known to
exist between species of a given genus and
between varieties within a given species.
Varietal variations have been most extensively
studied with tobacco. In fact, a sensitive
tobacco strain, Bel-W3, has been isolated and
developed for use as a biological indicator of
ozone injury.
The influence of light intensity on the
sensitivity of plants during growth appears to
depend on the phytotoxicant. Plants are more
sensitive to PAN when grown under high light
intensities, but are more sensitive to ozone
when grown under low light intensities. Re-
ported findings are in general agreement that
sensitivity of greenhouse-grown plants to oxi-
dants increases with temperature from 40° to
100° F. However, there is some indication
that this positive correlation may result from
the overriding influence of light intensity on
sensitivity.
The effects of humidity on tne sensitivity
of plants has not been well documented.
General trends indicate that plants grown
and/or exposed under high humidities are
more sensitive than those grown at low
humidities. Though there has been little
research in this direction, there are indications
that soil factors influence the sensitivity of
plants to phytotoxic air pollutants. Plants
grown under drought conditions are less
susceptible than those grown under moist
conditions. Studies indicate that plants appear
to be more sensitive when they are grown in
soil having low total fertility.
The age of the leaf under exposure is
important in determining its sensitivity to air
Table 6-8. SUMMARY OF EFFECTS OF OZONE ON BACTERIA AND PROTOZOA
Organisms
Bacteria
Streptococcus salivarius
Organisms sprayed in air
in Singleton fine broth
suspension and collected
on agar plates
E. coli
Ozone is admitted when
bacteria are inoculated
in Nelson's medium
Staphylococcus pyogenes,
Bacillus pyocyaneus,
Staphylococcus aureus.
Protozoa
Colpidium
Blepharisma
Paramecium
Amoeba
Didinium
Tillina
Concentration, ppm
0.025
4.0
10.0
3.0-4.6 (Acid
KI method)
8.0
Experimental conditions
30 minutes
Relative humidity =
60-80 percent,
20° C
1.5-4.5 hours
Between
4 minutes
(Colpidium) and
64 minutes
(Tillina),
in descending
order
Effects
90 percent
mortality
Retarded growth
Prevented
bacterial growth
No positive
germicidal action
100 percent
mortality
Reference
122
113
113
120
121
6-19
-------
pollutants. There is some evidence that oxi-
dant or ozone injury may be reduced by
pretreatment with the toxicant.
Identification of an injury to a plant as
being caused by air pollution is an arduous
undertaking. Even when the markings on the
leaves of a plant may be identified with an air
pollutant, it is often quite difficult to evaluate
these markings in terms of their effect on the
intact plant. Further difficulty arises in trying
to evaluate the economic impact of air pol-
lution damage to the plant.
The interrelations of time and concen-
tration, or dose, as they affect injury to
plants, are essential to air quality criteria.
There are, however, only scant data relating
concentrations and length of photochemical
oxidant exposure to chronic injury and
effects on reduction of plant growth, yield, or
quality. There is also a dearth of information
relating acute injury to concentrations and
duration of exposure to PAN or mixtures of
photochemical oxidants. A larger body of
information exists on the acute effects of
ozone but even in this instance, the informa-
tion is far from complete. Sufficient data do
exist, however, to present, in tabular form,
ozone concentrations which will produce 5
percent injury to sensitive, intermediate, and
resistant plants after given short-term ex-
posure, as shown in Table 6-5. Information
available lists 20 species and/or varieties as
"sensitive," 55 as "intermediate in sensi-
tivity," and 64 as "relatively resistant."
Bacteriostatic and bacteriocidal properties
of photochemical oxidants in general have
been demonstrated. The growth suppression
of microorganisms by ozone is a well-known
phenomenon, although ozone concentrations
for this activity are undesirable from a human
standpoint. The bacteriocidal activity of
ozone varies with its concentration, the rela-
tive humidity, and the species of bacteria.
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Escherichia coli at 1°. J. Gen. MicrobioL 75(2):381-385,
October 1956.
113.Haines, R.B. Effect of Pure Ozone on Bacteria. In:
Report of the Food Investigation Board for the Year
1935. London, Her Majesty's Stationery Office, 1936.
p. 30-31.
114.Nagy, R. Application of Ozone Form Sterilamp in
Control of Mold, Bacteria, and Odors. In: Ozone
Chemistry and Technology. Vol. 21, Advances in
Chemistry Series. Washington, D.C., American Chemical
Society, 1959. p. 57-65.
115.Ehrlich, R. Sterilizing with Ozone. Armour Research
Foundation, Chicago, Illinois. Frontier. 22(4): 16, 1960.
116. Torricelli, A. Drinking Water Purification. In: Ozone
Chemistry and Technology. Vol. 21, Advances in
Chemistry Series. Washington, D.C., American Chemical
Society, 1959. p. 453465.
117. GuinarcTi, P. Three Years of Ozone Sterilization of
Water in Paris. In: Ozone Chemistry and Technology.
Vol. 21, Advances in Chemistry Series. Washington,
D.C., American Chemical Society, 1959. p. 416-429.
118. Miller, S.et al. Disinfection and Sterilization of Sewage
by Ozone. In: Ozone Chemistry and Technolgy. Vol.
21, Advances in Chemistry Series. Washington, D.C.,
American Chemical Society, 1959. p. 381-387.
119. Witheridge, W.N. and C.P. Yaglou. Ozone in Ventilation
- Its Possibilities and Limitations. Trans. Amer. Soc.
Heating and Ventilating Engrs. 45:509-520, July 1939.
120. Jordan, E.O. and A.J. Carlson. Ozone: Its Bactericidal,
Physiologic and Deodorizing Action. J. Amer. Med.
Assoc. 67(13): 1007-1012, September 27, 1913.
121. Giese, A.C. and E. Christensen. Effects of Ozone on
Organisms. PhysioL ZooL 27(2): 101-115, April 1954.
122.Elford, W.J. and J. van den Ende. An Investigation on
the Merits of Ozone as an Aerial Disinfectant. J. Hyg.
42:240-265, May 1942.
123. Heck, W.W. and A.S. Heagle. Measurement of Photo-
chemical Air Pollution with a Sensitive Monitoring
Plant. JAPCA, 20 February 1970.
124. Heck, W.W., D.T. Tengey, and F.L. Fox. Effects of
Ozone on a Selected Group of Economically Important
Crops. USDHEW, PHS, EHS, National Ail Pollution
Control Administration. Raleigh, N.C. (Scheduled to be
published, July 1970).
6-23
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Chapter 7.
THE EFFECT OF OZONE ON MATERIALS
A. INTRODUCTION
The total extent of damage to materials
caused by atmospheric levels of ozone is not
known. Ozone may be a major contributor to
the degradation of materials which is now
attributed to "weathering." To date, the
majority of the research in this area has been
concerned with only two classes of materials,
the elastomers and textiles. Within these two
groups, certain specific organic compounds
are much more sensitive to attack by atmos-
pheric concentrations of ozone than animals
or humans. There may be, therefore, eco-
nomic incentives to control ozone levels well
below the concentrations which may be estab-
lished as hazardous to humans.
B. MECHANISMS OF OZONE ATTACK
Ozone is so active that, when concentrated,
it becomes a materials-handling problem. In
general, any organic material is incompatible
with concentrated ozone.1 Bailey has re-
viewed the literature thoroughly from 1939
to 1957 for reactions of ozone with organic
compounds, and he describes the reaction
mechanisms in detail.2 Although it is incor-
rect to assume that all of these reactions will
occur at atmospheric concentrations of
ozone, it is possible that some of these
mechanisms would be operant.
Many polymers are sensitive to atmospheric
concentrations of ozone.3 Both chain-
scissioning and crosslinking take place in
polymers exposed to ozone at atmospheric
levels. Chain-scissioning results in increased
fluidity and a loss in tensile strength. Cross-
linking increases the rigidity of the polymer,
reducing elasticity, and brittleness may result.
An example of chain-scissioning is as fol-
lows :3
RHC
=CHR'-^RHC-CHR'
•RHCOO + OCHR
The sensitivity of polymers to chain-
scissioning, therefore, is related to the pre-
valence of double bonds in their structure.
Since almost all rubbers possess such a chem
ical structure, they are prone to this type of
oxidative attack.4'5 A similar type of attack
has been proposed for the degradation of
dyes.6
C. THE EFFECT OF OZONE ON RUBBER
Rubber is an economically important mate-
rial that is highly sensitive to ozone attack.
The most vulnerable generic formulations are
natural, styrene-butadiene, polybutadiene,
and synthetic polyisoprene.7 These types
account for 85 percent by weight of the
estimated 1969 national production of rub-
ber.8 With the exception of natural rubber,
the major use for each of these elastomers is
in tires.9 Thus most of the rubber that is
susceptible to ozone-cracking is exposed to
the atmosphere in a state of tensile stress.
Butyl, halogenated butyl, polychloroprene,
vinyl-modified nitrile-butadiene, and carbo-
xylated nitrile rubbers have some ozone resist-
ance but require special formulation for opti-
mum performance. Synthetic rubbers with
saturated chemical structures, such as sili-
cones, ethylene-propylene, chlorosulfonated
polyethylene, polyacrylate, and fluorocarbon
rubbers have inherent ozone resist-
ance.4'10"16 These latter special-application
materials, however, are relatively expensive
and account for only a small fraction of the
market on a weight basis.
A tensile stress is necessary to produce
ozone-cracking of rubber. If strained as little
7-1
-------
as 2 or 3 percent and exposed to an atmos-
phere containing 20 to 40 jug/m3 (0.01 to
0.02 ppm) ozone, cracks will develop per-
pendicular to the stress axis.1';12 Rubber in
a relaxed state can be exposed for long
periods of time to relatively high concentra-
tions of ozone without visible cracking.17
The rubber is apparently protected by the
formation of an ozonide film on the surface.4
The embrittled film cracks when strained and
exposes fresh surface to the atmosphere. The
strong dependence of crack-growth on nomi-
nal tensile stress has been explained in terms
of fracture mechanics.18 However, the
"Griffith theory" only partially explains ob-
served relationships between number and size
of cracks as a function of strain.5'18 Crack
growth rate is also ozone concentration-
dependent,18 which suggests that the rate of
diffusion of ozone to the root of a crack is
the rate-controlling factor.
Andrews has taken advantage of the frac-
ture mechanics behavior of various rubbers to
compound for ozone resistance and other
desired properties.19 Blends of natural rubber
with an ethylene-propylene copolymer are
more resistant to ozone-cracking than natural
rubber alone. Specimens of blends from 0 to
50 percent ethylene-propylene, strained from
5 to 100 percent, were exposed to 980
mg/m3 (500 ppm) ozone in air. Micro -cracks
were observed in all of the blends, the
crack density increasing with a decrease of
ethylene-propylene rubber. The addition of
the ethylene-propylene copolymer raises the
critical stored energy necessary to propagate
the observed mz'cro-cracks into the macro-
cracks characteristic of ozone damage.
Antiozonant additives, such as p-phenyl-
enediamine derivatives, have been developed
and protect elastomers from ozone degrada-
tion. These chemicals are expensive, however,
and add to the cost of rubber products. One
company spent $2 million for research and
development prior to constructing a multi-
million-dollar plant to produce one type of
antiozonant.20 The addition of 1.5 percent
antiozonants to automobile tires costs up to
7-2
$0.50 per tire. With the 1969 production of
automobile tires reported to be over 203
million,21 the cost to the public of antiozon-
ants in tires alone could approach $100
million. Antiozonants are also used in con-
veyor belts, automotive rubber parts, wire and
cable, and other products as well as tires.
The use of antiozonants has its limitations.
The amount required to be effective increases
with the anticipated amount of ozone to be
encountered.22 In some cases these inhibitors
may provide only temporary protection
against ozone damage, because some of them
migrate to the surface of the rubber product
with usage.4 Oils, gasoline, and other chemi-
cals tend to extract antiozonants from the
rubber, leaving it again susceptible to ozone
attack. Thus, in spite of preventive measures,
ozone-cracking of rubber products is still a
major problem.
A number of factors affect the rate of
attack of ozone on rubber:4 (1) the amount
of tensile stress, (2) the type of rubber
compound, (3) concentration of ozone, (4)
period of exposure, (5) rate of diffusion of
ozone to the rubber surface, and (6) tempera-
ture. Dose-response data, therefore, are neces-
sarily dependent on these factors. Also, the
method for reporting damage varies from one
researcher to another. For example, damage
may be expressed as time to initiate either
micro -cracks or visible cracks, or it may be
expressed in crack-depth or crack-growth rate.
The following examples of dose-response data
should be considered with these factors in
mind.
Bradley and Haagen-Smit evaluated the
rubber formulation indicated in Table 7-1 for
susceptibility to ozone-cracking.1 3
This formulation was selected for its sensi-
tivity to ozone. Strips were strained approxi-
mately 100 percent by bending. These speci-
mens, if exposed to 39,000 mg/m3 (2 percent
or 20,000 ppm) ozone in air would crack
instantaneously and break completely within
1 second.
Results of Bradley and Haagen-Smit's
standard tests, using a gas flow rate of 1.5
-------
liters per minute through a 13-mm tube at
room temperature, are given in Table 7-2.
Edwards and Story have determined the
effects of ozone on "hot" (Polysar-S) and
"cold" (Polysar-krylene) stryene-butadiene
rubbers (SBR) containing various amounts of
antiozonant.2 2 The ingredients added to the
base polymer are listed in Table 7-3. The
results are given in Table 7-4.
Thin polybutadiene specimens were ex-
posed, under constant load, to room air for
which the average concentrations of ozone
had been determined.2 3 The specimens ex-
Table 7-1. FORMULATION OF HIGHLY
OZONE-SENSITIVE RUBBER
13
Ingredient 3
Rubber
Tire reclaim
SRF black
Stearic acid
Pine tar
Zinc oxide
Mercaptobenzothiazole
Diphenyl guanidine
Sulfur
Parts by weight
100
125
33
1.5
8.4
4.7
0.8
0.1
5
Percent by weight
35.91
44.88
11.85
0.54
3.02
1.69
0.29
0.03
1.79
40 minutes at 45 psi steam.
Table 7-2. EFFECT OF OZONE ON RUBBER3'13
Ozone concentration11
Mg/m3
40
510
880
ppm
0.02
0.26
0.45
Time to first sign of crack at 4X
magnification, minutes
65
5
3
aSpecial formulation of Bradley and Haagen-Smit, strained
100 percent.
Determined by neutral KI.
Table 7-3. TIRE SIDEWALL FORMULATION
22
Ingredient
Polymer (hot or cold SBR)
Circosol 2 X H
FEF Black
SRF Black
Zinc Oxide
Stearic Acid
Antiozonant (Santoflex AW)
Crystex
Parts by Weight
100
10
30
10
3
2
Variable
2
posed in the summer months, to average
ozone concentrations of about 94 /ug/ni3
(0.048 ppm), failed by breaking into two
separate parts after 150 to 250 hours. In the
fall, at average ozone concentrations of 82
Atg/m3 (0.042 ppm), specimens failed between
400 and 500 hours. In the winter, at average
ozone concentrations of 47 Mg/m3 (0.024
ppm), failures occurred between 500 and 700
hours. These data show the strong depend-
ence of cracking rate on the average concen-
tration of ozone.
The behavior of rubber exposed to ozone
under laboratory conditions correlates well
with the service behavior of tires in localities
where atmospheric ozone concentrations are
high.24 The relative susceptibility of white
sidewalls made from different formulations
remains the same, whether in a laboratory
test, in which they are exposed to as much as
980 Mg/m3 (0.5 ppm) ozone, or in the ambient
air of the Los Angeles area. The rate of
cracking is thus a function of ozone concen-
tration.
As the tread wear on passenger car tires
improves, more or better antiozonants will
Table 7-4. EFFECTS OF OZONE ON SIDEWALL
FORMULATIONS CONTAINING VARIOUS
ANTIOZONANT CONCENTRATIONS3'22
Polymer
"Hot" SBR
(Polysar-S)
"Cold" SBR
(Polysar-drylene)
Antiozonant
concentration,
(Santaflex AW),
percent
0
0.32
0.63
1.25
0
0.32
0.63
1.25
Rate of
cracking,
10'4
in./hr
0.92
0.69
0.35
0.13
1.58
0.85
0.57
0.24
Time to
first sign
of crack ,b
minutes
65
87
170
460
38
71
105
250
Specimens were strained initially at 100 percent and
exposed at 120 F to an ozone concentration of 490 ±100
Mg/m3 (0.25 ± 0.05 ppm).
bAdded to enable comparison with data in Table 7-2. First
sign of crack was assumed to be 10~4 inch crack depth, visible
at 4X magnification. Data are not found in reference 22.
7-3
-------
have to be added to sidewall formulations to
prevent sidewall cracking from becoming the
limiting factor in tire life. Thus, part of the
cost of premium tires will be due to atmos-
pheric ozone.
D. THE EFFECT OF OZONE ON FABRICS
AND DYES
1. Damage to Textile Fabrics
Ozone attacks cellulose by two mecha-
nisms.25 One is a free-radical chain mecha-
nism involving oxygen in the propagating
step, and the other appears to be an electro-
philic attack on double bonds. Bogaty et al.2 6
have shown that ozone attack at atmospheric
levels results in the deterioration of wet
cotton textiles. Two types of cotton fabric,
duck and printed cloth, were exposed, both
wet and dry, for 50 days to an atmosphere
containing between 40 and 120 jug/m3 (0.02
and 0.06 ppm) ozone. The deterioration of
the two fabrics was shown by comparing
dissolved fabric fluidity values before and
after exposure. The value for the wet duck
cloth increased from 2.6 to 9.5 rhe (a cali-
brated measure of fluidity which is inversely
proportional to viscosity), while the value for
the wet printed cloth increased from 8 to 16
rhe. Both fabrics, when wet, also showed a
20 percent loss in tensile strength due to the
exposure. When exposed dry, neither fluidity
values nor tensile strengths were changed
appreciably. The fabrics demonstrated that
increasing the ozone concentration increased
the amount of damage to the cellulose.
Morris and Young27 found in their labora-
tory experiments that light as well as humid-
ity is necessary to change appreciably break-
ing strength and cellulose fluidity. In the
absence of light, 980 jug/m3 (0.5 ppm) ozone
at 21° C (70° F) and 72 percent relative
humidity for 1,200 hours had little degrading
effect on Acala 4-42 and Pima S-l cotton
fabrics.28 In a later study, Kerr et al.29
showed that light was not necessary to de-
grade cotton in air containing ozone. Cot-
ton print cloth dyed with C. I. Vat Blue 29
was exposed at 25° C in an airtight chamber
containing a shallow pan filled with water so
as to increase the relative humidity in the
chamber. Purified air to which oxygen had
been added was passed through another cham-
ber containing three 4-watt ozone bulbs and
then directly into the exposure chamber. The
concentration of ozone was adjusted by vary-
ing the number of ozone lamps in operation,
the amperage used, and the amount of pure
oxygen added to the air intake. The concen-
tration of the ozone fed into the chamber was
1960 ± 200 /zg/m3 (1 ±0.1 ppm), and the
exit concentration, recorded with a Mast
Ozone Meter, was 980 jug/m3 (0.5 ppm).
Specimens were removed at 3-day intervals
and either washed or soaked. Control speci-
mens were kept in light-tight chambers at
21° C (70° F) and 65 percent relative
humidity and were given the same cycle of
washing or soaking. After 60 days of expo-
sure, the washed fabrics had an 18.2 percent
greater strength loss than did the controls.
Cellulose fluidity values also indicated degra-
dation caused by exposure to ozone. The
washed fabrics exposed to ozone had a
fluidity value of 9.27 rhe as compared to a
value for the control samples of 5.37 rhe.
Peters and Saville30 have reported that in
their experiments, the effects of high ozone
concentrations on breaking strengths are sig-
nificant for white nylon and polyester fabrics
but are not significant for cotton, acetate, or
fiberglass. Based on these results and the
results of other researchers, the relative sus-
ceptibility in increasing order of different
fibers to ozone attack is cotton, acetate,
nylon, and polyester.
2. Fading of Dyes
The first evidence of ozone causing the
fading of dyes was obtained when acetate
fiber samples dyed with Disperse Blue-27
(developed for nitrogen dioxide resistance)
were field-evaluated.31 These samples were
exposed to the atmosphere in light-tight
containers in Pittsburgh, Pa., which has a high
nitrogen dioxide concentration, arid Ames,
Iowa, where a low nitrogen dioxide concen-
7-4
-------
tration is recorded. After 6 months, samples
in Ames had faded but had not in Pittsburgh.
Laboratory exposure of similar samples to
200 Mg/m3 (0.1 ppm) ozone duplicated the
fading observed in Ames. It was further found
that all blue anthraquinone dyes were sensi-
tive to change as were certain anthraquinone
red dyes. Azo red and yellow dyestuffs and
diphenylamine yellow dyes were not sensitive
to ozone. Thus fading in Ames was attributed
to naturally occurring high levels of ozone.
In previously described research, Kerr et
al.29 measured the fading of vat-dyed cotton
fabrics caused by ozone. The results are
presented in Table 7-5 and indicate that the
rate of fading and the maximum amount of
the fading which will occur are both depend-
ent upon the environment. The soaked fabrics
faded in ozone more rapidly and to a greater
extent than did the laundered fabrics. It was
suggested that laundering produced a change
in the dye and improved its ozone resistance.
Salvin exposed wool, cotton, nylon,
acetate, orlon, and polyester fabrics, all dyed
with ozone sensitive dyes, to the atmosphere
of the cities of Chicago and Los Angeles and
the rural, nonindustrial areas of Sarasota,
Florida, and Phoenix, Arizona.32'33 In Los
Angeles, where ozone concentration is high,
the dyes were most affected, whereas those
exposed in Chicago were the least affected. In
humid Florida, dyes faded more than they did
in dry Arizona. The extent of ozone fading
was related to different concentrations and
durations of exposure in the different local-
ities.
Customer complaints of fading have been
attributed to attack by ozone.34'35 The
fading of polyester materials was not a pro-
blem until cotton/polyester fabrics were fin-
ished for permanent press. The type of
permanent press treatment which resulted in
fading used a magnesium chloride catalyst
which formed a soluble complex with the
blue dyes used on polyester. The dyes migrated
to the-finish, where they are susceptible to
ozone fading.34
A combination of high humidity and
ozone has caused fading of nylon carpets.35
The fading rates of any one dye in ozone-
containing atmospheres is a function of the
nylon structure as well as the environment.
This observation is attributed to the differ-
ences in adsorption onto and diffusion into
different nylons. The greater the surface area
exposed and the more open the microstruc-
ture, the more sensitive the nylon is expected
to be to ozone fading. Swelling of nylon due
to high humidity should increase both the
surface area and the rate of diffusion into the
fiber.35
By experimentations, combinations of fab-
rics, dyes, and treatments can be selected to
eliminate ozone fading.35 The additional ex-
pense both in research and the use of more
costly materials, however, is passed on to the
Table 7-5. SUBJECTIVE COLOR CHANGE OF DYED COTTON EXPOSED TO OZONE
CONCENTRATIONS BETT^EEN 980 and 1960 Mg/m3 (0.5 and 1.0 ppm) 29
Number of
days treated
12
24
36
48
60
Washed fabrics
Gray scale
4.0
2.5
2.5
2.0
2.0
NBS units3
1.5
4.5
4.5
6.0
6.0
Soaked fabrics
Gray scale
2.5
2.0
1.0
1.0
1.0
NBS units3
4.5
6.0
12.0
12.0
12.0
a NBS units = AL2 + Aa2 + Ab2wnere:
L = 10 \/Rd (Rd = reflectance)
a = measure of green to red color change.
b = measure of blue to yellow color change.
A= difference between exposed and unexposed.
7-5
-------
customer and is an indirect cost of ozone in
the atmosphere. Since dyes have been found
to fade also at ozone levels produced by
natural processes, it is extremely difficult to
determine what fraction of additional cost
may be due to man-made ozone levels.
E. THE NEED FOR FUTURE RESEARCH
It is highly probable that present know-
ledge of ozone damage to materials is only a
small fraction of the total. The interaction
effects between ozone and other pollutants
on materials has not been investigated. From
thermodynamics, it would be expected that
ozone would oxidize both nitrogen tetroxide
(N2 O4) and sulfur dioxide (SO2 ) to nitrogen
pentoxide (N2OS) and sulfur trioxide (SO3)
respectively. At the low concentrations found
in the atmosphere, the kinetics of the react-
ions in the gas phase may be too slow to be
considered. When adsorbed on solid surfaces
of materials, however, the reactions may be
catalyzed to appreciable rates. N2OS and SO3
form nitric acid and sulfuric acid respectively
when dissolved in water. Many materials are
attacked by these acids, and the diurnal
condensation-evaporation cycle of atmospher-
ic moisture on material surfaces would be
expected to concentrate these dissolved acids
if they did not react immediately with the
material. In this manner, damaging concentra-
tion levels could be reached.
An example of this type of behavior was
reported by Morris.2 8 A good statistical
correlation was obtained between breaking
strengths of cotton fabrics and the pH values
of water extracted from them. The breaking
strength decreased with a decrease in pH.
Correlations were also obtained with relative
humidity and the amount of sunlight at the
exposure sites. Breaking strength decreased
with increases of both humidity and amount
of sunlight. The amount of nonfibrous mater-
ial taken from fabric samples exposed in
California in May and June was 1.32 percent
and the pH of the water extract was 4.93. In
contrast, the value for the unexposed sample
was 0.29 percent, with a pH of 6.65.
Much more dose-response data are needed
7-6
before the economic impact of ozone can be
calculated. Although there may be sufficient
data for rubber, data for other organic mater-
ials such as fabrics, dyes, paints, and plastics
are sadly lacking. There have been no investi-
gations to determine the dose-response re-
lationships of combinations of ozone with
other pollutants on either organic or inorganic
materials.
F. SUMMARY
Although the total extent of ozone-associ-
ated damage to materials is not known, ozone
may very well be a major contributor to the
"weathering" of materials. Ozone is an ex-
tremely active compound, and generally any
organic material is incompatible with concen-
trated ozone. Many organic polymers are
subject to chemical alteration from exposure
to very small concentrations of ozone, includ-
ing some ambient concentrations. This sensi-
tivity usually increases with the number of
double bonds in the chemical structure of the
polymer.
Rubber is an economically important ma-
terial that is highly sensitive to ozone attack.
The most vulnerable generic groups of rubber
are natural, styrene-butadiene, polybutadiene,
and synthetic polyisoprene. Although a ten-
sile stress is necessary for ozone to produce
cracking of rubber, rubber products are
usually used in this state. Other factors which
determine the rate of ozone-attack on rubber
are the type of rubber compound, the concen-
tration of ozone, the period of exposure, the
rate of diffusion of ozone to the rubber
surface, and temperature. Although rubber in
a relaxed state can be exposed for long
periods of time without visible cracks form-
ing, cracks can develop from exposure to an
atmosphere containing 20 to 40 Mg/m3 (0.01
to 0.02 ppm) ozone if the rubber is under a
strain of as little as 2 or 3 percent. Antiozon-
ant additives have been developed and are
capable of protecting elastomers from ozone
degradation. These additives are expensive,
and they sometimes migrate with usage to the
surface of the rubber product and thus afford
only Limited protection. Oils, gasoline, and
-------
other chemicals may extract antiozonants
from rubber and thus also decrease the
resistance of the rubber product to ozone
attack.
Ozone attacks the cellulose in textile fab-
rics through both a free-radical chain-mechan-
ism and an electrophilic attack on double
bonds. Light and humidity appear to be
factors which must be present before an
appreciable alteration occurs in the breaking
strength and fluidity of fibers. The relative
susceptibility of different fibers to ozone
attack, in increasing order, appears to be:
cotton, acetate, nylon, and polyester.
Certain dyes are susceptible to fading
during exposure to ozone. The rate and
extent of fading appear to be dependent on
ozone concentration, length of exposure, type
of material used, and environmental factors,
such as relative humidity and the presence or
absence of other atmospheric pollutants.
Technology is capable of selecting combina-
tions of fabrics, dyes, and processing which
can eliminate ozone fading, but the cost of
this will be passed on to the consumer in the
form of increased costs.
To calculate the economic costs of ozone
air pollution, dose-response relationships must
be formulated. At present, this type of data
exists only for rubber. Little, if any informa-
tion is available on dose-response relationships
of the effect of combinations of ozone with
other air pollutants on materials.
G. REFERENCES
1. Cloyd, D. R. and W. J. Murphy. Technology Survey:
Handling Hazardous Materials. National Aeronautics and
Space Administration. Washington, D. C. NASA
SP-5032. September 1965. p. 67.
2. Bailey, P. S. The Reactions of Ozone with Organic
Compounds. Chem. Rev. 55:925-1010, 1958.
3. JeUinek, H. H. G. Fundamental Degradation Processes
Relevant to Outdoor Exposure of Polymers. In: Applied
Polymer Symposium No. 4: Weatherability of Plastic
Materials, Kamal, M. R. (ed.). New York, Interscience
Publishers, 1967. p. 41-59.
4. Jaffe, L. S. The Effects of Photochemical Oxidants on
Materials. J. Air Pollution Control Assoc. 77:375-378,
June 1967.
5. Newton, R. G. Mechanism of Exposure-Cracking of
Rubber (with a Review of the Influence of Ozone). J.
Rubber Res. 14:21-62, March-April 1945.
6. Salvin, V. S. Ozone Fading of Dyes. Text. Chemist
Colons! 7(ll):22-28, May 21, 1969.
7. Crabtree, J. and A. R. Kemp. Accelerated Ozone
Weathering Test for Rubber. Ind. Eng. Chem. (Anal.
Ed.). 18:169-114, March 1946.
8. The Rubber Industry. Rubber Age. 101:45-41, January
1969.
9. Year End Report: Rubber in 1968-A Complete Recov-
ery. Rubber World. .759(4): 34, January 1969.
10. Materials in Design Engineering. August 1966.
11. Crabtree, J. and F. S. Malm. Deterioration of Rubber
From Use and with Age. In: Engineering Uses of Rubber,
McPherson, A. T. and A. Klemin, (eds.). New York,
Reinhold Publishing Corp., 1956. p. 140-170.
12. Fisher, H. L. Antioxidation and Antiozonation. In:
Chemistry of Natural and Synthetic Rubbers. New York,
Reinhold Publishing Corp., 1957. p. 49-55.
13. Bradley, C. E. and A. J. Haagen-Smit. The Application of
Rubber in the Quantitative Determination of Ozone. J.
Rubber Chem. Technol. 24(4):750-755, October-
December 1951.
14. Symposium on Effect of Ozone on Rubber. ASTM
Special Technical Publication Number 229. Philadelphia.
American Society for Testing Materials, 1958. 130 p.
15. Gaughan, J. E. Ozone Cracking of Natural and Synthetic
Rubbers. Rubber World. 7J5(6):803-808, March 1956.
16. Soininen, A., A. L." Pehu-Lehtonon, and E. Auterinen.
Atmospheric Ozone in Helsinki and Its Effects on
Rubber. Rubber Chem. Technol. 36(2):S 16-526, April-
June 1963.
17. Van Rosem, A. and H. W. Talen. The Appearance of
Atmospheric Cracks in Stretched Rubber. Kaut-schuk.
7:79,1951.
18. Braden, M. and A. N. Gent. The Attack of Ozone on
Stretched Rubber Vulcanizates. I. The Rate of Cut
Growth. II. Conditions for Cut Growth. J. Appl. Polym.
Sci. 3(7):90-99, 100-106, January-February 1960.
19. Andrews, E. H. Resistance to Ozone Cracking in Elasto-
mer Blends. J. Rubber Chem. Technol. 40:635-649,
1967.
20. Hopkins, F.A. Marketing of Rubber Chemicals. Uniroyal,
Inc. Presented at American Society Division of Chemical
Marketing and Economics Symposia. San Francisco.
April 1968. 7 p.
21. Current Business Statistics. Survey Curr. Business. 49(5,
Pt. I):S-37,May 1969.
22. Edwards, D. C. and E. B. Storey. A Quantitative Ozone
Test for Small Specimens. Chem. in Canada. 77:34-38,
November 1959.
23. Meyer, D. A. and J. G. Sommer. The Development of
Weather and Aging Resistant Pneumatic Tires and
Mechanical Rubber Goods. The Dayton Rubber Co.
Final Technical Report, AD 143312. June 30, 1957.
24. Hofmann, C. M. and R. L. Miller. Resistance to
Atmospheric Exposure of Passenger Tires. Presented at
American Society for Testing and Materials Meeting.
Atlantic City. February 1, 1968
25. Katai, A. A. and C. Schuerch. Mechanism of Ozone
Attack on Methyl Glucoside and Cellulosic Materials. J.
Polym. Sci. Part A-l. 4:2683-2703, October 1966.
26. Bogaty, H., K. S. Campbell, and W. D. Appel. The
Oxidation of Cellulose by Ozone in Small Concentra-
tions. Text. Res. J. 22:81-83, February 1952.
7-7
-------
27. Morris, M. A., M. A. Young, and T. A.-W. Molvig. The
Effect of Air Pollution on Cotton. Text. Res. J.
54:563-564, June 1964.
28. Morris, M. A. The Effect of Weathering on Cotton
Fabrics. California Agricultural Experiment Station.
Davis. Bulletin Number 23. June 1966.
29. Kerr, N., M. A. Morris, and S. H. Zeronian. The Effect of
Ozone and Laundering on a Vat-Dyed Cotton Fabric.
Amer. Dyestuff Reptr. 5
-------
Chapter 8.
TOXICOLOGICAL APPRAISAL OF
PHOTOCHEMICAL OXIDANTS
A. INTRODUCTION
Photochemical oxidants such as ozone,
oxides of nitrogen, and peroxyacyl nitrates
are gases which tend to exert their toxic
effect by entering the body through inhala-
tion. If present in sufficient concentrations,
these gases are capable of causing death to
various organisms. At sublethal concentra-
tions, they may alter, impair, or otherwise
interfere with normal respiratory processes.
Alterations in pulmonary function and in
the mechanical properties of the lungs are
among the effects found as a result of
inhalation of these compounds. Other effects
which have been investigated include path-
ological changes in the lungs, chemical and
biochemical changes both in the lungs and in
other organs, and eye irritation.
The toxicological effects of three major
pollutant groups, ozone, "oxidants" (mix-
tures of substances produced by photochem-
ical reactions), and peroxyacyl nitrates, are
discussed in this chapter. Each pollutant
group is treated separately, and human and
animal data are treated separately within each
section.
B. OZONE
1. Animal Data
a. Acute Toxicity
The earliest experiments to determine the
acute toxicity of ozone on a variety of animal
species were carried out by Bohr and Maar'in
1904 and by Hill and Flack in 1912.2 Gross
examination of the respiratory organs showed
acute inflammation of the respiratory tract,
often with hemorrhage and edema (abnormal
accumulation of fluid). Death due to this
reaction sometimes occurred within several
hours after the exposure was terminated, but
usually within 24 hours.
Mittler et al.3 have determined the LD50
for ozone in a variety of laboratory animals.
The LDS o of a toxic substance is defined as
that dose expected to kill 50 percent of a
population of experimental animals. These
results are shown in Table 8-1. In most of the
studies carried out, animals were exposed to a
constant level of ozone for a given period of
time. There were no pathological changes in
the lungs of rats exposed to concentfations up
to 6,290 Mg/m3 (3.2 ppm) for 18 to 22 hours.
Data from other sources, although less com-
prehensive, indicate that the observations of
Mittler et al. might occur at much lower
concentrations. 4>s With exposures from
7,800 to 11,800 Mg/m3 (4 to 6 ppm) there
were hemorrhagic changes in the lung; above
6 ppm, both hemorrhage and edema occurred
(Table 8-2). There are no data at present on
the extent of penetration of ozone, but the
occurrence of edema at the alveolar level
presumably reflects some local damage. Very
little is know of the uptake of ozone by
pulmonary tissues or of its half-life following
uptake.
Dose, length of exposure, and fate of ozone
Table 8-1. LD50 OF OZONE FOR VARIOUS SPECIES
AFTER 3-HOUR EXPOSURE 3
Species
Guinea pigs
Rabbits
Mice
Rats
Cats
Ozone, ppm
51.7
36.0
21.0
21.8
34.5
8-1
-------
Table 8-2. EFFECTS OF EXPOSURE OF RATS TO NONLETHAL CONCENTRATIONS
OF OZONE 3
Ozone,
ppm
(C)
3.64.0
3.0-3.5
2.8-3.2
4.4
3.84.4
3.54.1
5.0-5.8
6.0-7.7
Duration of
exposure (t),
hours
18
20
22
18
20
22
18
18
Cxt,
ppm x hours
64.8-72.0
60.0-70.0
61.6-70.4
81.2
76.0-88.0
77.0-90.2
90.0-104.4
108.0-138.6
Gross appearance of lungs,
shown by range of C x t
> Normal, 60.0-72.0
1 Slightly hemorrhagic,
76.0-90.2
Hemorrhagic, 90.0-104.4
Hemorrhagic and
edematous, 108.0-138.6
are not the only factors which determine
toxicity. In a recent review, Stokinger has
listed other factors which influence the res-
ponse to a specific level of ozone.6 These
include:
1. Age: When exposed to 7,800 pg/m3 (4
ppm) for 4 hours, young mice were found
to be 2 or 3 times more susceptible to the
acute toxic effects of ozone than older
animals.
2. Temperature: Susceptibility of rats and
mice to the toxic effects of ozone is
doubled when the temperature is raised
from 75° to 90°F.
3. Exercise: Exercise enhances the tox-
icity of ozone for rats. 1,960 jug/m3 (1
ppm), a level without obvious acute effects,
becomes lethal if animals are made to
undergo forced activity intermittently for a
few minutes each hour during exposure to
the gas.
4. Dosage Rate: The LDS 0 dose of ozone
decreases with increase in the length of
exposure up to 3 hours; it then remains
constant. This appears to be valid over a
concentration range of from 1,960 to
98,000 jug/m3 (1 to 50 ppm).
5. Respiratory Infection: Mice infected
with Klebsiella pneumoniae (a disease-pro-
ducing bacterium) and then exposed to
1,960 /zg/m3 (1 ppm) ozone have shown
shortened survival time and increased mor-
tality. Mice infected with streptococcus
(Group C) and then exposed to 160 ng/m3
(0.08 ppm) ozone for 3 hours exhibited
increased mortality. This decreased resis-
tance to respiratory infection is noted
when the ozone exposures occur either
prior to or following infection.
6. Reducing Agents and Drugs: Prophylac-
tic administration of reducing agents (de-
oxidizing compounds) such as ascorbic acid
(vitamin C), both alone and in combination
with cysteine (an amino-acid) and glucuro-
nate, substantially reduced the edemagenic
response of animals to 03.
7. Intermittent Exposure: The edemage-
nic response, and the associated alterations
in pulmonary function, are reduced mar-
kedly by interruption of ozone administra-
tion and exposure to air. Intervals as brief
as 15 or 20 minutes in repeated 30-minute
exposures to 7,800 Mg/m3 (4 ppm) ozone
reduced edema and mortality among lab-
oratory animals.
In addition to these factors, Skillen7 con-
firmed Fairchild's observation8 of a variation
in the effect of ozone exposure on rats with
varying thyroid status. Three groups of rats
were used. The first received meal containing
0.15 percent propylthiouracil (PTU), a drug
which decreases thyroid activity; the second
received meal containing 0.01 percent strong
desiccated thyroid; the third received untreat-
ed meal. After 4 weeks of feeding, these
animals were continuously exposed to 11,800
8-2
-------
jug/m3 (6 ppm) ozone. The average survival
times of the three groups were: greater than
10 hours for those rats with reduced thyroid
function; 6.7 hours for rats with unaltered
thyroid activity; and 2.2 hours for those rats
with stimulated thyroid function.
(1) Effects on the pulmonary organs.
Changes in pulmonary function.
Several workers have determined the extent
of pulmonary edema and change in pulmon-
ary function in animals following exposure to
ozone. Scheel5 et al. exposed 75 rats to 3,900
/ig/m3 (2 ppm) ozone for 3 hours. After their
removal from the exposure chamber the
oxygen uptake, tidal volume, and frequency
of breating of the rats was measured on a
closed circuit respirometer. The rats were
killed in groups of five, without further
exposure, at intervals over a period of 960
hours. The lungs were excised and weighed
before and after drying. The results are shown
in Figures 8-1 and 8-2. It was found that the
water-content of the lungs increased during
the post-exposure period, the increase reach-
ing a maximum after 12 hours. These authors
expressed pulmonary edema in terms of water
in the lung per kilogram body-weight instead
of per unit dry-lung-weight (Figure 8-1). If
this exposure to ozone is considered a stress,
then changes in body-weight might be ex-
pected to occur, especially over the long
post-exposure periodof 1.000 hours. No data
are given on changes in body weights and
therefore the changes in lung-water-content
given in this paper must be interpreted with
caution.
The authors also reported an increase in the
dry-lung weights during the first 250 hours of
the post-exposure period (Figure 8-1). Again
the results are expressed with reference to
13
11
i
o
I4I£RJNJ-UNG/KG OF RAT
NORMAL WATER IN LUNG/KG OF RAT
DRY LUNG/KG OF RAT
NORMAL DRY LUNG/KG OF RAT
100
300 500 700
TIME AFTER EXPOSURE, hours
900
Figure 8-1. Changes in lung water and tissue of rats exposed to 3,900 |ug/m3 (2 ppm)
ozone for 3 hours.5
8-3
-------
MINUTE VENTILATION
(xlO-1)
OXYGEN CONSUMED/minute —
0 40 80 120 160 200 240 280
HOURS AFTER EXPOSURE
Figure 8-2. Average respiratory response
of 75 rats exposed to 3,900 Mg/m3 (2 ppm)
ozone for 3 hours.5
body-weight. Inspection of the data shows an
apparent twofold increase in the dry-lung-
weight, which can presumably be ascribed to
residual cells, protein, etc., resulting from
pulmonary edema. The increase could also be
partly due, however, to an acute loss of
body-weight.
A decrease in minute ventilation (the
volume of air breathed per minute), tidal
volume (volume per breath), and oxygen
uptake occurred immediately after exposure
and reached minimum recorded values 8
hours after exposure (Figure 8-2). At 20
hours after exposure, all measurements had
returned to initial values. The initial decrease
in the minute ventilation and oxygen uptake
of the animals could have reflected a decrease
in activity (metabolic rate) as a secondary
result of the irritating effects of the exposure.
One factor which might cause a decrease in
activity is the occurrence of pulmonary
edema. The simultaneous increase in minute
ventilation and decrease in oxygen consump-
tion after 40 hours suggests that delayed
impairment occurred. All the data given in
this study on changes in pulmonary function
were expressed with reference to hours after
exposure.
In a second series of experiments, Scheel5
et al. exposed rabbits to ozone concentrations
increasing from 15,700 to 88,200 jug/m3 (8 to
45 ppm) for 1 hour each week. As in the rat
experiments, there was a reduction in tidal
volume and oxygen uptake, reaching a mini-
mum within 1 hour after exposure (Figure
8-3). These parameters increased during the
120
Ill
100
80
z
o
Q_
1/5 «
HI 0)
oi .t so
< E
oc.
20
T
T
T
T
OXYGEN CONSUMED/minute —
TIDAL VOLUME
I I I
10 20 30 40 50
HOURS AFTER EXPOSURE
60
Figure 8-3. Average respiratory response
of eight rabbits following first exposure to
29,000 /jg/m3 (15 ppm) ozone for 30 minutes.5
following 4 hours of the post-exposure
period, but remained below the pre-exposure
values for more than 2 days. After repeated
exposures to ozone, the rabbits showed not
only a marked decrease in tidal volume as a
result of the exposure, but also changes in
oxygen consumption. For example, the nor-
mal control animals consumed 104 to 136 cc
of oxygen per minute, whereas the repeatedly
exposed animals were able to consume only
68 to 98 cc of oxygen per minute before the
tenth exposure. This may have been the
consequence, however, of their subjection to
considerable stress for 2-1/2 months. De-
creased oxygen uptake could be the result of
decreased activity or of loss of weight, both
of which could be secondary to the effects of
ozone.
Murphy9 et al. exposed guinea pigs to
from 590 to 2,650 jug/m3 (0.3 to 1.35 ppm)
8-4
-------
ozone for a period of 2 hours. Measurements
of respiratory rates, tidal volumes, and total
respiratory flow resistances were made before,
during, and after exposure. It was observed
that respiratory rates increased and tidal
volumes decreased during exposure to all con-
centrations (Figure 8-4). The maximum
changes were significantly different (p <
0.05) from the pre-exposure control values
obtained for each concentration shown.
After a maximum response was reached, the
effects tended to remain constant for the
remainder of the test period. Respiratory
rates and tidal volumes tended to return to
pre-exposure control levels when the animals
were returned to clean air. Total respiratory
flow resistances were not significantly altered
during inhalation of ozone concentrations of
670 to 1,330 Mg/m3 (5 to 7 ppm) for 2
hours.10 Measurement of flow resistance, fre-
quency of breathing, tidal volume, and lung
compliance were made before, during, and
after exposure. The results are shown in
Figure 8-5. A threefold increase in flow
resistance occurred during exposure and
reached a maximum after 1 hour. There was a
50 percent increase in frequency of breathing
and a small decrease in tidal volume. Lung
compliance (a parameter which had not been
measured previously) decreased 50 percent.
After exposure, all measurements returned to
pre-exposure values within 180 minutes.
Pathological changes.
Gross autopsy findings of pulmonary
edema and hemorrhage following acute ozone
exposure have been known for some time.11
Scheel5 et al. have provided histopatho-
logic evidence of injury caused by a single
acute exposure of 1,960 or 6,270 /zg/m3(1.0
or 3.2 ppm) ozone for 4 hours in mice and by
repeated intermittent exposures of 15,700 to
88,200 Mg/m3 (8 to 45 ppm) ozone for 1 hour
in rabbits. No gross pulmonary edema was
observed in mice killed immediately after
exposure to 1,960 Mg/m3 (1 ppm), but moder-
ately engorged blood vessels and capillaries
containing an excess of leukocytes (white
blood cells) were found. Mice killed 20 hours
after exposure showed mild edema and migra-
tion of the leukocytes into the alveolar
spaces. Superficial desquamation of the epi-
thelium (peeling away of surface cells) in the
bronchi and bronchioles was also observed.
Inhalation of 6,270 jug/m3 (3.2 ppm) pro-
duced grossly visible edema during or shortly
after exposure. The perivascular lymphatic
vessels were distended and filled with edemat-
ous precipitate. Hyperemia (excess blood),
mobilization of leukocytes, and varying de-
grees of extravasation of red cells (migration
of cells from the capillaries into the tissues)
accompanied the edema. Damage to the res-
piratory tract consisted of loss of epithelium
from the bronchioles, and sheets of desqua-
mated epithelial cells were seen in the lumen.
Repeated exposures of rabbits to ozone
have resulted in damage to the epithelium of
the respiratory tract, increasing in severity
from the lower trachea to the bronchioles.
Growth of fibrous tissue was found in the
walls of the bronchioles and in the alveolar
ducts. The external surface had a puckered
and granular appearance in one rabbit after
the 49th exposure, suggestive of shrinkage of
fibrous tissue. The time of onset of the
fibrous changes was not determined, but the
respiratory tract of one rabbit killed after the
25th exposure contained no such lesions.
Chemical and biochemical changes.
The elastic behavior of the lungs is deter-
mined by both fixed tissue elements and
other substances, such as surfactant (a natural
surface-active agent lining the alveoli), or by
edema. There is evidence that these factors
might be affected by the chemical changes
that have been observed in the lung tissue
following exposure to ozone.
Lung tissue "ground substance" may in-
clude hyaluronic acid, chondroitin sulfuric
acids A, B and C, heparin, keratosulfate, and
the proteins collagen and elastin. Theoreti-
cally, the latter compounds would be expect-
ed to be oxidized by ozone to yield alde-
hydes. In one experiment, Buell12 et al. used
8-5
-------
i 1.2
RESPIRAT|ON RATE
\
\
X
V
N^
Q nnm
0.30
0.68
1.08
1.35
NO. TESTED
5
10
10
4
/ /
/'
'
»
J
*. ^ \
\ \\
.—-T». \ "-
^
•' X
,•' r
0.8
1.3
MINUTE VOLUME ^
N
» *
/
8-6
H-
-OZONE EXPOSURE-
TIME, hours
Figure 8-4. Effect of ozone exposure on respiration of guinea pigs.9
-------
o
a:
H
Z
8
HI
o:
ts>
o
CL
X
Ul
350
300
250
200
150
100
50
— 1
v—i
/
-OZONE, 5-7 ppm-
— —FLOW RESISTANCE
'• — •FREQUENCY
«••—— MINUTE VENTILATION
—-— TIDAL VOLUME
••—"LUNG COMPLIANCE
**»>
\ \
\ ^
v_ •
-AIR-
30
60
90 120
TIME, minutes
150
180
210
Figure 8-5. Respiratory response and recovery of guinea pigs exposed to ozone.
four litter-mate rabbits; 2 were exposed to
1,960 Mg/m3 (1 ppm) ozone for 1 hour, 1 of
which was sacrificed immediately after expos-
ure and the other 24 hours later. Another was
killed immediately after exposure to 9,800
/ug/rn3 (5 ppm) for 1 hour. The fourth was
used as a control. After hydrolysis of the
protein fraction of the lung tissue by the
enzymes hyaluronidase, pepsin, elastase, and
collagenase, the present of carbonyl com-
pounds (e.g., aldehydes and ketones) was
observed. The carbonyl compounds were
identified spectrophotometrically as the cor-
responding dinitrophenyl-hydrazones. It was
concluded that the carbonyl compounds were
most likely derived from lung proteins and
that structural changes in lung tissue might
have occurred. Ozone might also affect the
ground substance, since the data suggest that
oxidative degradation of hyaluronic acid
could have occurred. The similarity of data
obtained from animals sacrificed immediately
after exposure and 24 hours after exposure
suggests that no reversal of the process occur-
red within that period of time. The authors
suggested that decreased slippage and decrea-
sed flexibility of elastic protein molecules
might occur if the ground substance is des-
troyed by ozone. The effect could be en-
hanced by intra- and inter-molecular cross-
8-7
-------
linking of aldehydes with the fibers of elastic
protein molecules.
This experiment confirmed the results of
preliminary experiments in which three sets
of rabbits were used, one set to develop the
methodology and two sets to determine if the
observation was real.13 In all cases, no car-
bonyl compounds were found in the lungs of
control rabbits.
Mendenhall and Stokinger have exposed
saline washings obtained from the lungs of
mice to 9,800 to 15,700 pg/m3 (5 to 8 ppm)
ozone and noted rapid increases in the film
pressure (the force opposing surface ten-
sion).14 The authors suggested that if analo-
gous changes were to occur in vivo, the
consequence would be an increase in the
distensibility of the lungs, considered by the
authors to be conducive to the development
of emphysema. This effect was not confirmed
in another study in which saline washings
from the lungs of dogs were exposed in vitro
to similar concentrations of ozone. If pulmon-
ary edema were to supervene because of
ozone exposure, one would expect to observe
an effect different from that seen by Menden-
hall and Stokinger; that is, there would be a
reduction of surfactant and an associated
increase in surface tension especially at low
lung volumes, a resultant decrease in alveolar
stability, and a reduction in distensibility of
the lungs.15
Frank16 et al. have exposed the right lung
of rabbits to 4,300 to 23,500 jug/m3 (2.2 to
12.1 ppm) ozone for 3 hours, the left lung
having been collapsed prior to exposure.
When edema occurred in the right lung,
changes in surfactant behavior were observed
in the left lung of some animals; no such
changes were observed in the absence of
edema in the right lung. These results suggest
that ozone is not only capable of inducing
chemical changes in exposed lungs but also
that the products of such changes are capable
of producing deleterious effects or compen-
satory responses in non-exposed lungs.
Skillen17 et al. have induced pulmonary
edema in rats by exposing them to 11,800
jug/m3 (6 ppm) ozone for 4 hours. The
animals were sacrificed immediately after
exposure and their lungs removed. Significant
increases (p < 0.001) in lung weight, lung
protein content and lung serotonin (5-hydroxy-
tryptamine) were observed. The source of
the increase in lung serotonin could have been
due in part to the increase in the number of
pulmonary mast-cells and their subsequent
disintegration. Whether this increase in seroto-
nin is related to pulmonary edema remains to
be demonstrated.
(2) Systemic effects.
Biochemical changes.
Several experiments described in greater
detail later in this chapter have provided
evidence that ozone may exert an effect at
the cellular level which is similar to that of
radiation. 18~20 In these studies, free radicals
have been suggested as the basic biochemical
mechansim of ozone-associated cellular dam-
age; this same chemical species is also believed
to mediate radiation-induced cell damage.
Based on cellular changes of human red blood
cells in vitro after exposure to 78,000 jig/m3
(40 ppm) ozone for 2 hours, and mouse red
blood cells in vivo after exposure to 15,700
jug/m3 (8 ppm) for 4 hours, Goldstein21"23 et
al. have suggested that ozone-induced cellular
damage may be mediated by its ability to
react with the double-bonds of unsaturated
fatty acids, resulting in the formation of free
radicals and other intermediate species which
might be responsible for the cellular damage.
These free radicals (from ozonide and peroxide
intermediates) may also enter into similar
reactions with other unsaturated fatty acids,
initiating a chain reaction of cellular damage.
Thus, Goldstein et al. imply that cellular
damage may result both directly from ozon-
olysis and secondarily from lipid peroxida-
tion initiated by the products of ozonolysis.
Immunology.
Scheel5 et al. reported the presence of
circulating antibodies (precipitins) in the se-
rum of rabbits exposed to ozone. Ordinarily,
8-8
-------
such antibody responses are elicited after
introduction of a foreign protein into an
animal. After exposing eight rabbits to 19,600
/jg/m3 (10 ppm) ozone for 1 hour each week
for a 6-week period, these investigators re-
ported a positive precipitin test when serum
from the exposed rabbits was overlaid with an
antigen prepared by exposing a 0.1 percent
solution of egg albumin to dry gas containing
4,500 to 4,900 Mg/m3 (2,300 to 2,500 ppm)
ozone. The data indicate that the interaction
of ozone and albumin resulted in denatura-
tion or' change in the conformation of the
albumin.
Buell24 undertook to reproduce Scheel's
results but was unable to confirm the precipi-
tin reaction using the exposure of rabbits to
ozone. Buell also employed a variety of
sensitive techniques in an attempt to demon-
strate immunologic responses in other ways.
It is likely that cross-reactions between native
and heat-denatured ovalbumins of the type
described by Scheel25 are largely due to the
impurities conalbumin or ovomucoid.
A report by Erban2 6 indicates that various
noxious stimuli may evoke or elicit nonspe-
cific responses in rabbits. The serum globulin
fraction, for example, in particular the alpha-
globulin fraction, increased in rabbits exposed
daily for 9-1/2 hours to 36 mg/m3 sulfur
dioxide (13.8 ppm) for 80 days. Thus, it
should be concluded that an immunological
response attributable to ozone exposure is not
yet proven, although the possibility exists
that exposures to ozone might aggravate
pre-existing sensitivity or immunologic pro-
cesses.
Brinkman1 8 et al. have shown that inhala-
tion of 390 to 490 /zg/m3 (0.20 to 0.25 ppm)
ozone for periods of 30 to 60 minutes by
mice, rats, rabbits, and man increased the rate
of sphering of red cells in vitro, the cells
losing their characteristic biconcave shape
more rapidly following exposure of diluted
blood to radiation. This would indicate an
acceleration in the aging of the cells. These
changes were largest after 1 hour and dimin-
ished toward the control after 6 hours expo-
sure.
Mountain27 has reported that the glu-
tathione content of lung extracts of mice
was reduced following acute ozone exposure.
Glutathione is known to be essential to the
integrity of the red blood cell.2 8 It exists in
both the oxidized (GSSG) and reduced (GSH)
form and may be enzymatically converted
from one form to the other. Only GSH is
physiologically active, and it is this form
which has been measured by various investiga-
tors. It is possible that exposure to ozone
either oxidizes the sulfhydryl group of glu-
tathione or prevents the formation of the
reduced form. Either possibility would result
in an abnormal excess of the oxidized form.
GSSG is known to combine with hemoglobin
in vitro,29 resulting in a decreased affinity of
the blood for oxygen; this in turn causes a
decrease in the amount of oxygen released to
the tissues. The presence of GSH inhibits the
formation of the hemoglobin-GSSG complex
due to the presence of its free sulfhydryl
group,29 and thus oxidation of glutathione
must be almost complete if the mechanism is
to be effective in vivo.
Effects of ozone on other organs.
Chemical and biochemical changes have
been observed in the heart, liver, and brain of
animals following inhalation of ozone. Brink-
man et al. have exposed adult mice to 390
Mg/m3 (0.2 ppm) ozone for 5 hours daily for 3
weeks.18 Structural changes in the cell mem-
branes and in the nuclei of myocardial muscle
fibers were produced which were reversible
after about 1 month following exposure. The
physiological implications of these changes
were not discussed. Skillen30 et al. have
demonstrated a significant decrease (p <
0.001) in brain serotinin following exposure
of rats to 11,800 MS/™3 (6 ppm) for 4 hours.
The mechanism of this response is unknown.
Acute exposure of laboratory animals to
high concentrations of ozone causes stimula-
tion of the activity of the liver. Scheel5 et al.
8-9
-------
exposed rats to 17,990 jug/m3 (9.2 ppm)
ozone for 45 minutes. A large increase in the
liver RNA/DNA ratio was observed during the
first 4 hours after exposure, but the ratio
rapidly returned to normal. Murphy31 et al.
found significant increases (p < 0.01) in
liver-weight per unit body-weight and liver
alkaline phosphatase activity following a sin-
gle exposure of rats to 6,100 jug/m3 (3.1
ppm) for 20 hours. No significant increases
were observed after an exposure of 7,470
;itg/m3 (3.8 ppm) for 4 hours. In both of these
studies, no attempt was made to determine
the minimal exposure conditions which would
produce these effects. The role of alkaline
phosphatase within the animal body is only
partially known, although it has frequently
been used as an index of the response to
stress.32
Since inhaled ozone itself can directly
affect only the lining of the respiratory tract,
changes in extra-pulmonary organs may be
the result of the breakdown of material
within the lung with a secondary systemic
effect. It should be emphasized that the
biochemical changes which take place in the
liver and brain are the result of abnormally
high exposures to ozone, and, subject to the
animal's survivial, are potentially reversible.
b. Effects of Prolonged Exposure to Ozone
According to Stokinger's review, at least
three long-term effects of repeated exposures
to ozone have been recognized.6 These are:
(1) long-term pulmonary effect, (2) lung
tumor acceleration, and (3) aging. An addi-
tional effect, (4) the development of toler-
ance following low level exposure to ozone, is
also related to chronic toxicity.
(1) Long-term pulmonary effects.
Stokinger33 et al. reported that chronic
bronchitis, bronchiolitis, and emphysema-
tous and fibrotic changes in the lung tissues
occur in mice, rats, hamsters, and guinea pigs
exposed 6 hours daily, 5 days a week for 14-
1/2 months to a concentration slightly above
1,960 Mg/m3 (1 ppm) ozone. These irreversi-
ble changes also develop in animals tolerant to
acute inflammatory effects.
(2) Lung tumor acceleration.
Acceleration of lung tumorigenesis (adeno-
ma) in a strain of mice susceptible to such
tumors occurred from daily ozone exposures
of about 1,960 Mg/m3 (1 ppm). At 15
months, a tumor incidence of 85 percent was
seen in the ozone-exposed, as against 38
percent in the control mice; the average
number of tumors per exposed mouse was
1.9 compared with 1.5 in the controls.34
(3) Agjng.
There are some suggestive data that expo-
sure to ozone may accelerate the aging pro-
cess. Bjorksten has presented evidence that
aging may be due to irreversible cross-linking
between macromolecules, principally proteins
and nucleic acids.35' 36 He included alde-
hydes in his list of active cross-linking agents.
Aldehydes are potential cross-linking agents,
and may be produced in the lung by ozone
exposure.
Hueter37 et al. exposed mice and guinea
pigs for 23 months to irradiated automobile
exhaust containing 390 to 1,960 /ig/m3 (0.2
to 1.0 ppm) ozone; also present in the
mixture were 23 to 115 mg/m3 (20 to 100
ppm) carbon monoxide, 6 to 36 ppm hydro-
carbons, and 0.7 to 3.9 ppm nitrogen oxides.
It was noted that irradiated auto exhaust
increased susceptibility to pulmonary infec-
tion and chronic disease (bronchitis), partic-
ularly in the latter half of the animal's life,
although no change in immunological re-
sponse was demonstrated.
Stokinger6 reports an accelerated or prema-
ture aging in rabbits after 1 year of weekly
1-hour exposures to ozone. His evidence
included: premature calcification of the stern-
ocostal cartilage, unthrifty appearance and
coarseness of the pelage (hairy system of the
body), severe depletion of body fat, and
general signs of senescence, such as dull
cornea and sagging conjunctivae.
8-10
-------
It has been suggested that the radiomimet-
ic properties of ozone are implicated in its
effects on aging. Fetner,19 in demonstrating
chromosome breakages in human cell cultures
from exposure to 15,700 ,ug/ni3 (8 ppm)
ozone for 5 or 10 minutes, suggested that the
effects of ozone and irradiation are additive.
Tliis is supported by the data of Brinkman20
et al.
Buell13 suggested that the interaction of
ozone and moisture (water) results hi the
formation of atomic- or radical-oxygen and
molecular oxygen, while Alder38 postulated
the formation of a variety of radicals. Al-
though high-energy sources such as X-radiation
undoubtedly decompose water into a variety
of free radicals, it has not been shown that
ozone can form more than one.
(4) Development of tolerance
to low-level exposures.
One feature of the response to oxidants,
and in particular, ozone, which has stimulated
considerable interest is the apparent develop-
ment of tolerance to the short-term effects of
these agents in laboratory animals. Tolerance
is the acquired capacity of a pre-treated host
to exhibit a lesser response to a challenge than
would be observed in a comparable but naive
(non-pretreated) host. Tolerance is demon-
strable directly at a single brief 1 hour or less
exposure to very low levels, from 590 to
5,900 Mg/m3 (0.3 to 3.0 ppm) ozone.
Tolerance occurs after a nonedemagenic as
well as an edemagenic dose. In rats, a toler-
ance is sometimes developed that lasts for a
month or longer, while in mice, a tolerance up
to 14 weeks has been observed.
It must be emphasized that ozone is not
the only compound which is capable of
producing tolerance. Nitrogen dioxide, phos-
gene, and phenylthiourea are among many
others. It is interesting that tolerance evoked
by .one agent can provide cross-protection
against one or more irritants. For example, a
single exposure of rats or mice to 980 to
9,800 Mg/m3 (0.5 to 5 ppm) ozone for 1 to 5
hours will induce protection against the acute
pulmonary effects of nitrogen dioxide, hydro-
gen peroxide, ketene, phosgene, hydrogen
sulfide, and nitrosyl chloride.39 The develop-
ment of pulmonary edema is the toxic effect
shown by all of these compounds. Although
pretreatment by injection of phenylthiourate
will provide tolerance against inhalation of a
lethal dose of ozone, the reverse is not true;
inhalation of ozone will not provide a cross-
tolerance against challenge by injection of
thiourate. The development of tolerance to
ozone has also been noted by Coffin40 et al.,
employing altered response to bacterial in-
fection as the parameter (Table 8-3).38 This
suggests that the cellular mechanism respon-
sible for resistance to infection, presumably
the macrophage system, is capable of exhibit-
ing ozone tolerance. In the reported experi-
ments, however, tolerance on the basis of
edema development cannot be precluded.
since the ozone concentration of 1,960 Mg/m3
(1 ppm) is probably edemagenic for mice.
Experiments reported by Pace41 et al., in
which in vitro exposure of standard tissue
cultures of live cells were employed, indicate,
however, that protection can be conferred by
previous exposure to ozone. This argues
strongly that an epicellular or membrane effect
or an intra-cellular mechanism is responsible
for tolerance, since isolated cells in synthetic
medium should be uninfluenced by hormonal
or other mechanisms mediated through humo-
ral agents.
Henschler42 has demonstrated tolerance to
nitrogen dioxide in mice. It was found that
those mice which had been pregassed only
once were almost totally protected, whereas
those which were repeatedly pregassed were
only partially protected. It was concluded
that the first exposure protected against the
following exposures, thus inhibiting increased
tolerance build-up.
In another experiment, Henschler43 induc-
ed tolerance and eventually managed to chal-
lenge the animals with a lethal dose. It is
significant that none died with pulmonary
edema; the predominant gross findings were
8-11
-------
Table 8-3. DEVELOPMENT OF TOLERANCE TO THE
MORTALITY-ENHANCING EFFECT OF OZONE ON
STEPTOCOCCAL INFECTION
40
Percent mortality from streptococcal
aerosol following exposure to:
~" Number
of mice
per group
20
20
20
20
20
Ambient
air
35
40
20
20
10
1 ppm ozone
for 3 hours
75
90
65
80
70
1 ppm ozone for 3 hours,
repeated 24 hours later
40
70
35
55
10
100 25%a 76%a
^he differences in mortality between the group exposed to
ambient air and the group exposed to 1 ppm for 3 hours,
and between the latter group and the group exposed twice
to ozone, were statistically significant (p < 0.001).
massive hemorrhage. The mechanisms of toler-
ance are uncertain. The possibility that a
gaseous irritant will produce tolerance is
apparently governed partially by its solubility.
Gases and vapors with a relatively low solu-
bility can contact all parts of the respiratory
tract from the nasal passages down to the
bronchioli and alveoli. Irritants which reach
these inner recesses of the lung are referred to
as deep lung irritants, and it is these which are
capable of producing tolerance. Irritants
which ordinarily do not reach the
alveoli in sufficient concentration, however,
appear to be devoid of tolerance develop-
ment. Thus materials such as sulfur dioxide,
chlorine, ammonia, and isocyanate, when
inhaled in low concentrations, do not have
the ability to promote protective tolerance
against subsequent challenge.
The development of tolerance produces
certain characteristics after such a challenge.
These are:
1. Pathology: The usual changes asso-
ciated with pulmonary edema are
either reduced or absent.
2. Water content: The usual increase in
lung water content is either reduced
or does not occur.
3. Biochemistry: The activity of serum
alkaline phosphatase and of adrenal
succinic dehydrogenase remains ei-
8-12
ther normal or only slightly altered in
tolerant animals. In addition, there is
significantly less oxidation of lung
GSH in the animal pretreated with
ozone.
It must be pointed out that the existing
data suggest that rodents are particularly
likely to develop tolerance. Quilligan44 etal.,
using several different conditions of exposure
and challenge, were unable to demonstrate
tolerance to ozone in baby chicks. It is not
known whether humans can develop tolerance
to ozone.
It would appear that the development of
tolerance is a useful tool to determine the
mechanism for the production of ozone-
induced pulmonary edema. In the light of
Henschler's observation that repeated inter-
mittent exposures of mice to nitrogen dioxide
produced less protection against challenge
with a lethal dose than a single pre-exposure,
tolerance may not be significant in popula-
tions continuously exposed to low levels of
oxidants. Also, indices other than mortality
need to be developed in animals before
tolerance development can be appraised in
humans.
c. Interaction with Other Agents
(1) Increased Susceptibility
to bacterial infection
It has been observed that animals chal-
lenged with aerosols of infectious organisms
suffer a higher incidence of infection when
previously exposed to ozone, irradiated auto
exhaust, or other common air pollutants. The
suggested explanation is that the various
pollutants inhibit, inactivate, or otherwise
impair two distinct functions: the mucociliary
streaming, that is, the action of cilia (tiny,
hair-like, mobile, projections of cells) in the
nasal and upper respiratory passages to clear
particulates and prevent them from entering
the lungs; and phagocytosis by the alveolar
macrophages which surround and digest for-
eign particles in the lungs.
Coffin4°.4S et al. studied the effect of
ozone exposure on rabbits by means of
-------
pulmonary lavage to obtain data on alteration
of the cells. They found that exposure for 3
hours to ozone at concentrations from about
1,960 jug/m3 (1 ppm) and above elicited an
influx of heterophilic (polymorphonuclear)
leukocytes into the pulmonary airway (p <
0.001); this is illustrated in Figure 8-6. The
elevation of heterophiles was noted imme-
diately after cessation of the 3-hour exposure,
peaked at 6 hours, and was still evident in
reduced amounts 24 hours later (Figure 8-7).
The authors interpreted this finding as indi-
cating an acute reversible inflammatory re-
sponse to irritation. At the higher exposure
levels used, there was correlation with inflam-
mation noted in tissue sections, while at lower
levels, cells obtained by lavage indicated an
irritation response not detected by histologic
examination.
These same investigators noted by similar
lavage techniques that administration of
ozone also reduced the number and in vitro
phagocytic abilities of the pulmonary alveolar
macrophages. The reduction in phagocytosis
was noted following 3-hour exposures to
concentrations of 1,310 to 7,800 jug/m3 (0.67
to 4 ppm) ozone (p < 0.005). The authors
suggest that this reduced phagocytosis con-
ferred by ozone may play a role in the
increased survival in the lungs of bacteria,
with consequent enhancement of infection
for ozone-exposed animals. (Table 8-4).
Table 8^». DEPRESSION OF PHAGOCYTOSIS AFTER
3-HOUR EXPOSURE TO OZONE 4S
23456
OZONE, ppm
Figure 8-6. Cellular response to exposure
to ozone for 3 hours.45
i
Q_
o
I 1 I 1 L I T T
• EXPOSURE 3 hours
MEAN OF 5 RABBITS ±
STANDARD ERROR
90
80
70
60
50
40
30
20
10
0 2 4 6 8 " 10 "12 14 16 18 20 252627
TIME, hours
Figure 8-7. Increase in percent heterophiles
following exposure to 9,800 jug/m3 (5 ppm)
ozone for 3 hours.45
Ozone dose,
ppm
None
0.67
1.25
2.50
3.75
5.00
9.50
Phagocytic
index x 100
498
442
341
303
281
286
291
Number of
rabbits
20
6
6
6
6
6
6
Holzman46 et al., on the basis of determi-
tions from pulmonary wash-out fluid, have
demonstrated that a 3-hour exposure to 9,800
jug/m3 (5 ppm) ozone reduced the activity of
the bactericidal enzyme, lysozyme, presum-
ably due to in vivo oxidation of the enzyme.
In experiments reported by Coffin40 et al.
and Stokinger and Coffin,47 mice were ex-
posed to ozone at various levels for 3 hours
and subsequently to a bacterial aerosol of
streptococcus (Group C). Enhancement of
mortality occurred from ozone con-
centrations of 160 Mg/m3 (0.08 ppm) and
above (p < 0.05); these data are shown in
Table 8-5. The same investigators also showed
that prolongation of pulmonary bacterial
8-13
-------
Table 8-5. MORTALITY OF MICE EXPOSED TO
STREPTOCOCCAL AEROSOL FOLLOWING A 3-HOUR
OZONE EXPOSURE 40
Ozone,
ppm
.52
.35
.30
.28
.20
.18
.17
.10
.08
.07
07
Number of mice
per group
40
40
40
40
40
40
40
40
40
40
40
Percent Mortality
Strep
only
13
0
8
3
8
0
8
8
15
15
8
Strep +
ozone
80
60
63
40
50
63
45
35
38
35
5
Difference
percent
67a
60a
55a
37a
42a
63a
37 a
27 a
23 a
20
-3
"p <0.05.
survival time and acceleration of bacterial
growth can be conferred by ozone exposure.
Miller and Ehrlich48 studied the effect of
exposure to ozone on the susceptibility of
mice and hamsters to respiratory infection
caused by inhalation of Klebsiella pneu-
moniae aerosol. The ozone exposures were
from 2,550 to 8,580 Mg/m3 (1.3 to 4.4 ppm)
for 3 hours or 1,650 Mg/m3 (0.84 ppm) for 4
hours per day, 5 days a week for 2 weeks.
The observation period for this experiment
was 2 weeks. The parameters measured were
mortality and survival time. The mortality
due to K. pneumoniae infection was signifi-
cantly greater (p< 0.05) in every case and at
each exposure level for animals exposed to
ozone than for their paired controls. No
deaths were obtained from ozone exposure
alone. Autopsy of the animals exposed to K.
pneumoniae which died within the 2-week
observation period showed the presence of
the infectious organism in the lungs and heart.
K. pneumoniae was absent in those animals
which survived the 2-week observation period.
It was concluded that exposure to ozone
siginificantly reduces the resistance of mice
and hamsters to subsequent respiratory infec-
tion due to K. pneumoniae. Statistical evalua-
tion of the data indicated higher mortality,
shorter survival time, and a lower LD5 0 for K.
pneumoniae in animals exposed to ozone as
compared with controls.
In a similar series of experiments con-
ducted by Purvis49 mice were exposed to
7,470 to 8,000 ME/m3 (3.8 to 4.1 ppm)
ozone for 3 hours. The exposures took place
1 to 27 hours before and 3 to 27 hours after
challenge with K. pneumoniae aerosol. It was
found that, within 19 hours after exposure to
ozone, the resistance of mice suffering from
respiratory infection initiated by challenge
with an aerosol of K. pneumoniae was signifi-
cantly reduced. The same effect was observed
in infected animals exposed to ozone up to 27
hours after the challenge with the infectious
aerosol.
(2) Increased susceptibility to histamine
In an attempt to define a mechanism for
the edemagenic effect of ozone, Easton1 ° et
al. noted that ozone-exposed guinea pigs ap-
peared to be more susceptible to the toxic
action of histamine, a chemical substance
released by the tissues in allergic reactions. It
was observed that pre-exposure to 9,800
Mg/m3 (5 ppm) ozone for 2 hours followed by
a histamine challenge of from 0.9 to 1.4
mg/kg (injected 1.5 to 2.0 hours after the end
of exposure) resulted in increased mortality
compared with an air-exposed control group;
these results are illustrated in Figure 8-8.
Autopsy of the dead animals showed that
the members of both groups died of acute
bronchoconstriction. The increased suscepti-
bility to histamine was detectable for 12
hours after the termination of exposure to
ozone. The minumum concentration of ozone
necessary to produce such an increase in
susceptibility was found to be 980 to 1,960
Mg/m3 (0.5 to 1.0 ppm). This concentration is
only one-twentieth of that required to pro-
duce death from pulmonary edema due to
ozone alone. Since there was no significant
8-14
-------
difference between lung water content in the
two groups, it was concluded that pulmonary
edema did not contribute to the increased
susceptibility to histamine. It was found that
the increased susceptibility only occurred
when exposure to ozone took place before
challenge with histamine. There was no in-
crease in susceptibility in guinea pigs injected
with histamine prior to exposure. This is in
contrast to the increased susceptibility to K.
pneurnoniae before and after exposure to
ozone.
d. Mechanisms of Ozone Toxicity in Animals
The existing data suggest that ozone exerts
its toxic effect primarily on the respiratory
system and secondarily on the other extra-
pulmonary systems. In the latter case, some
of the responses are essentially those of stress
and are not specific for ozone. The exact
mechanisms by which ozone causes damage to
the respiratory system, however, are still
unknown. Research to elucidate such mecha-
nisms is currently being conducted in three
major areas^the acute toxic edema reaction,
the effects on oxygen transport by the red
cells, and the development of tolerance. The
latter is used frequently as a model system to
determine the mechanism of the edema reac-
tion.
100
90
sc
70
60
50
40
30
20
10
I II I III
5 ppm OZONE
EXPOSURE.
2 hours
AIR EXPOSURE
2 hours —
I I I I
0.5 1.0 1.5
CONCENTRATION OF HISTAMINE, mg/kg
Figure 8-8. Effect of ozone exposure on
histamine toxicity in guinea pigs.10
In animals, it is suggested that some re-
sponses to ozone are due to irritation at the
local levels. An example is the immediate
increase in pulmonary flow resistance ob-
served during exposure to ozone, and its rapid
return to normal after exposure. Because of
the delayed edemagenic response observed
frequently after short-term exposure to high
concentrations of ozone, it is likely that the
formation of pulmonary edema operates by
some other mechanism. Data are available
from various sources which suggest that ozone
exerts a direct effect on the cell membrance
and not by way of a neural or hormonal
pathway.
Fairchild5! et al. provided evidence that
ozone interacts with sulfhydryl groups along
the respiratory tract and in the lung. Their
conclusions were based on the protection
against the effects of ozone provided by
administration of organic sulfur-containing
compounds. How ozone reaches the active
sulfhydryl groups is open to some question. It
is possible that the intact molecule reacts with
the receptor site, but it is more likely that,
since ozone is so reactive, it reacts with water
to form molecular oxygen or other active
forms of oxygen.1 3
Glutathione is one compound which con-
tains a free sulfhydryl group and which has
been implicated in the mechanism for the
formation of pulmonary edema. It has been
observed that lung GSH levels were main-
tained in ozone-tolerant animals but not in
non-tolerant animals.39 This situation could
be brought about in two ways—either through
interaction of ozone with the sulfhydryl
group or through interference with the enzy-
matic pathways (pentose phosphate shunt)
which are responsible for maintaining ade-
quate levels of reduced glutathione. It should
be pointed out that glutathione is not itself
diminished, but is converted to the oxidized
form and is therefore inactive. The processes
of inflammation and repair are accompanied
by an increased utilization, by glucose, of the
pentosephosphate pathway in the injured
area.52 The decrease in the levels of GSH
8-15
-------
would inhibi*.this pathway and hence inhibit
the process of repair. This would explain the
delayed edemagenic response frequently ob-
served after exposure to acute concentrations
of ozone.
Buell12 et al. have demonstrated changes in
the formation of lung proteins and ground
substances in rabbits after exposure to ozone;
these changes were not reversible within 24
hours after exposure. The potential intra- and
inter-molecular cross-linking of aldehydes
with fibers of elastic protein molecules would
result in decreased flexibility of the latter and
hence imply a simultaneous reduction in the
elasticity of the lung. It would be desirable
for such a study to be put on a quantitative
basis so that the extent of and subsequent
renaturation or replacement of lung tissue
could be determined.
The radiomimetic properties of ozone have
been suggested as a basis for its edemagenic
response, although the data obtained so far
provide conflicting conclusions which have
already been noted in this report. The evi-
dence in support of this theory, however, is as
follows:
1. The reducing agents which protect
against ozone also protect against
irradiatipn effects;
2. Both ozone and X-radiation produce
chromosomal aberrations; and
3. Both ozone and UV-radiation retard
deoxygenation of hemoglobin in the
capillaries.
Dixon and Mountain5 3 have suggested that
the liberation of histamine, thought to result
from ozone exposure, has a role in the
formation of pulmonary edema. However,
Easton1 ° et al. were unable to demonstrate a
significant depletion of lung histamine in
guinea pigs exposed to ozone. Additional
evidence that ozone or one of its reaction
products exerts its edemagenic effect by a
direct interaction with the cell membrane is
given by Stokinger in a recent review.6 He
cites a personal communication from Pace
who has shown that ozone affects cultures of
liver and HeLa cells (cultured human cancer
cells) in much the same way as it affects the
cells of an intact animal.
It must be concluded that, although there
are a number of facts which are suggestive of
certain mechanisms, the data obtained so far
are inadequate to provide a mechanism for
ozone-induced pulmonary edema. The re-
sponses of the extra-pulmonary organs to
exposures of high concentrations of ozone
(possibly excluding effects on oxygen trans-
port by red blood cells) are essentially those
of stress. These are not specific for ozone and
are frequently encountered in animals as-
saulted by a variety of toxic chemicals. A
neuro-humoral mechanism has been sug-
gested,3 3 but its exact nature is still unclear.
e. Summary
A detailed summary of the effects of ozone
in animals is shown in Table 8-6. The concen-
trations listed are the lowest for which the
observed effect has been recorded. Based on
experimental data, it has been found that:
1. Pathological changes, including
bronchitis, bronchiolitis, emphy-
sema, and fibrosis, are produced by
prolonged exposure to 390 to 1,960
Mg/m3 (0.2 to 1.0 ppm) ozone.
2. Changes in pulmonary function are
produced by exposure to 590 Mg/m3
(0.3 ppm) ozone for periods of up to
2 hours. These changes, which revert
to normal following exposure, are
decreased tidal volume, increased fre-
quency of breathing, and increased
flow resistance.
3. Chemical changes in the structural
proteins of the lung are found fol-
lowing exposure to 1,960 jug/m3 (1
ppm) for 1 hour.
4. Mortality rates resulting from
histamine, bacterial infections, age,
and exercise are increased as a result
of exposure to from 1,960 to 9,800
Mg/m3 (1 to 5 ppm) ozone for 2 to 6
hours.
5. Biochemical changes in the lung and
other organs are found following
exposure to 5,900 to 11,800
8-16
-------
Table 8-6. SUMMARY OF THE EFFECTS OF OZONE IN ANIMALS
Ozone,3
/ig/m3
160
670
1,330
1,960
1,960
2,120
2,550
3,900
6,290
9,800
9,800
11,800
20,000
41,000
41,000
67,980
71,000
101,370
1,650
Ozone,3
ppm
0.08
0.34
0.68
1.00
1.00
1.08
1.30
2.00
3.20
5.00
5.00
6.00
15.00
21.00
21.80
34.50
36.00
51.70
0.84
Length of
exposure
3 hours
2 hours
2 hours
1 hour
4 hours
2 hours
3 hours
3 hours
4 hours
2 hours
3 hours
4 hours
30 min.
3 hours
3 hours
3 hours
3 hours
3 hours
4 hours/
5 days/2
wk
Observed effect(s)
Local effects
Short-term exposures
Increased susceptibility to strep-
toccoccus (Group C)
30% increase in frequency of breathing;
20% decrease in tidal volume
No significant increase in flow
resistance
Chemical changes in ground substance
and lung protein
Engorged blood vessels and excess leuco-
cytes in lung capillaries -
Increased flow resistance
Increased susceptibility to Klebsiella
pneumoniae
Increased lung weight, decreased tidal
volume, decreased minute ventilation
Gross pulmonary edema
Increased lung compliance, increased
susceptibility to histamine
Decreased activity of bacteriocidal
lysozyme
Gross pulmonary edema, increased lung
serotonin
Decreased tidal volume, decreased
02 consumption
50% mortality
50% mortality
50% mortality
50% mortality
50% mortality
Long-term exposures
Increased susceptibility to Klebsiella
pneumoniae
Species
Mice
Guinea pigs
Guinea pigs
Rabbits
Mice
Guinea pigs
Mice,
hamsters
Rats
Mice
Guinea pigs
Mice,
rabbits
Rats
Rabbits
Mice
Rats
Cats
Rabbits
Guinea pigs
Mice,
hamsters
Reference
Coffin40 et al.
Murphy9 et al.
Murphy9 et al.
Buell12 et al.
Scheel5 et al.
Murphy9 et al.
Miller and
Ehrlich48
Scheel5 et al.
Scheel5 et al.
Easton and
i n
Murphy
Holzman46 et al.
Skillen17etal.
Scheel5 et al.
Mittler3 et al.
Mittler3 et al.
Mittler3 et al.
Mittler3 et al.
Mittler3 et al.
Miller and
Ehrlich48
aThe concentrations of ozone listed are the lowest for which the observed effect has been recorded.
8-17
-------
Table 8-6. (continued).-SUMMARY OF THE EFFECTS OF OZONE IN ANIMALS
Ozone,a
Mg/m3
1,960
15,700
to
88,000
390
390
1960
6100
7800
11800
_ - _. 390
Ozone,a
ppm
1.00
8 to
45
0.20
0.20
1.00
3.10
4.00
6.00
0.20
Length of
exposure
continuous
1 hi/wk up
to 49 wk
30 min.
6 hours
6 hours
20 hours
4 hours
4 hours
5 hr/day/
3 wk
Observed effects)
Bronchitis, bronchiolitis, emphysematous
and fibrotic changes; acceleration of
lung tumor development
Damage to epithelium of the lower
trachea and bronchioles; flbrosis
Systemic effects
Short-term exposures
Increased sphering of red blood cells
when irradiated
Decreased voluntary running activity
60% increase in mortality as a result of
exercise for 15 min/hr
Increased liver weight; increased liver
alkaline phosphatase
Decreased mortality with age: young 50%
mortality, old 10% mortality
Decreased brain serotonin
Long-term exposures
_ Structural changes in heart myocardial
fibers
Species
Mice
Rabbits
Rabbits,
rats, mice
Mice
Rats
Rats
Mice
Rats
Mice
Reference
Stokinger33etal.
Scheel5 et aL
Brinkman18 et al.
Stokinger6
Stokinger6
Murphy31 et al.
Stokinger6
Skillen30 et al.
Stokinger
aThe concentrations of ozone listed are the lowest for which the observed effect has been recorded.
(3 to 6 ppm) ozone for periods of
more than 4 hours.
6. Increased susceptibility to bacterial
infection is produced by a 3-hour
exposure to 160 Mg/m3 (0.08 ppm)
ozone.
2. Human Data
Much of the data on effects of exposure to
ozone in humans depend on measurement of
pulmonary function. Definitions of the vari-
ous measures of pulmonary function may be
found in any one of a number of textbooks
on pulmonary physiology, or in the Air
Quality Criteria for Paniculate Matter,
NAPCA Publication No. AP-49.54
a. Occupational Exposures to Ozone
References to human occupational ex-
posures to ozone are numerous. Dadlez55 in
1928, found that 2,940 Mg/m3 (1.5 ppm)
ozone rendered the atmosphere intolerable.
He cites an investigation by D'Arsonval who
found that 780 Mg/m3 (0.4 ppm) ozone in the
atmosphere produced symptoms of discom-
fort and irritation which were apparent in
about 30 minutes. In 1931, Flury56 gave the
following symptoms characteristic of ozone
exposure: 920 Mg/m3 (0.47 ppm) causes
distinct irritation of mucous membranes,
1,840 /zg/m3 (0.94 ppm) causes coughing,
irritation, and exhaustion within 1.5 hours;
and 5,900 Mg/m3 (3 ppm) causes sleepiness in
1 hour. At higher concentrations, ozone
causes increased pulse, sleepiness, and contin
ued headache. It may also result in dyspnea
(difficult breathing), pulmonary edema, and
peribronchial complications.
More recently (1957), Kleinfeld57 et al.
have reported several cases of severe ozone
intoxication in welders using a consumable
electrode technique which was new at that
8-18
-------
time. Three plants were investigated, and in all
cases the ozone concentration was monitored
at the breathing zone of the consumable
electrode machine. In the first case, an ozone
concentration of 490 Mg/m3 (0.25 ppm) was
found. The workers had no complaints, and
clinical findings were noncontributory. In the
second case, the ozone concentration ranged
from 590 to 1,570 Mg/m3 (0.3 to 0.8 ppm).
Two out of four welders complained of chest
constriction and throat irritation. Clinical
examination disclosed no abnormalities. In
the third case, the ozone concentrations were
17,990 MS/m3 (9.2 ppm). A trichloroethylene
degreaser was located about 50 feet feet from
the welding area. Concentrations of nickel
carbonyl and nitrogen oxides were negligible.
Air tests for phosgene in the welding area
were negative. The authors gave case histories
of three workers, although others also com-
plained of severe headaches, throat irritation,
and lassitude. One of the cited patients
developed severe dyspnea and substernal op-
pression and, on admission to a hospital, he
was found to be in pulmonary edema. Chest
x-rays showed diffuse peribronchial infiltra-
tion consistent with peribronchial pneumo-
nia. The patient made a slow recovery over a
2-week period but still complained of fatigue
and exertional dyspnea after 9 months. The
two other workers had similar but less critical
symptoms.
Challen5 8 et al. have performed a similar
clinical and environmental survey. Ozone con-
centrations of 1,570 to 3,330 Mg/m3 (0.8 to
1.7 ppm) were found. Eleven out of 14
workers who were directly involved in weld-
ing complained of respiratory symptoms. No
further symptoms were reported when ozone
concentrations were reduced to 390 Mg/m3
(0.2 ppm). The results of this study, however,
were complicated by the fact that concentra-
tions of trichlorethylene up to 1,275 mg/m3
(238 ppm) were also present.
Young5 9 et al. have made the first study of
pulmonary functional changes in workers
exposed to ozone. Seven men engaged in
argon-shielded electric arc welding, all smok-
ers, were studied. The concentration of ozone
in the welding shop was estimated by the
rubber cracking technique and found to be
390 to 590 Mg/m3 (0.2 to 0.3 ppm). The
following measurements of pulmonary func-
tion were made: vital capacity (VC), func-
tional residual capacity (FRC), maximal
midixpiratory flow rate (MMFR), 0.75-sec-
ond forced expiratory volume (FEV 0.7 s )>
and carbon monoxide diffusing capacity
(DLCO) at rest and at exercise. There was no
convincing evidence that functional impair-
ment develops in association with long-term
exposure to 390 to 590 Mg/m3 (0.2 to 0.3
ppm) ozone in these seven smokers. Similar
exposures and studies in non-smokers should
be conducted.
The available data on occupational expo-
sures of humans to ozone are summarized in
Table 8-7.
b. Human Experimentation
Experiments on human subjects were first
carried out by Jordan and Carlson in 1913.60
Three men were exposed to 9,800 to 19,600
Mg/m3 (5 to 10 ppm) ozone for a brief period.
The subjects developed headache and drowsi-
ness, one of them to the point of falling
asleep. The authors suggested that the head-
ache was due to irritation and hyperemia
(abnormal congestion of blood) in the frontal
sinuses. Similar findings were observed in dogs
exposed to ozone.
Griswold6 l et al. have reported change's in
pulmonary function in a single subject ex-
posed to 2,940 to 3,920 Mg/m3 (1.5 to 2
ppm) ozone for 2 hours. High temperatures
complicated the exposure and may have
influenced the results. At this concentration,
ozone was associated with a lack of coordina-
tion and inablility to express thoughts, plus
respiratory symptoms such as chest pain and
cough. Measurements of vital capacity were
made before and immediately after exposure.
No measurements of diffusing capacity were
made. There was a slight (13 percent) reduc-
tion in vital capacity, which returned to
normal after 22 hours. The forced expiratory
8-19
-------
Table 8-7. SUMMARY OF AVAILABLE DATA ON OCCUPATIONAL EXPOSURE OF HUMANS TO OZONE
Ozone,
/ug/m'
490
590
to
1,570
17,990
(peak
concen-
tration)
390
1,570
to
3,330
390
to
590
780
920
1,840
5,900
Ozone,
ppm
0.25
0.3
to
0.8
9.2
(peak
concen-
tration)
0.2
0.8
to
1.7
0.2
to
0.3
0.4
0.47
0.94
3.0
Subjective complaints
None
Chest constriction
and throat irritation
in 2 to 4 subjects
Severe headaches,
throat irritation, and
lassitude in 7 or 8
subjects
Cough, choking,
dyspnea, and
substernal oppression
in 3 of 8 subjects
Very severe head-
ache; dyspnea,
sub sternal oppres-
sion in 1 of 8
subjects
Dry mouth and throat,
irritation of nose and
eyes, disagreeable
smell in 1 1 of 14
subjects
Irritating odor,
soreness of eyes,
and dryness of
mouth, throat, and
trachea in 1 of 7
subjects
Discomfort and irri-
tation in about 30
minutes
Distinct irritation of
mucous membranes
Coughing, irritation,
and exhaustion, with-
in 1-1/2 hours
Sleepiness within
1 hour
Clinical findings
attributed to ozone
None
None
By X-ray, molted
densities in both
lungs, clearing
after 9 days
Severe pulmonary
edema. By X-ray,
peribronchial in-
filtration consis-
tent with peri-
bronchial pneumonia
None
None
None
None
None
None
None
Measurements of
pulmonary function
None
None
None
None
None
None
None
VC decreased in
3 of 7 subjects.
FRC decreased in
2 of 7 subjects.
DL^o decreased
in 1 of 7 subjects.
None
None
None
None
Other comments
_
_
Negligible nickel
carbonyl and
oxides of nitro-
gen. Trichloro-
ethylene de-
greaser located
50ft from
welding area.
Tests for
phosgene
negative.
Concentration
of trichloroethy-
lene up to 238
ppm found
All decreases in
pulmonary func-
tion measure-
ments were small.
All subjects
were smokers.
_
_
Reference
Kleinfeld57
etal.
Kleinfeld57
etal.
Kleinfeld57
etal.
Challen58
etal.
Challen58
etal.
Young59
etal.
Dadlez55
(D'ArsonvaJ)
Flury56
Flury56
Flury56
8-20
-------
volume (FEV 3-0)was reduced by 16.8 per-
cent and was still slightly below normal after
22 hours. There was a slight reduction in the
maximum breathing capacity. It is possible
that the very slight reduction in vital capacity
was due, in part, to the symptoms noted.
Bennett62 has exposed two groups of six
volunteers to ozone for 3 hours a day, 6 days
a week, for 12 weeks; one group at a
concentration of 390 ng/m3 (0.2 ppm), the
other at 980 ng/m3 (0.5 ppm). Ozone was
produced by an ultraviolet ozone generator in
which pure oxygen was used to prevent the
simultaneous formation of nitrogen oxides.
Measurements of vital capacity and forced
expiratory volume (FEV l -0) were made. The
group exposed to 390 Mg/m3 (0.2 ppm) ozone
experienced no symptoms, and their vital
capacity and forced expiratory volume
showed no significant change. The subjects
experienced an average of 0.66 upper respira-
tory infections per person during the period
November through January, compared with
an average of 0.95 per person suffered by a
control group in a nearby laboratory. The
group exposed to 980 Mg/m3 (0.5 ppm) had
no symptoms, although they could detect the
ozone by smell. Their vital capacities showed
a light downward trend, but the decreases
were not significant. Their forced expiratory
volume (FEVj -0) showed a significant de-
crease during the last few weeks of exposure
(Figure 8-9). The results given in this paper
represent only the average value for the entire
group, and no information was given concern-
ing the range of response among individuals.
The conclusions of the author that airway-
narrowing had taken place are quite plausible,
since vital capacity was not altered.
Young6 3 et al. have made a detailed study
of the effect of low concentrations of ozone
on pulmonary function in man. These authors
exposed 11 subjects, 10 men and 1 woman,
aged 20 to 45 years, to 1,180 to 1,570
•AVERAGE FORCED VITAL CAPACITY, 0.2 ppm
.AVERAGE FORCED VITAL CAPACITY, 0.5 ppm
i AVERAGE 1 sec. FORCED EXPIRATORY VOLUME, 0.2 ppm
AVERAGE 1 sec. FORCED EXPIRATORY VOLUME, 0.5 ppm
8 10
EXPOSURE, weeks
12 14 16 18
-NO OZONE EXPOSURE »4
Figure 8-9. Effect of exposure to 390 and 980 jug/m3 (0.2 and 0.5 ppm) ozone on six
subjects.62
8-21
-------
(0.6 to 0.8 ppm) ozone for 2 hours. The
ozone was generated by the action of two
small ultraviolet bulbs on a stream of dry,
filtered, air which was fed into the inspired air
just before it reached the mixing box. Satis-
factory evidence was obtained that the gener-
ator was not producing nitrogen oxides si-
multaneously. In this experiment, the subjects
served as their own controls by breathing air
instead of ozone for a period of 2 hours prior
to exposure; in addition to the 16 ozone
experiments, 11 experiments using air as a
control were performed on the 11 subjects.
Pulmonary function measurements were de-
termined immediately before the experiments
and at 24 and 48 hours after the completion
of the breathing periods. In two subjects,
mixing efficiency was determined by the
helium dilution method, and the mechanical
properties of the lungs were studied before
and after inhalation of ozone. Ten of the 11
subjects experienced substernal soreness and
tracheal irritation for 6 to 12 hours. There
was a 25 percent reduction in the carbon
monoxide diffusing capacity (DLCO) with
inhalation of ozone for 2 hours (Table 8-8).
There was also a 7 percent drop in the DLC o
after breathing air for 2 hours. The drop was
attributed to the progressive shift in perfusion
distribution in the lung, which had occurred
as a result of rest in the upright position. The
results of individual experiments, however,
showed that change in the DLC o after breath-
ing air was scattered in a random manner,
whereas a decrease in the DLCO following
ozone exposure was noted in every one of the
16 experiments. The results of ventilatorv
tests carried out in 10 of the 11 subjects are
shown in Table 8-9. Vital capacity and the
forced expiratory volume (FEV0.7S) were
unaffected by 2 hours of air breathing but fell
about 10 percent after breathing ozone. This
difference was not statistically significant.
The maximal mid-expiratory flow rate
(MMFR) fell about 15 percent, but this
change was not statistically significant. The
authors point out that one subject had such
large decreases in all of these measurements
Table 8-8. EFFECT OF INHALING EITHER AIR OR 1,180 TO 1,570 Mg/m3
(0.6 to 0.8 ppm) OZONE FOR 2 HOURS ON PULMONARY DIFFUSING CAPACITY
(DLCO) OF 11 SEATED NORMAL SUBJECTS63
Control
exposure
Exposure to air
for 2 hours
Change (A air)
Control
exposure
Exposure to
ozone for
2 hours
Change (A ozone)
Difference
in effect of
exposures
(A ozone - A air)
DLCO,
ml CQ/min/mmHg
20.7
19.3
-1.4
22.5
17.1
-5.4
-4.0
Standard
deviation
5.00
4,40
0.822
3.4
2.8
0.84
3.84
t
1.64
6.40
3.31
P
0.2 to 0.1
0.001
0.01 to 0.001
8-22
-------
that his changes were responsible for almost
half of the effect shown by the whole group.
The mixing efficiency and dynamic compli-
ance of the lung remained normal after ozone
exposure. The airway resistance was slightly
greater after ozone than before, however, in
each of the two subjects measured, but
remained within normal limits. It was con-
cluded that the lowering of the diffusing
capacity was due to a thickening of the
alveolar wall. It was calculated that an in-
crease of 50 percent in the thickness of the
alveolar capillary membrane was necessary to
produce the change observed; this could be
achieved by only 13 ml of edema fluid. The
authors suggested that injury might be con-
fined to the lower regions of the lungs, since
they are known to receive a higher portion of
the ventilation than the upper regions.
Although it was not proved, the speed of
recovery indicated that edema rather than
inflammation was responsible for such
changes. The small reduction in vital capacity
could be due to a physical limitation.
Hallett64 exposed ten subjects to 1,960 to
7,800 Mg/m3 (1 to 4 ppm) ozone for periods
of up to 30 minutes. Measurements of vital
Table 8-9. EFFECT OF INHALING EITHER AIR OR
1,180 to 1,570 Mg/m3 (0.6 to 0.8 ppm) OZONE FOR
2 HOURS ON VITAL CAPACITY (VC), INDIRECT
MAXIMAL BREATHING CAPACITY (FEV0 75 x 40),
AND MAXIMUM MID-EXPIRATORY FLOW RATE
(MMFR), ON 10 MALE SUBJECTS 63
INHALANT
Air
Before
After
Change (A air)
P
Ozone
Before
After
Change (A ozone)
P
p ( A ozone - A air)
VC,
liters
4.40
4.44
+ 0.04
0.3-0.2
4.43
4.06
-0.37
0.10-0.05
0.05-0.02
rFEV075x40,
| liters/min.
135
136
+ 1
0.7-0.6
131
118
-13
0.05-0.02
0.05-0.02
MMFR,
liters/sec
3.80
3.94
+0.14
0.6-0.5
3.60
3.08
-0.52
0.05-0.02
0.10-0.05
capacity, 1- and 3-second forced expiratory
volumes, and maximal breathing capacities
were made with a Collins spirometer. Maxi-
mum expiratory How rate was measured using
a Wright peak flowmeter, and functional
residual capacity was determined using the
closed circuit helium technique. Carbon
monoxide diffusing capacity was determined
by the steady-state method. Ozone was gen-
erated from pure oxygen and was monitored
by a Mast ozone meter but, due to a calibra-
tion problem, there was some uncertainty
about the actual exposure. Results are given
for 11 subjects, 6 of whom could not tolerate
the dose for a full 30 minutes. All had
symptoms after 10 minutes. The symptoms
usually lasted for more than an hour and, in
some, for several hours, especially headache
and shortness of breath. Measurements of
pulmonary function are confusing, since some
showed increases and some showed decreases.
Measurements of vital capacity showed four
out of eight subjects exhibiting decreases of
greater than 10 percent; five out of eight
subjects showing a decrease in the forced
expiratory volume (FEV x .0) of greater than
10 percent; five out of six subjects showing
a decrease in maximum expiratory flow
rate; five out of eight subjects showing a
decrease in maximal breathing capacity; and
seven out of eleven subjects showing a de-
crease in the carbon monoxide diffusing
capacity, the smallest decrease being 20
percent. Since no measurements were made
of the mechanical properties of the lungs,
it is difficult to relate these changes to any
one factor. It is possible that both me-
chanical changes and irritative symptoms
contributed to the changes.
Goldsmith65 et al. have attempted to
demonstrate changes in airway resistance fol-
lowing exposure to ozone. Four subjects were
exposed to 200, 780, 1,180, and 1,960 Mg/m3
(0.1, 0.4, 0.6, and 1.0 ppm) ozone for periods
of 1 hour. During exposure, simple pulmon-
ary function tests such as Wright peak -flow-
meter and puffmeter (used to estimate
MMFR) were used to detect any rapid unto-
ward reaction, but none was observed. Airway
8-23
-------
resistance was measured in triplicate, using
the body plethysmograph technique before,
immediately, 1 hour, and 24 hours after
exposure; these data are shown in Figure
8-10. The subject who had the highest pre-
exposure airway resistance showed a 45
percent increase after exposure to 200 jug/m3
(0.1 ppm), and had slight hemoptysis (expect-
oration of blood). The pooled data show
increased airway resistance with increasing
concentrations which became significant at
1,960 jug/m3 (1.0 ppm). To pool the data, all
of each subject's tests were averaged and the
relative value, a percent of this average, was
calculated.
c. Summary of Human Exposure to Ozone
Prolonged exposure of humans to ozone,
under occupational and experimental condit-
ions, has produced the following effects:
1. No apparent effects were observed at
u
•z.
LLJ
ID
Z
<
X
U
z
<
LLI
OZONE EXPOSURE, ppm
0.1
0.4
0.6
-EXPOSURE
1 hour
Figure 8-10. Effect of ozone on airway resistance.®^
8-24
-------
concentrations up to 390 Mg/m3 (0.2
ppm).
2. The threshold level at which nasal and
throat irritation will result appears to be
about 590 Mg/m3 (0.3 ppm).
3. Concentrations of 980 Mg/m3 (0-5 ppm)
have caused a 20 percent decrease in
forced expiratory volume, observed after
8 weeks of intermittent exposure (3
hours a day, 6 days a week); this change
has returned to normal during a post-
exposure period of 6 weeks.
Experimental appraisal of short-term ex-
posures to ozone show the following results
(Table 8-10):
1. Up to 200 Mg/m3 (0.1 ppm) for 1 hour is
apparently without significant effect.
2. Concentrations of 200 to 780 Mg/m3
(0.1 to 0.4 ppm) for 1 hour have not
been shown to produce effects, but there
is a lack of information for this concen-
tration range
3. Exposure to concentrations of 980 to
1,960 Mg/m3 (0.5 to 1.0 ppm) for
periods of 1 to 2 hours produces changes
in pulmonary function. These are: in-
creased airway resistance, decreased vital
capacity, decreased carbon monoxide
diffusing capacity, and decreased forced
expiratory volume.
4. Some people are unable to tolerate
concentrations of 1,960 to 5,900 Mg/m3
(1.0 to 3.0 ppm) over a period of about
2 hours. Extreme fatigue and lack of
coordination are experienced.
5. Concentrations of about 17,600 Mg/m3
(9.0 ppm) produce severe pulmonary
edema and possible acute bronchiolitis.
C. OXIDANTS
In addition to the experimental exposure
of both animals and humans to ozone, con-
siderable work has been performed to evalu-
ate the effects of exposure to "oxidants."
These exposures have usually involved photo-
chemical smog obtained from either ambient
air or the synthetic irradiation of automobile
exhaust, and thus ozone has generally been
one of the substances present in these "oxi-
dant mixtures."
1. Animal Data
a. Direct Effects of Photochemical Oxidants
(1) Effects on pulmonary tissue.
Changes in pulmonary tissue.
Studies carried out to show the effect of
both ambient air and high concentrations of
auto exhaust on pulmonary function in labor-
atory animals have indicated that some in-
crease in lung flow resistance occurs as a
result of exposure to oxidants.
Swann66'67 et al. have studied the effect
of ambient air on the flow resistance of
guinea pigs. The first study took place over a
period of 2 years. Guinea pigs were located at
three stations within the Los Angeles area. At
each station, one group was exposed to
filtered air and a second group exposed to
ambient air. Measurement of expiratory flow
resistance (mostly airway resistance) at
monthly intervals, using the forced pressure
oscillation technique, showed no essential
difference between the two groups in each
station.
These data provided a basis for further
study of guinea pigs exposed to ambient air
when the oxidant level was above 40 percent
of the alert, or greater than 390 Mg/m3 (0.2
ppm). It was observed that some ambient air
breathers could show a significant increase in
resistance on the days during which oxidant
levels reached 980 Mg/m3 (0.5 ppm) or higher.
The animals exposed to charcoal filtered air,
however, also experienced this increase in
resistance, although to a lesser extent. The
ambient-air-breathing animals also showed an
increase in resistance on days when the
oxidant levels were considerably lower, 590
Mg/m3 (0.30 ppm). It is possible that other
components of ambient air, such as hydrocar-
bons and oxides of nitrogen, may also have
been elevated on the days when resistance was
elevated. The data provided in this paper are
inadequate to permit analysis of the relative
importance of these various pollutants on
respiratory resistance, although cold, wet days
8-25
-------
oo
K>
CTs
Table 8-10 (continued). SUMMARY OF DATA ON HUMAN EXTERMENTAL EXPOSURE TO OZONE
up to
7,800
200
780
1,180
1,960
up to 4 0
0.1
0.4
0.6
1.0
10-30
minutes
1 hour
1 hour
1 hour
1 hour
11
4 male
4 male
4 male
4 male
Headache, shortness
of breath, lasting
more than 1 hour
Odor
Odor
Throat irritation
and cough
VC: mean decrease
16.5% (4/8 subjects
showed decrease ^"10%),
FEVj Q: mean decrease
20% (5/8 subjects
showed decrease >10%);
MMFR: mean decrease
10.5% (5/6 subjects
showed a decrease);
MBC: mean decrease 12%
(5/8 subjects showed
a decrease),
DLco: decreased 20-50% in
7/11 subjects, increased
10-50% in 4/11 subjects.
Airway resistance.
mean increase 3.3%
at 0 hours after
exposure (1/4 sub-
jects showed an in-
crease of 45%);
Airway resistance:
mean increase 3.5% at
0 hours after exposure
(1/4 subjects showed
an increase of 60%),
mean increase 12.6%
1 hour after exposure;
Airway resistance:
mean increase 5.8% at
0 hours after exposure
(1/4 subjects showed
an increase of 75%),
mean increase 5%
1 hour after exposure;
Airway resistance:
mean increase 19.3%
at 0 hours after
exposure (3/4 subjects
showed an increase of
> 20%); mean increase
5% 1 hour after
exposure.
Only 5/11 toler-
ated dose for
full 30 mins.
Wide variation in
DLco-
One subject
had history of
asthma, and ex-
perienced hem-
optysis 2 days
after 1 ppm.
Hallctt64
Goldsmith
and Nade!65
-------
Table 8-10. SUMMARY OF DATA ON HUMAN EXPERIMENTAL EXPOSURE TO OZONE
Ozone,
Mg/m3
9,800
to
19,600
2,940
to
3,920
390
980
1,180
to
1,570
Ozone,
ppm
5 to 10
1.5 to 2
0 2
0.5
0.6-0.8
Length of
exposure
Not avail-
able
2 hours
3 hr/day,
6 days/wk,
for 1 2 wk
3 hr/day,
6 days/wk,
for 1 2 wk
2 hours
No. of
subjects
3 male
1 male
6 male
6 male
11
10 male.
1 female.
Subjective
complaints
Drowsiness,
headache
C.N S. depression,
lack of coordina-
tion, chest pain.
cough for 2 days,
tiredness for
2 weeks
None
No irritating
symptoms but could
detect ozone by
smell
Substernal soreness
and trachcal im-
tation 6-12 hours
after exposure, dis-
appearing within
12-24 hours in
10/11 subjects
Measurements of
pulmonary function
None
VC: decreased 13%,
returned to normal in
22 hours,
FEV3 0: decreased 16.8%,
slightly below normal
after 22 hours,
MBC: decreased very
slightly.
VC: no change
FKVj Q no change
VC: slight decrease
but not significant;
FEVj Q significant
decrease toward end
of 12 weeks. Returned
to normal during
6 weeks after exposure.
DL^Q: mean decrease of
25% f 11/11 subjects);
VC: mean decrease of
10% which was signifi-
cant (10/10 subjects);
FEVQ 75 x 40: mean de-
crease of 10% which
was significant
(10/10 subjects);
MMFR: mean decrease
of 15% which was not
significant;
Mixing efficiency:
no change (2/2 sub-
jects);
Airway resistance'
slight increase but
within normal limits;
Dynamic compliance:
no change (2/2 sub-
jects).
Other
comments
Measurement of 03
probably inaccurate
0.66 upper respir-
atory infections/person
in 12 weeks -Cf
control group had
0.95 in the same
period
0 80 upper respir-
atory infections/person
in 12 weeks
Reference
Jordan&O
et al
Gnswold61
et al.
Bennett62
Young63
et al.
oo
to
-J
-------
would appear to be associated with an in-
crease in resistance.
Murphy68 et al. exposed guinea pigs to
irradiated and nonirradiated auto exhaust for
periods of 4 hours. Intact unanesthetized
guinea pigs were exposed through face masks
attached to an exposure manifold, and were
placed in body plethysmographs. Before, dur-
ing, and after exposure, measurements were
made of tidal volume, respiratory rate, and
total respiratory (lung and chest wall) flow
resistance, as described by Mead.69 The re-
sults of these measurements are shown in
Figures 8-11 and 8-12. Chemical differences
were noted between the two forms of auto
exhaust. Comparison of concentrations in
irradiated and nonirradiated atmospheres of
approximately equal dilution ratios show the
photochemical formation of aldehydes, nitro-
gen dioxide, and total oxidant at the expense
of nitric oxide and olefin (Table 8-11).
Marked increases in total expiratory flow
resistance occurred rapidly during exposure to
irradiated exhaust. This was accompanied by
a decrease in respiratory rate and a small
increase in tidal volume. These functions
rapidly returned to baseline levels following
removal of the animals to a clean-air atmo-
sphere. The response to nonirradiated exhaust
was relatively small, and when it occurred
could possibly have been due to carbon
monoxide. In this study, the increase in flow
resistance was associated with a decrease in
frequency of breathing and an increase in
tidal volume. In this respect, the response was
similar to that of guinea pigs exposed to
sulfur dioxide10 and different from guinea
pigs exposed to ozone or to nitrogen diox-
ide.9 The increase in flow resistance noted in
this experiment occurred at low oxidant levels
compared to the concentration of ozone
(1,960 Mg/m3 or 1 ppm) required to produce
changes in flow resistance. The data suggest
that components of the exhaust other than
oxidants play a role. It must be pointed out
that changes in resistance were of only bor-
derline significance when concentrations of
auto exhaust comparable to those found in
ambient air were used (1-1142 in Figure 8-12;
experiments H and I in Table 8-11).
Pathological changes.
Bils7 ° and Bils and Romanovsky71 have
reported ultrastructural alterations of the
alveolar tissue of mice exposed to heavy Los
Angeles smog containing 780 MS/m3 (0.4
ppm) total oxidants and to synthetic photo-
chemical smog prepared by irradiating 14,000
jug/m3 (8 ppm) propylene, and 3,440
(2.8 ppm) NO to yield 1,470 to 980
Table 8-11. CHEMICAL AGENTS IN EXHAUST-CONTAMINATED ATMOSPHERES 68
Experiment
A. Irr.
B. In.
C. Nonirr.
D. Irr.
E. Irr.
F. Irr.
G. Nonirr.
H. Irr.
I. Irr.
Dil. ratio-
air/ex.
150
155
160
360
330
407
375
1,350
935
Concentrations*
COC
290
310
300
86
95
85
85
34
47
Total
oxidant
0.78
0.80
0.02
0.82
0.57
0.45
0.00
0.35
0.33
NO 2
5.50b
2.66
1.58
1.64
2.23
2.95
0.38
0.49b
0.43
NO
1.00b
0.21
4.27
0.16
0.20
0.59
2.58
0.25 b
0.17b
Form aid.
1.93
2.42
0.12
1.11
1.02
1.39
0.38
0.54b
0.39b
Aerolein
0.17b
0.20b
0.07
0.11
0.09
0.10
002
Olefin
8.90b
12.90
17.80
3.20
1.60
1.53
5.37
0.57b
1.22b
HC/NOX
ratio
4.0
3.5
2.9
2.5
2.1
2.6
2.4
2.9
aAll concentrations in ppm except olefins in jug per liter.
blndicates analysis at manifold was not obtained and figure refers to a representative analysis at the irradiation chamber.
cCarbon monoxide concentration calculated from raw exhaust/dilution ratio.
8-28
-------
u
<
IS)
UJ
0^0.8
a:
o
i-
<
K
a.
x
UJ
%••
\ ^,—
v'-
A
/V
'.
•I--.
^r
>- £
Oi-x
CL
1/5
UJ
OL
\l
4O
4.0
-I O
O .t
< E
2 2.0
1.0
4
O
r- ----
—•% /
— • •'' — '
AIR
EXHAUST
AIR
_ ^\
V
\^-*>
\^ ^,_
EXP.
• AIR ONLY
IRRAD.
AIR EX.
0
150:1
NUMBER OF
ANIMALS
14
5
Z E
X'V. __ — >.
TIME, hours
Figure 8-11. Respiratory response of guinea pigs breathing auto exhaust.66
8-29
-------
(0.75 to 0.5 ppm) total oxidants. Exposure to
natural smog was for 2 to 3 hours, whereas
exposure to synthetic smog was for 3 hours.
The data from these experiments are summar-
ized in Tables 8-12 and 8-13. The pattern of
the ultrastructural changes appeared to be the
same for both natural and synthetic smog.
The severity of the changes appeared to
increase with increase in age, with irreversible
changes (loss of wall cells) appearing at about
age 15 months. The lining epithelium and
basement membrane seemed to withstand
smog well even though the endothelium was
seriously affected. The edema-like condition
was only apparent in the lining epithelium
when the mice reached 20 to 21 months.
In additions to these studies, Rounds and
Bils72 treated cultures of alveolar wall cells
from rats and rabbits in vitro with NaNO2; it
was assumed that NaNO2 simulated the intro-
duction of nitrogen dioxide to the cell. A
reversible inhibition of respiratory activity of
the cells was observed. Electron microscopy
of the living cells and of fixed material during
NaNO2 treatment showed that there were
changes in the shape of the nucleus and
ultrastructure of the mitochondria of the
alveolar wall cell. These changes occurred as a
2.2
2.0
1.8
1.6
1.4
1.2
1.0
0.8
0)
1
a.
AIR EXHAUST DILUTION RATIO:
I = IRRADIATED
Nl = NONIRRADIATED
*— POST-EXPOSURE—+\
EXPOSURE, hours
Figure 8-12. Effect of auto exhaust on expiratory flow resistance of guinea pigs.
68
8-30
-------
Table 8-12. ULTRASTRUCTURAL ALTERATIONS IN ALVEOLAR TISSUE OF MICE AFTER
EXPOSURE TO MORE THAN 780 Mg/m3 (0.4 ppm) OXIDANT FOR 2 TO 3 HOURS70
Age
Time of investigation
Cellular effects and pathology
5 months
9 months
9 months
21 months
During and after exposure.
During exposure.
14 hours after exposure
During exposure.
No apparent change.
Few normal mitochondria in epithelial cell walls.
Disrupted cytoplasm containing lamellar inclusions or
fragments.
Some epithelial and endothelial swelling.
Marked recovery.
Difficult to distinguish between experimental and
control animals.
Similar to 9-month-old mice, but cytoplasmic fragments
and proteinaceous material were present in alveoli.
Practically no epithelial wall cells present.
Table 8-13. ULTRASTRUCTURAL ALTERATIONS IN ALVEOLAR TISSUE OF MICE AFTER 3-HOUR EXPOSURE TO
FROM 980 TO 1,470 jjg/m3 (0.50 TO 0.75 ppm) OXIDANT IN SYNTHETIC PHOTOCHEMICAL SMOG
Age
6 monflis
8 months
15 months
20 months
Time of investigation
Immediately
after exposure
Immediately
after exposure
18 hours after
exposure
Immediately
after exposure
6 to 8 hours
after exposure
24 hours
after exposure
Immediately
after exposure
18 hours
after exposure
Cellular effects and pathology
Difficult to distinguish treated from control tissues. Possibly an increase in
breakage of the endothelial membrane in treated animals.
Wall cells contained fewer normal mitochondria. These cells were vacuolated with many
lamellar inclusions, possibly indicating increased mitochondria! transformation.
Slight epithelial and endothelial swelling.
Alveolar tissue recovered so that it was difficult to distinguish treated from
controls.
Swelling and disruption of both epithelial and endothelial lining of alveolar cell.
Basement membrane still intact. Increase in number of alveolar phagocytes. Observed
decrease in wall cells, seen also in controls and therefore attributed to aging.
Disrupted wall cell cytoplasm but some normal wall cells remained. Large alveolar
phagocytes, some in almost complete contact with epithelial lining. Serious disorgan-
ization of the connective tissue in some localized interstitial areas.
Most wall cells seemed to be lost. Some epithelial and endothelial lining cells re-
mained intact. Integrity of basement membrane maintained. Rupture of the lining
membranes was apparent.
Cytoplasm of large alveolar cell walls quite disorganized. Most of the surrounding
basement membranes, connective tissue, and lining membranes also severaly altered.
Disruption of both epithelial and endothelial lining membranes. Most alveolar
phagocytes appeared normal.
Exaggerated swelling of cell lining. Both epithelial and endothelial blebs contained
substances that could have produced an edematous condition. Remains of degenerating
wall cells present. Remaining wall cells contained same type of dense membranous
material as that seen in alveoli.
8-31
-------
result of both a single exposure to 37,600
Mg/m3 (20 ppm) nitrogen dioxide for 1 hour
and chronic exposure to 28,200 jug/™3 (15
ppm) nitrogen dioxide for 4 hours a day for
10 days. Increasing the dose of nitrogen
dioxide to 150 Mg/m3 (80 ppm) for 55
minutes produced more drastic and irrevers-
ible lamellar transformation of the wall cell
mitochondria.
Development of lung tumors.
Certain studies have reported that aging
experimental mice breathing air with rela-
tively high levels of photochemical oxidant
pollution show increased incidence of benign
pulmonary adenomas. Gardner73 has exposed
several strains of mice at four exposure
stations in the Los Angeles area. Monthly
average "oxidant" concentration varied from
40 to 140 Mg/m3 (0.02 to 0.07 ppm), and
daily 24-hour maxima averaged from 140 to
490 jug/m3 (0.07 to 0.25 ppm). The results
indicated a trend toward an increased inci-
dence of pulmonary adenomas in aging exper-
imental mice breathing ambient air when
compared to the incidence in control animals
who breathed filtered air.
In an attempt to confirm this observed
trend, Gardner74 et al. conducted an addi-
tional study utilizing rats exposed to either
ambient or filtered Los Angeles air. The
results of this second study indicated that
there was an increased incidence of chronic
nephritis in male rats exposed to ambient air,
although no statistically significant differ-
ences concerning the incidence of lung tumors
were noted between the mice exposed to the
ambient atmosphere and their respective con-
trols.
Catcott and Kotin75 did not find an
increase in lung tumors in dogs from polluted
areas of Los Angeles, although this species
seems to be resistant to pulmonary lesions for
anatomical reasons.
Kotin7 6 >7 7 et al. exposed A-strain and Cs7
black mice to 1,960 to 7,470 jug/m3 (1.0 to
3.8 ppm) oxonized gasoline. The results are
shown in Table 8-14. These data show an
association between exposure to ozonized
gasoline and an increase in lung tumor in-
cidence.
Kotin and Falk78 have pointed out that
the physical state of natural carcinogenic
hydrocarbons is .one of adsorption on soot
particles in a size range compatible with
deposition and retention of particles. They
have also noted that atmospheric irritants,
including photochemical oxidants, cause res-
piratory epithelial changes which facilitate
deposition and retention of particles.
It is often implied that an increase in the
frequency of pulmonary adenoma is equiva-
lent to a demonstration that the exposure in
question had produced or enhanced a carcino-
genic effect. True carcinomas in C57 black
mice have been produced by the combined
exposure to ozonized gasoline and to in-
fluenza virus,79'80 and it has recently been
Table 8-14. LUNG TUMOR INCIDENCE IN MICE AFTER EXPOSURE
TO EITHER OZONIZED GASOLINE OR WASHED AIR 76-77
Group
Washed air
Ozonized gasoline
Washed air
Ozonized gasoline
Strain
CS7
C57
A-strain
A-strain
Week of
first tumor
appearance
56
71
28
24
Number of
mice
surveyed
376
155
45
15
Number of
tumor-
bearing
mice
6
15
11
6
Percent
tumor-
bearing
1.6
9.6
24.0
40.0
8-32
-------
reported that experimental animals pre-
exposed to sulfur dioxide and then exposed
to inhaled polynuclear hydrocarbons develop-
ed a true metastasizing bronchial car-
cinoma.81 Other combinations, such as poly-
nuclear hydrocarbons with soot and with
hematite, have been reported to produce
experimental lung cancer in animals. No true
lung cancers have been reported, however,
from experimental exposures to either ozone
alone or any other combination or ingredient
of photochemical oxidants.
(2) Systemic effects.
Changes in fertility and neonatal mortality
Hueter et al.,37 in studying the effect of
irradiated auto exhaust on mice, observed
decreased fertility and survival rate of off-
spring in those mice exposed to irradiated
auto exhaust containing ozone in concen-
trations of 1,180 to 1,960 Mg/m3 (0.6 to 1.0
ppm); other pollutants present in the exhaust
were carbon monoxide (70 to 115 mg/m3, or
60 to 100 ppm), hydrocarbons (20 to 36
ppm), and nitrogen oxides (2.9 to 3.9
ppm).37 Similar results have been obtained
by Lewis82 et al., who studied the effect of
irradiated auto exhaust on the reproduction
of mice. One hundred-fifty virgin females
were preconditioned to either filtered air of
irradiated auto exhaust for a period of 16
hours daily for 46 days. Estimates of total
oxidant levels ranged from 200 to 980 Mg/m3
(0.1 to 0.5 ppm) in the first experiment and
590 to 1,960 Mg/m3 (0.3 to 1.0 ppm) in the
second experiment; carbon monoxide, hydro-
carbons, and nitrogen oxides were also pres-
ent. At 12 to 13 weeks, the mice were
permitted to mate with randomly paired,
similarly preconditioned males for an 11-day
mating period. Results of the first experiment
indicated that preconditioning of males with
irradiated auto exhaust doubled the non-
pregnancy average of their mates. It was
determined, moreover, that the reproductive
tracts and gonads of the nonpregnant females
and their respective mates were normal.
In the second experiment, it was found
that preconditioning of males to irradiated
auto exhaust resulted in an increased mortal-
ity in neonatal mice. The authors suggest that
air pollutants in irradiated auto exhaust may
alter the genetic composition and possibly
other cellular components of sperm.
Stress response.
Exposure to photochemical oxidants has
produced stress responses in animals. It is well
known that an increased urinary 17-ketogenic
steroid output is found in response to a wide
variety of stresses. Harvey83 et al. subjected
guinea pigs to psychological and physiological
stresses and measured their elevated 17-keto-
genic steroid output by Selye's general alarm
reaction. The guinea pigs were then exposed
to a Los Angeles photochemical smog. At the
end of the stress period, the levels rapidly
returned to normal. The subsequent exposure
to smog increased the 17-ketogenic steroid
output, but the differences were small com-
pared to the control group. It was suggested
by the authors that smog stress induces the
general alarm reaction.
Hueter37 et al. reported a stress adaption
response in mice exposed over a period of 2
years to irradiated auto exhaust containing a
concentration of ozone of 80 to 390 Mg/m3
(0.04 to 0.2 ppm). Their indices to stress
adaptation included a reduction in the spon-
taneous activity of the mice, followed by a
return to pre-exposure activity level.
b. Indirect Effects of Photochemical
Oxidants
Altered response to other agents.
Exposure to photochemical oxidants has
been shown to lower the resistance of animals
to certain other deleterious agents. Levels of
lab oratory-synthesized smog, with oxidant
levels well below the peak concentrations
found in heavily polluted areas, have en-
hanced mortality from streptococcal pneu-
monia.
Murphy68 et al. have studied the combined
effects of the edemagenic agent a-naphthyl-
thiourea (ANTU) with both irradiated and
nonirradiated auto exhaust. These data are
shown in Table 8-15. Except for one experi-
8-33
-------
ment (G), there was a consistently higher
mortality rate due to ANTU in the exhaust-
exposed group. Although the mortality differ-
ences between the two groups were small,
they were statistically significant (p < 0.02).
The authors concluded that increased mor-
tality was due to increased stress and not due
to the lethality of the exhaust itself.
Coffin and Blommer84 have studied the
susceptibility of laboratory animals to bac-
terial infection following exposure to auto
exhaust. Mice were exposed to auto exhaust
containing 13,800 to 115,000 jug/m3 (12 to
100 ppm) carbon monoxide and 160 to 1,310
/zg/m3 (0.08 to 0.67 ppm) oxidant for four
hours. Clean air was used in control ex-
periments. Immediately after exposure, the
animals were subjected to a bacterial aerosol
of streptococcus (Group C) introduced at a
rate of 100,000 organisms per mouse. It was
observed that exposure to exhaust containing
115,000 /Mg/m3 (100 ppm) carbon monoxide
and an oxidant range of 690 to 1,310 Mg/m3
(0.35 to 0.67 ppm) caused enhanced mortali-
ty from streptococcal pneumonia. Mortality
was 53 percent for those pretreated with
exhaust and 11. percent for the controls. A
"no effect" level was reached at 28,750
3 (25 ppm) carbon monoxide and 240
3 (0.12 ppm) oxidant. It was concluded
that laboratory-synthesized photochemical
smog can enhance mortality to streptococcal
pneumonia at levels of carbon monoxide and
oxidant which are well below the peak con-
centration in heavily polluted air. In view of
the fact that ozone at 160ME/m3 (0.08 ppm)
and above has been shown to enhance morta-
lity from respiratory infection,40 it would
appear reasonable to ascribe the enhancement
reported in this experiment to the oxidant
content of the auto smog.
c. Summary
Several general statements can be made
regarding the experimental exposure of lab-
oratory animals to mixtures of photochemical
oxidants.
1. Long-term exposure to ambient air in
Los Angeles produces an increase in flow
resistance in guinea pigs during peak oxi-
dant periods when the oxidant level ex-
ceeds 980 /ug/m3 (O-5 PPm)-
2. Long-term exposure to irradiated auto
exhaust with oxidant levels from 390 to
1,960 Mg/m3 (0.2 to 1.0 ppm) produces a
decrease in fertility, an increase in neonatal
mortality, and a stress adaptation response
in mice.
3. During short-term exposure to irra-
diated auto exhaust containing up to 1,570
Mg/m3 (0.8 ppm) oxidant for periods of up
to 6 hours, the following changes in pul-
monary function are observed in guinea
pigs: increased tidal volume, increased
minute volume, and increased flow re-
sistance. These changes return to normal
Table 8-15. EFFECT OF IRRADIATED AND NONIRRADIATED EXHAUST ON MICE TREATED WITH ANTUa
68
Experiment
A. Irr.
B. Irr.
C. Nonirr.
D. Irr.
E. Irr.
F. Irr.
G. Nonirr.
Dilution
ratio,
air/exhaust
150
155
160
360
330
407
375
Number
treated
per group
10
15
15
20
15
15
15
Mortality, percent
0 hr post exposure
Ail
0
27
13
0
0
27
13
Exhaust
10
47
40
5
6.7
53
0
3 hr post exposure
Air
0
27
13
5
0
40
20
Exhaust
40
47
47
15
6.7
60
20
24 hr post exposure
Air
20
27
13
5
20
60
20
Exhaust
50
47
47
15
33
80
20
ANTU (ff-naphthylthiourea) injected intrapcritoneally, 30 minutes before exposure, at dosage of 15 mg/kg in all experiments
except F''; experiment F, 20 mg/kg.
8-34
-------
immediately following exposure. In addi-
tion, irreversible alveolar tissue changes in
aged mice, decreased spontaneous running
activity, and increased susceptibility to
streptococcal pneumonia in young adult
mice are observed.
It should be noted that experimental ex-
posure to irradiated auto exhaust usually
involves variable concentrations of carbon
monoxide, hydrocarbons, and nitrogen oxi-
des, as well as "oxidants." The studies of the
effects of oxidants on animals are summarized
in tabular form in Table 8-16. Apart from the
production of eye irritation, no studies have
been carried out on the effects of photo-
chemical oxidant mixtures on humans.
D. PEROXYACYL NITRATES
1. Animal Data
Lethality
Data on the lethality of peroxyacetyl ni-
trate (PAN) are sparse, but that which is
available suggests that it is less lethal to mice
than ozone, about the same as nitrogen
dioxide, and more lethal than sulfur dioxide.
Campbell8 5 et al. exposed mice to high
concentrations of PAN, 480 to 700 Mg/m3
(97 to 145 ppm) as measured at the chamber
outlet, for 2 hours at 80° F The studies
demonstrated that the majority of mice ex-
posed to 540 Mg/m3 or 110 ppm or more,
PAN died within a month (Figure 8-13). It
was observed that mice exposed to higher
concentrations died earlier than those ex-
posed to the lower concentrations. Median
lethal exposures characteristically produced a
delayed mortality pattern, with most deaths
occurring in the second and third week after
exposure. Mortality was greater among older
mice than younger mice, and it was greater at
higher temperatures. It was not influenced
appreciably by changes in relative humidity.
2. Human Data
Effects on Pulmonary Function
Experiments carried out on humans have
suggested that exposure to PAN results in
increased oxygen uptake during exercise.
Smith8 6 has carried out a group of studies on
male college students averaging 21 years of
age. The subjects were exposed to 1,485
Mg/m3 (0.3 ppm) PAN by breathing through
the mouth (nose clamps were used) for 5
minutes while at rest, and then the subjects
were engaged immediately in 5 minutes of
exercise on a bicycle ergotometer. Both air
containing PAN and air free of PAN were
used without the knowledge of the subjects.
Since the pollutant has no characteristic smell
or taste, it was considered that the experi-
ment was carried out in a "blind" fashion.
Some of the data are presented in Table 8-17,
and it can be noted that there was a statisti-
cally significant increase in oxygen uptake
during exercise, without any change at rest.
Expiration velocity was reduced after exer-
cise. The changes could possibly be a reflec-
tion of an increase in the work of breathing or
due to an increase in airway resistance.
Because the report of this work does not
adequately describe the experimental design
or the statistical analysis, these results merit
replication before conclusive statements can
be made.
3. Discussion
The data obtained so far on the effects of
PAN in animals and man are too incomplete
to enable conclusions to be drawn regarding
any effects of this pollutant at ambient
concentrations.
E. SENSORY IRRITATION
1. Animal Data
Effects of Air Pollutants on the Eye
Experiments with various types of air
pollutants have thus far failed to show sig-
nificant physical or chemical effects on the
eyes of exposed rabbits. Mine87 et al. ex-
posed healthy albino rabbits to pure sulfur
dioxide at 26,200 Mg/™3 (10 ppm); nitrogen
dioxide at 37,600 Mg/m3 (20 ppm); and
ozone, 3,720 to 5,490 Mg/m3 (1.9 to 2.8
8-35
-------
9°
u>
ON
Table 8-16. SUMMARY OF THE EFFECTS OF PHOTOCHEMICAL OXIDANTS IN ANIMALS
Oxidant,
Mg/m3
> 240
650
to
1,610
> 780
> 980
1,960
to
7,470
650
to
1,610
200
to 980
390
to
1,960
590
to
1,960
Oxidant,
ppm
>0.12
0.33-0.82
> 0.4
> 0.5
1.0-3.8
0.33-0.82
0.1-0.5
0.2-1.0
(inlet)
0.3 - 1.0
Source
Irr. auto
exhaust
In. auto
exhaust
Smog
Smog
Ozonized
gasoline
Irr. auto
exhaust
Irr. auto
exhaust
Auto
exhaust
Irr. auto
exhaust
Length of
exposure
4 hours
4 hours
2-3 hours
Continuous
Continuous
6 hours
16 hour
day/46 days
Continuous
16 hour
day/46 days
Observed effect(s)
Local effects
Short-term exposures
Increased mortality from streptococcal pneumonia.
Increased expiratory flow resistance— 20 to 120%,
increased inspiratory flow resistance - 40%.
Decreased respiratory frequency - 15-35%.
Alveolar tissue changes in animals aged 9 months
or over. Increased severity with age. Damage
at 9 months reversible, at 21 months
irreversible.
Disruption of epithelial walls; cytoplasmic
fragments and proteinaceous material in
alveoli.
Long-term exposures
Increase in flow resistance (increase also
occurred at lower oxidant levels).
Increased frequency of lung tumors seen
after 24 weeks
Systemic effects
Short-term exposures
8 to 80% decrease in spontaneous running
activity.
Long-term exposures
Decrease in fertility. Doubling of
non-pregnancy average.
Stress adaptation response, i.e. reduction
in spontaneous running activity returning
to pre-exposure levels.
Increased neonatal mortality due to
preconditioning of males.
Species
Mice
Guinea pigs
Mice
Guinea pigs
Mice
Mice
Mice
Mice
Mice
Reference
Coffin and
Blommer84
Murphy68
et al.
Bils70
Bils and
Romanovsky
Swann66 et al.
Swann and
Balchum67
Kotin and Falk76
T7
Kotin " et al.
77
Kotin' et al.
Murphy68 et al.
Lewis82 et al.
Hueter37 et al.
O'J
Lewis et al.
-------
Table 8-17. COMPARISONS OF MEANS AND
PERCENTAGE CHANGE IN OXYGEN
UPTAKE IN HEALTHY MALE COLLEGE
STUDENTS AFTER INHALATION OF
1,485 Mg/m3 (0.3 ppm) PEROXYACETYL
NITRATE AND FILTERED AIR 86
Activity
Rest for 5 minutes
Exercise for 5 minutes
Recovery for 5 minutes
Oxygen uptake,
liters/min
Air
1.65
10.32
3.30
PAN
1.66
10.55
3.34
Change, percent
0.19
2.3a
1.2
ppm); and to the vapors of acrolein, 4,580 to
18,320 Mg/m3 (2 to 8 ppm); and a di-epoxide
(3 to 12 ppm). These compounds were also
used in various mixtures, with and without
the addition of a saline aerosol. Two types of
synthetic smog were also used: UV-irradiated
ozonized gasoline, with or without nitrogen
dioxide, and irradiated auto exhaust. The
parameters measured were the regeneration
rate of excoriated corneas, changes in the
degree of chemosis (excessive edema of the
conjunctiva), and iritis (inflammation of the
iris). A single 4-hour exposure or 25 to 34
intermittent 1-hour exposures to the various
gases produced no significant effects. In a
Statistically significant (p < 0.05).
100
90
80
70
o
Q.
?• 50
a:
o
30
20
10
MORTALITY FOLLOWING EXPOSURE
>-
I-
<
-|-
-O
-o
•z.
<
I-
o
6?
o
o
102-1 10-
-111-117 -j [• 122-
PAN CONCENTRATION, ppm
QC
Figure 8-13. Cumulative mortality of mice from exposure to PAN.
8-37
-------
similar study, Mettier8 8 et al. were unable to
demonstrate ophthalmologic or biochemical
effects on intact and de-epithelialized corneas
of exposed rabbits.
2. Human Data
a. Olfactory Effects
Witheridge and Yaglou89 have reported
that the odor of ozone could be detected by
people with a keen sense of smell at 20 ng/m3
(0.01 ppm), and that normal people could
detect the odor at 30 ng/m3 (0.015 ppm); the
measuring techniques used in this study were
less accurate at these low concentrations than
methods of later studies. The authors con-
ducted a series of experiments in which a
number of subjects were placed in a poorly
ventilated room and body odor intensity was
allowed to reach a point of equilibrium. An
ozonator was turned on and adjusted to
produce the minimum ozone intensity con-
sistent with minimal body odors. The subjects
then evaluated the ozone and body odors.
The authors claimed that the ozone odor
intensity was not affected by the presence or
absence of body odor. They found that the
perceived body odor was due to the effect of
the ozone on the mucous membranes of the
nose, rather than on the odor agents them-
selves.
Henschler90 et al. have performed careful
studies of the olfactory threshold and
symptoms in 10 to 14 male volunteer test
subjects exposed for 30 minutes to a series of
different concentrations of ozone. Changes in
sensation were recorded by the subjects at
5-minute intervals while in the chamber. The
lowest concentration of ozone used, 40
Mg/rn3 (0.02 ppm), was recognized immedi-
ately by 9 of 10 exposed subjects. Thus
Henschler et al. indicate that the odor thresh-
old is below 40 jug/™3 (0.02 ppm). Following
exposure to 40 ug/m3 (0.02 ppm), the sub-
jects reported that the odor diminished rap-
idly. Within a period of 30 seconds to 12
minutes (average of 5 minutes), the odor was
no longer perceptible. At 100 ug/m3 (0.05
ppm) ozone, 13 of 14 subjects indicated that
the odor was considerably stronger and the
odor perception lasted longer (2 to 30 min-
utes, with an average of 13 minutes).
b. Experimental Studies of Eye Irritation
The most obvious reaction of humans
exposed to photochemical air pollution is the
development of eye irritation with, in some
instances, lacrimation. A number of compli-
cated problems arise, however, when attempts
are made to provide precise experimental
measurements of eye irritation and to deter-
mine exactly what factors are responsible for
reported irritation.
Ozone, the principal contributor to ambi-
ent oxidant levels, is not an eye irritant.91
The major photochemical products identified
as eye irritants are acrolein, peroxyacetyl
nitrate (PAN), and peroxybenzoyl nitrate
(PBzN).91'93 The recently discovered PBzN
compound has been demonstrated to exhibit
an eye irritation potency 200 times that of
formaldehyde.93 Problems associated with
studies of eye irritation generally fall into one
of two categories: (1) Human experimental
studies have been directed toward a definition
of the substances responsible for irritation,
and attempts have been made to correlate
experimental data with those obtained from
epidemiological studies, and (2) Difficulties
have been encountered in experimental
studies resulting from variables which include
the measurement of a subjective response,
individual differences in sensitivity, synthetic
atmospheres, and the multiphasic nature of
photochemical reactions.
First, there is the problem of obtaining
clean air samples for irradiation, that is,
samples which are uncontaminated with
hydrocarbons and nitrogen oxides. It is diffi-
cult to cleanse the residual traces of reacted
products from previous experiments from
exposure chambers. Thus, additional impuri-
ties often build up.
Second, problems stem from the fact that
measurement of eye irritation in humans is
necessarily the measurement of a subjective
response. Physiologic and psychologic factors
contribute to the sensitivity of a particular
8-38
-------
individual. Wide variations in response to a
given irritant may depend on differences in
sensitivity between individuals and between
irritants; age, the older persons being more
sensitive and sustaining irritant effects for
longer periods; inflamation due to other
causes; and choice of experimental subjects.
A third complication is the nature of
photochemical reactions themselves, which
are fundamentally multiphasic with a com-
plex time course (Figure 8-14). Thus it takes
several hours for reactions to take place at
realistic concentrations of hydrocarbons and
nitrogen oxides. Both in chamber irradiations
of hydrocarbons and nitrogen oxides and in
polluted atmospheres, the earliest reaction is
the conversion of nitric oxide to nitrogen
dioxide. This is followed, about an hour later,
by a peak in eye irritation response, and then
by the maximal oxidant or ozone value,
which occurs about 2 hours after peak eye
irritation. The measured oxidant level, for
practical purposes, may be considered as a
weighted sum of the nitrogen dioxide and
ozone.
3. Discussion
The characteristic pungent odor of ozone
can be detected instantaneously at very low
concentrations (less than 40 ng/m3, or 0.02
ppm, depending on individual acuity); at 100
Mg/m3 (0.05 ppm), the odor is considerably
stronger and persists longer. The odor per-
sisted for an average of 5 minutes after the
lower exposure, and an average of 13 minutes
after the higher exposure.
The following conclusions can be reached
on the basis of the existing data on eye
irritation:
1. The effective eye irritants are the
products of photochemical reactions.
2. Although oxidant concentrations
may correlate with the severity of
eye irritation, a direct cause-effect
relationship has not been demon-
strated. Ozone, the principal contrib-
180
HOUR OF DAY
Figure 8-14. Analytical data for auto exhaust chamber experiments.
8-39
-------
utor to ambient oxidant levels, is not
an eye irritant, although the possibil-
ity that this compound contributes
to eye irritation by a synergistic
mechanism cannot be ruled out.
The precursors of the eye irritants
are organic compounds in combina-
tion with oxides of nitrogen, the
most potent being aromatic hydro-
carbons.
The chemical identities of the effec-
tive irritants in synthetic systems are
known. They are formaldehyde,
PBzN, PAN, and acrolein, although
the latter two contribute only to a
minor extent.
The substances causing eye irritation
in the atmosphere have not been
completely defined. It is possible
that aldehydes and peroxybenzoyl
nitrate contribute to a major extent,
but it is probable that unidentified
compounds are also responsible.
A thorough discussion relating to the eye
irritation effects of air pollution will be found
in the companion document, AP.-64, Air
Quality Criteria for Hydrocarbons.
F. SUMMARY
The data have been presented separately
for both human exposures and animal studies;
effects of ozone, oxidants, and PAN have been
discussed and summarized separately. Table
8-18 summarizes the toxicologic studies of
ozone exposure, and Table 8-19 summarizes
the toxicologic studies of oxidant exposure.
The data existing on the effects of PAN are
extremely limited at the present time.
Table 8-18. SUMMARY OF TOXICOLOGIC STUDIES OF OZONE EXPOSURE
Effect
Moibidity
Local effects
Perception of pungent odor (man)
Increased frequency of breathing. Decreased tidal volume
(guinea pigs)
Chemical changes in lungs (rabbits)
Engorged blood vessels and excess leukocytes in lung
capillaries (mice)
Increased flow resistance (guinea pigs)
Increased lung weight. Decreased tidal volume, decreased
minute ventilation (rats)
Gross pulmonary edema (rats)
Decreased lung compliance (guinea pigs)
Gross pulmonary edema. Increased lung serotonin (rats)
Decreased tidal volume, decreased oxygen consumption
(rabbits)
Bronchitis, bronchiolitis, emphysematous and fibrotic
changes; acceleration of lung tumor development (mice)
Systemic effects
Decreased voluntary running activity (mice)
Increased liver weight. Increased liver alkaline
phosphatase (rats)
Decreased brain sertonin (rats).
Structural changes in heart myocardial fibers (mice)
Ozone
concentrations,
ppm
0.02
0.34
1.00
1.00
1.08
2.00
3.20
5.00
6.00
15.00
1.00
0.20
3.10
6.00
0.20
Mg/m3
40
670
1,960
1,960
2,120
3,920
6,290
9,800
11,800
29,000
1,960
390
6,100
11,800
390
Length of
exposure
< 5 minutes
2 hours
1 hour
4 hours
2 hours
3 hours
4 hours
2 hours
4 hours
30 minutes
continuous (at
least 1 year)
6 hours
20 hours
4 hours
5 hours/day/
3 weeks (total
105 hours)
Reference
Henschler90et al.
Murphy et al.
Buell12 et al.
Scheel5 et ai
Murphy' et at
Scheel5 et al.
Scheel5 et al.
Easton1^ et al.
Skillen1 7 et al.
Scheel5 et al.
Stokinger33et al.
Stokinger6
Murphy-^ et aL
Skillen30 et aL
Brinkman18etal.
8^0
-------
Table 8-18. (continued) SUMMARY OF TOXICOLOGIC STUDIES OF OZONE EXPOSURE
Effect
Mortality
Increased susceptibility to Streptococcus (Group C)
Increased susceptibility to Klebsiella pneumoniae
(mice, hamsters)
Increased susceptibility to Klebsiella pneumoniae
(mice, hamsters)
Increased susceptibility to histamine (guinea pigs)
Increased mortality with exercise (15 minutes/hour)
(rats)
Decreased mortality with age. Young-50% mortality;
old- 10% mortality
Decreased survival time due to stimulated thyroid
activity (rats)
LDjQ mice
LDjQ rats
LDjQ cats
LDjQ rabbits
LD<;Q guinea pigs
Ozone concentrations,
ppm
0.08
0.84
1.30
5.0
1.0
4.0
6.0
21.0
21.8
34.5
36.0
51.7
Mg/m3
160
1,650
2,550
9,800
1,960
7,800
11,800
41,000
42,000
67,980
71,000
101,400
Length of
exposure
3 hours
4 hours/5 days/
2 weeks
3 hours
2 hours
6 hours
4 hours
4 hours
3 hours
3 hours
3 hours
3 hours
3 hours
Reference
Coffin40 et al.
Miller48 et al.
Miller48 et al.
Easton10 et al
Stokinger6
Stokinger6
Skillen7
Mittler3 et al.
Mittler3 et al.
Mittler3 et al.
Mittler3 et al.
Mittler3 et al.
TABLE 8-19. SUMMARY OF TOXICOLOGIC STUDIES OF OXIDANT EXPOSURE ON ANIMALS
Effect
Morbidity
Local Effects
Increased flow resistance; decreased frequency of
breathing (guinea pigs)
Changes in alveolar tissue in mice
Increase in flow resistance (guinea pigs)
Increase in lung tumors (mice)
Systemic Effects
Decrease in spontaneous running activity (mice)
Decrease in fertility. Doublingof non-pregnancy
average (mice)
Mortality
Increased neonatal mortality due to pre-conditioning
of males (mice)
Increased mortality from streptococcal pneumonia
Oxidant concentration,
ppm
0.33-0.82
>0.4
>0.5
1.0-3.8 (from
ozonized
gasoline)
0.33-0,82
0.1 -0.5
0.3 - 1.0
>0.12
Mg/m3
650-
1,610
780
980
1,960-
7,470
650-
1,610
200-
980
590-
1,960
240
Length of exposure
4 hours
2-3 hours
continuous
24 weeks
6 hours
16 hours day/
46 days (total,
736 hours)
16 hours day/
46 days (total,
736 hours)
4 hours
Reference
Murphy68 et al.
Bils70'71 etal.
Swann66' 67 et al.
Kotin76' 77et al.
Murphy68 et al.
09
Lewisoz et al.
Lewis8" et al.
Coffin and Blommer84
8-41
-------
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71. Bils, R.F. and J.C. Romanovsky. Ultrastructural Altera-
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72. Rounds, D.E. and R.F. Bils. Effects of Air Pollutants on
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Med. Assoc. 753 (6): 331-3 35, September 15, 1958.
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79. Wiseley, D.V. et al. The Combined Effect of Repeated
Viral Infection and Exposure to Carcinogenic Aerosols
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8-44
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Chapter 9.
EPIDEMIOLOGICAL APPRAISAL OF PHOTOCHEMICAL OXIDANTS
A. INTRODUCTION
The possibility that photochemical air pol-
lution could be a major health hazard has
been of growing concern. A number of
systematic studies have been conducted in an
attempt to obtain an association between
episodes of high oxidant pollution and general
mortality, acute illness, aggravation of chronic
respiratory disease, impairment of per-
formance, or untoward symptoms such as eye
irritation. The purpose of this chapter is to
review the data and conclusions of these
studies. In some cases, the data have been
reanalyzed. Areas of insufficient knowledge
and the relevance of -the existing data to air
quality criteria are emphasized.
B. ACUTE EFFECTS OF PHOTO-
CHEMICAL OXIDANTS
To identify the acute health effects of
photochemical oxidant pollution, observations
of the same populations or communities are
made during periods of high-level pollution
and during periods of low-level pollution.
These health effects are associated with
short-term pollutant concentrations measured
as 24-hour averages, hourly maxima, or in-
stantaneous peak concentrations.
1. Daily Mortality in Relation to
Variations in Oxidant Levels
a. Mortality Among Residents Age 65
Years and Older
A study of the relationship between daily
concentrations of photochemical oxidants
and daily mortality among residents of Los
Angeles County age 65 years and older was
reported in March 1955, March 1956, and
February 1957.1 The number of deaths per
day was related to 2 indices: daily tem-
perature at the downtown weather bureau,
and oxidant concentrations from August
through November of 1954 and July through
November of 1955. (Table 9-1 and Figure
9-1) Daily mortality clearly exceeded the
average during a heat-wave occurring in late
August and early September of 1955. High
concentrations of photochemical oxidants oc-
curred immediately before, during, and after
the heat-wave. Daily mortality decreased,
however, when the temperatures dropped
while elevated oxidant levels persisted.
Thus the oxidant level did not inde-
pendently affect daily mortality counts. An
inconsistent pattern was observed during
other months when daily mortality was com-
pared with both temperature and oxidant
gradients (Table 9-1). For example, on days
when the maximum temperature fell to be-
tween 70°-79° F, variations in oxidant levels
from low to medium to high showed no
consistent relationship to the average number
of deaths. For the months covered by this
study, therefore, daily mortality among per-
sons age 65 years and older in Los Angeles
County was strongly influenced by a heat
wave, but was not altered consistently by
variations in oxidant concentrations.
b. Mortality and Heat Waves
Since there is a meteorological association
between high temperatures and high oxidant
concentrations in the Los Angeles basin, the
conclusions of the previous paragraph do not
preclude a relationship between increased
mortality and the simultaneous occurrence of
high temperatures and high oxidant concen-
trations. That is, high oxidant concentrations
may augment the mortality effect of high
temperature. The results of a study by Oechsli
9-1
-------
to
Table 9-1. AVERAGE NUMBER OF DEATHS PER DAY DUE TO CARDIAC AND RESPIRATORY CAUSES AMONG RESIDENTS OF
LOS ANGELES COUNTY, AGE 65 AND OLDER, AS RELATED TO TEMPERATURE AND OXIDANT CONCENTRATIONS BY MONTH, 1954-1955'
Concentration,
ppm
August, 1954
Low (00 - .24)
Medium (.25 - .49)
High (.50 +)
September, 1954
Low (00 - .24)
Medium (.25 -.49)
High (.50 +)
October, 1954
Low (00 - .24)
Medium (.25 - .49)
High (.50+)
November, 1954
Low (00 - .24)
Medium (.25 - .49)
High (.50 +)
July, 1955
Low (00 - .24)
Medium (.25 - .49)
High (.50 +)
No Readings
August, 1955
Low (00 - .24)
Medium (.25 - .49)
High (.50 +)
No Readings
September, 1955
Low (00 - .24)
Medium (.25 - .49)
High (.50+)
No Readings
Totals
Number
of days
8
22
1
1
25
4
9
14
8
16
14
4
11
2
14
5
16
4
6
5
13
7
5
Average
number
of deaths
29.9
32.2
32.0
26.0
32.1
33.3
39.4
37.1
36.3
38.6
37.9
35.0
34.8
42.0
37.5
36.8
38.4
37.2
37.8
29.0
61.5
50.3
34.8
50°-59°F
Number
of days
1
Average
number
of deaths
39.0
60°-69° F
Number
of days
1
1
5
4
1
Average
number
of deaths
31.0
43.0
36.0
36.8
33.0
Temperature readings, T^ !
70°-79°F
Number
of days
4
7
1
1
5
6
10
3
4
5
1
5
1
10
3
4
1
4
Average
number
of deaths
28.2
30.1
32.0
26.0
29.6
38.2
36.0
36.7
42.0
34.8
28.0
34.4
42.0
38.7
27.3
30.8
32.0
33.2
80°- 89°F
Number
of days
4
12
16
4
2
2
5
6
5
3
6
1
4
4
16
4
4
1
3
1
Average
number
of deaths
31.5
31.8
35.1
33.3
47.5
39.5
36.0
38.6
41.8
37.3
35.2
42.0
34.5
35.5
38.4
37.2
38.5
30.0
43.7
28.0
90°-99°F
Number
of days
3
4
1
2
1
3
1
Average
number
of deaths
39.0
36.0
37.0
36.5
52.0
40.7
41.0
100° F and above
Number
of days
1
5
2
Average
number
of deaths
42.0
98.8
85.0
-------
and Buechley2 of mortality associated with
three Los Angeles heat-waves-in 1939, 1955,
and 1963-provide information on this mul-
tiple-relationship. Daily mortality during
these heat-waves was compared with daily
mortality occurring immediately before and
after each heat-wave and with mortality dur-
ing the same season in 1947, when no
heat-wave occurred.
Significant increases in the mortality ratio
were observed with increases in temperature
during each of the three heat waves. Above
average deviations were greatest among the
more elderly persons. Of the three incidents,
the one occurring in 1963 is notable for a
considerable diminution of excess mortality,
even though temperatures reached the same
peak levels as in 1939 and 1955. It has been
surmised that the use of air conditioning was
one of several possible reasons for the re-
duction in mortality in 1963. There was no
discernible difference in the magnitude of the
mortality response to heat in 1939 and 1955.
It can be assumed that considerably less
photochemical oxidant pollution accom-
panied the 1939 heat wave than waspresent in
1955, although oxidant was not being mea-
sured in 1939. The comparison of the 1939
and 1955 heat waves suggests, under the
above assumption, that high photochemical
oxidant concentrations do not augment the
mortality effect of high temperatures.
320
300
to
I
I-
<
UJ
Q
LL
o
a:
LU
cfl
5
z
3 10 17 24 31 7 14 21 28 7 14 21 28 2 9 16 23 30 7 14 21 28
-JULY >4* AUG. »4< SEPT. +\* OCT. >f* NOV. »-|
PERIOD, days
Figure 9-1. Comparison of deaths of persons, 65 years of age and over, and
maximum daily temperatures, Los Angeles County, July 1 to November 30,
1955.1
9-3
-------
c. Mortality of Nursing Home Residents
An attempt was made to establish whether
nursing home patients, many of whom were
chronically ill and thought to be unusually
susceptible to atmospheric pollution, ex-
perienced greater mortality on or immediately
after days of high oxidant concentrations.1
Deaths and transfers to hospitals among res-
idents of 16 Los Angeles nursing homes
having a total of 358 beds were recorded for
1954. An unusually large number of patients
appeared to have been transferred to hospitals
following a particularly heavy episode of
smog during 1 week of the study period. A
larger study of the nursing home population
was conducted from July through December
of 1955, during which all such homes in Los
Angeles County containing 25 or more beds
were surveyed. The number of institutions
ranged from 90 to 92, with a total of 3,734 to
3,826 beds. Daily mortality, the corres-
ponding maximum daily temperature, and the
occurrence of smog-alert days with ozone
concentrations of 590 /Jig/m3 (0.30 ppm) or
higher are shown in Figure 9-2. The heat-wave
in late August and early September again
showed a striking effect on mortality; at all
other times, variations in daily mortality did
not appear to be related to the occurrence of
smog-alert days.
d. Two-Community Study
Massey3 et al. compared daily mortality in
two areas of Los Angeles County. These areas
were selected for both similarities in tem-
perature and differences in air pollution lev-
els. Two synthetic communities containing a
combined population of 944,391 persons
were thus formed. The pollutant variables
used in this analysis were the daily maximum
and mean oxidant levels as established using
the KI method, and sulfur dioxide and carbon
monoxide concentrations. The synthetic com-
munities were subdivided into smaller units,
110
100
LU
Q
o
X
o
z
CO
o:
f = DAYS OF OFFICIAL ALERTS,
ozone 0.30 ppm or higher.
20
10
90
80
70
60
CO
LU
o:
Qi
LU
Q.
LU
>-
_i
<
50 ±E
X
40
30
1 5 10 15202530 4 9 14192429 3 81318 2328 3 813 182328 2 7 12 172227 2 7 12 1722 27 31
•JULY »4*— MJG.—»U SEPT. »[«— 3CT.—*4"* NOV- *4* DEC.-
PERIOD, days
Figure 9-2. Comparison of nursing home deaths, maximum daily temperature, and
"-smog alert" days in Los Angeles County, July through December 1955.1
-------
each of which was represented by a single
temperature or air pollution station. The
mean number of daily deaths in the low
pollution area was subtracted from the mean
number of deaths in the high pollution area,
and the differences were examined by cor-
relation and regression analysis with respect
to differences in pollution. No significant
correlations between mortality differences
and differences in pollutant levels were ob-
served.
e. Mortality from Cardiac and
Respiratory Diseases
Hechter and Goldsmith4 analyzed the ef-
fect of pollutant concentrations on average
dailv mortality from cardiac and respiratory
diseases in Los Angeles County for the years
1956 through 1958. Daily mortality, averaged
within each month of the study, fluctuated
between 1.0 and 1.3 per 100,000 population.
These fluctuations were approximately 180
degrees out of phase with fluctuations in
oxidant and temperature values, and ap-
proximately in phase with maximum carbon
monoxide concentrations (Figure 9-3). To
remove the major effect of season of year, the
authors fitted Fourier curves to the data and
found a single cycle of Fourier functions to fit
oxidant and temperature fluctuations in car-
bon monoxide and cardiorespiratory mortali-
ty (Figure 9-4). The residual variations from
X
o
X
o
z
o
5
Z
O
CD
YEAR
YEAR
Figure 9-3. Comparison of maximum concentrations of oxidant and carbon monoxide,
maximum temperature, and daily death rate for cardiac and respiratory causes, Los
Angeles County, 1956-1958.4
9-5
-------
these fitted curves for each of the variables
were presumed to be independent of season.
The relationship between pollution or tem-
perature on 1 day with the value of the same
variable on the successive or following days
was also accounted for in the analysis. When
residuals from the fitted curves were thus
analyzed, no significant correlations between
pollutants and mortality for cardiorespiratory
diseases were found. Neither were there signi-
ficant correlations when a lag of 1 to 4 days
was applied.
Mills5 has attempted to relate cardiorespi-
ratory deaths to the occurrence of smog in
Los Angeles. Although he observed an associa-
tion between oxidant levels and excess deaths,
he failed to take into account seasonal fluctu-
ations of each, thus precluding the compari-
son of this observation with other studies in
this section.
The analysis of mortality data by fitting
them to Fourier curves derived from the same
data may mask a real effect of environmental
factors on mortality. In the absence of a
simultaneous study of a less-polluted com-
parison community, no conclusive statement
can be made regarding the effect of oxidant
levels on community mortality.
/ Discussion
A variety of methods have been used to
examine whether short-term variations in pho-
tochemical oxidant concentrations have been
associated with excess mortality in Los Ange-
les. The results have not demonstrated such
an effect. Studies comparing the mortality
TEMPERATURE
..•--.
\\
^
•
»*
OXIDANT
//
//""^ —
/ \
20
15
10
Z
<
Q
X
O
X
o
o
z
o
u
20
16
12
/ /
//
//
A'"\
CARBON MONOXIDE /-
CARDIAC AND RESPIRATORY
DEATH RATE
1.4
1.3
1.2
1.1
1.0
< O
o; o
— o
n: ^
Q i
Z .
< LJJ
(J ^
<
0.9
0.8
J FMAMJJASONDJ FMAMJJASONDJ FMAMJJASON
-1956-
»l<
-1957-
> H
-1958-
YEAR
9-6
Figure 9-4. Fourier curves fitted to data in Figure 9-34
-------
experience of Los Angeles with that of a
less-polluted community are needed before
firm conclusions can be drawn about the
observed lack of a pollutant-related mortality.
2. Hospital Admissions in Relation to
Oxidant Levels
a. Los Angeles County Hospital
Admissions, 1954
A study of hospital admissions for the
period September through December of 1954
has examined records on admissions to Los
Angeles County Hospital in several cate-
gories,1 namely, admissions for asthma in
children under 10 years of age, for tuber-
culosis, for other respiratory conditions, and
for other causes. Total admissions, the num-
ber of persons with acute conditions in all
units, and the number who died, were tabu-
lated. No significant associations with oxidant
levels were observed. Weekly admissions to an
additional group of hospitals with a total of
2,224 beds were similarly examined. The data
appeared to show some seasonal trend, par-
ticularly for certain diseases of the lung, but
no association between oxidant air pollution
and hospital admissions due to diseases of the
cardiovascular or respiratory systems was ob-
served.
Brant6'7 studied patients with respiratory
or cardiovascular diagnoses who were ad-
mitted to or discharged from Los Angeles
County Hospital between August 8 and De-
cember 25, 1954. Patients were excluded who
were younger than 9 or older than 90 years of
age, as were those who had not resided for at
least 3 years in an area within 8 miles of
downtown Los Angeles. Meteorological data
including temperature and relative humidity
were included in the analysis. Although the
method of selection of patients for the study
was not described, the process of selection
yielded 246 cardiovascular admissions and
122 respiratory admissions. Total oxidant as
measured about a mile from the hospital was
used as an index of air pollution. Multiple
regression analyses were used to relate hos-
pital admissions to atmospheric and meteoro-
logical variables. Calculations included re-
gressions of hospital admissions as late as 4
weeks after the occurrence of a given set of
environmental measurements, and a signifi-
cant correlation between periods of high
oxidant, low relative humidity, and low tem-
perature, and hospital admissions weeks later
for cardiovascular conditions was observed.
Because there is no biologically plausible
explanation for this correlation, the associa-
tion must be considered fortuitous. In con-
trast, there was a negative correlation between
admissions for cardiovascular disease and oxi-
dant levels either on the day of admission or
for 2 weeks prior to admission.
b. Hospital Admissions in the Los Angeles
Metropolitan Area
Based on Blue Cross records, Sterling,8'9 et
al. assembled data from Los Angeles hospitals
for the period of March 17 to October 26,
1961. Diagnoses were grouped according to
"highly relevant," "relevant," and "irrele-
vant" disorders. Classified as "highly rele-
vant" were allergic disorders, inflammatory
diseases of the eye, acute upper respiratory
infections, influenza, and bronchitis. "Rele-
vant" disorders were considered to include
diseases of the heart, rheumatic fever, vascular
diseases, and other diseases of the respiratory
system. All other illnesses were classified as
"irrelevant."
The authors found that the mean number
of admissions varied by day of week. They
were higher in the first-half than in the
second-half of the week. They also observed
(1) oxidant precursors were exceptionally low
on Sundays, (2) both oxidant and ozone
levels were low on Saturdays and Sundays, (3)
nitric oxide was exceptionally low on Wednes-
days. After correcting for the day of the week
with respect to pollutant and admission fre-
quencies, "highly relevant" and "relevant"
illnesses were found to show significant cor-
relations with oxidant levels, carbon monox-
ide, and ozone. "Highly relevant" conditions
were also correlated with oxides of nitrogen
and particulate matter. No significant correla-
tions between hospital admissions and tern-
9-7
-------
perature were found, in contrast to the
findings discussed in section B.I and in Figure
9-3, although only data for March and April
were used. Using the same data, Sterling9 et
al. studied the association of duration of
hospital stay and air pollution. The correla-
tions were not statistically significant.
Because of the limited period of the year
utilized for study, and extremely low correla-
tion coefficients, it is difficult to conclude
that a meaningful relationship has been dem-
onstrated by these studies.
c. Discussion
Studies reviewed in this section have failed
to adequately demonstrate any relationship
between daily hospital admissions and varia-
tions in concentrations of photochemical
oxidants.
3. Aggravation of Respiratory Diseases
by Oxidant Pollution
a. Aggravation of Asthma
As a result of reports by physicians that
asthmatic attacks are frequently associated
with smog periods, Schoettlin and Landau1 °
undertook a study to determine whether such
a phenomenon does take place. Five physi-
cians selected 157 patients, 137 of whom
participated in the study. All resided and
worked in the Pasadena area. Fifty-four of the
patients were younger than 15 years of age.
Most had had asthma for at least 2 years, and
all but 17 had been residents of the Los
Angeles area for 5 or more years. Daily
records of the time of onset and severity of
asthmatic attacks were maintained by the
patients for the period September 3 through
December 9, 1956. Relatively high air pollu-
tion levels occur during these months of the
year. The data were collected weekly. In the
event a subject neglected to submit a report,
the investigators telephoned and requested
one.
The study showed that the peak period for
asthma attacks was between midnight and
6:00 a.m., while the maximum oxidant levels
were recorded between 10:00 a.m. and 4:00
p.m. A delay in response to the inciting agent
9-8
might explain this late period for asthma
attacks. Of the 3,435 attacks reported, less
than 5 percent were spontaneously associated
with smog by the patients, and none of these
were severe. One-third of the attacks spon-
taneously associated with smog were reported
by a single patient. The correlation-coefficient
between the number of attacks per day and
the maximum oxidant reading was 0.37.
Addition of other variables to the analysis did
not significantly alter these results. There was
no significant difference in the average num-
ber of attacks per day for days above the
median maximum oxidant level (0.13 ppm by
the phenolphthalein method) compared with
days below the median. However, there was a
significant increase in the mean number of
attacks on days when daily maximum oxidant
levels exceeded 0.25 ppm by the phenolph-
thalein method, the equivalent of 250 Mg/m3
or 0.13 ppm by the KI method, contrasted
with days when the daily maximum oxidant
level fell below this level. The authors sug-
gested that this may indicate a threshold-level
for oxidants above which there could be a
physiologic response. There was also a signifi-
cant association between attack-rates on days
in which plant damage occurred, with oxidant
concentrations of about 200 jUS/m3 (0.10
ppm) by the KI method, in contrast to days
without plant damage. This effect was most
pronounced for persons who had lived in the
area 10 or more years. The data were exam-
ined further to see whether a small number of
the subjects might be responsible for the
observed correlation. Eight individuals, or 6
percent of the total panel, were identified
whose attacks corresponded most often to
days on which plant damage occurred, but
there was no attribute common to these
individuals. Thus a small portion of people
suffering from asthma appeared to be re-
sponsive to levels of photochemical oxidants
sufficient to cause vegetation damage.
b. Aggravation of Emphysema and
Chronic Bronchitis
Several studies have been conducted to
determine if air pollution aggravates the con-
-------
dition of subjects suffering from chronic
bronchitis and emphysema.
Motley11 et al. reported on the results of
lung function tests on 66 volunteers, 46 of
whom had pulmonary emphysema. Lung
function tests were performed on subjects in
rooms from which the oxidants were removed
by activated charcoal filters. Twenty-one sub-
jects stayed in the filtered rooms for periods
between 2 and 4 hours, 20 subjects between
18 and 20 hours, and 25 subjects between 40
and 90 hours. No accurate measurements of
oxidants were obtained but, during the pe-
riods of the study, oxidant concentrations
ranged from 390 to 1,370 Mg/m3 (0.2 to 0.7
ppm) and oxone from 390 to 1,040 Mg/m3
(0.2 to 0.53 ppm) at monitoring stations
several miles from the chamber. Air was
classified as smoggy when there was a definite
odor of ozone, reduced visibility, eye irrita-
tion, and the prediction of smog by the Los
Angeles Air Pollution Control District. Lung
function measurements were made of vital
capacity, FEV3 0, and maximal breathing
capacity. Residual volume and air distribution
measurements were also recorded. An im-
provement in lung function was observed,
particularly a decrease in the residual lung
volume in emphysematous subjects who re-
mained in the chamber for 40 or more hours
and who entered it on smoggy days. No
significant changes in lung volume measure-
ments were obtained when normal subjects
breathed filtered air. No significant changes
were observed when emphysematous subjects
entered the chamber on non-smoggy days.
Variations in the smoking habits of test
subjects could have significantly influenced
the results, but no information on such
variations was reported.
At Los Angeles County Hospital, Remmers
and Balchum1 2 utilized a room with an air
conditioning system and a filter which could
be used at the discretion of the investigator to
remove photochemical oxidants, ozone, and
nitrogen oxides from ambient air and partially
remove particulate matter. Studies were con-
ducted in September and October of 1964
and from March to November of 1965.
Subjects performed lung function tests one or
more times daily while they lived in the room.
In general, they spent 1 week in the air in the
room without air filtration, and 1 week with
the air filtered. During both weeks, air-
-conditioning was adjusted to maintain a
room temperature of 72° ± 3°F and a relative
humidity of 50 ± 5 percent. A third week was
spent in a room arranged for exposure to
ambient atmosphere. Respiratory function
tests of airway resistance, diffusing capacity,
other pulmonary function tests, blood oxygen
tension, and oxygen consumption during ex-
ercise were performed. Several tests were
repeated while the patients were exercising.
Because of the elaborate nature of the ex-
perimental system, only a small number of
subjects could be studied. Eleven subjects
were cigarette smokers, and one stopped
smoking when he entered the study. Most
subjects had moderate to severe respiratory
impairment from bronchitis or emphysema.
Hence, any impairment of respiratory func-
tion could be interpreted as a fairly serious
deterioration of pulmonary status.
Preliminary examination of the data indi-
cated that airway resistance was affected by
elevated oxidant concentrations when obser-
vations were made over a range of 100 to 450
Mg/m3 (0.05 to 0.23 ppm). Determination of
a threshold level for this effect cannot be
made from these data because of the infre-
quent observations over the entire range of
exposure. The subjects were also exposed to
ambient air containing not only oxidants, but
other substances as well. It is possible that the
observed effects were caused partially by
removal of other pollutants such as aerosols,
particulates, PAN, or aldehydes. Cigarette
smoking also varied and apparently was more
frequent when the ambient air was not being
filtered, thus possibly confounding the re-
sults. Another test which seemed to show
significant changes with air pollution was the
consumption of oxygen during exercise. Al-
terations in rate and depth of breathing could
also have accounted for some of these effects,
9-9
-------
but these possibilities were not investigated.
Further analyses of these data were carried
out for purposes of this report, and the results
are shown in Table 9-2.
In view of the possible influence of ciga-
rette smoking on these test results, data for
cigarette smokers must be interpreted cau-
tiously. The majority of the nonsmokers in
this study did show decreases in airway
resistance corresponding to decreases in oxi-
dant exposure, but observations were far too
infrequent for inferences to be drawn
about a possible threshold level for this effect.
Rokaw and Massey1 3 conducted a study of
the effects of environmental variables on
pulmonary function in a group of 25 patients
in a chronic disease hospital in Los Angeles,
over a period of 18 months. All of the
patients had chronic, nontuberculous, respira-
tory diseases, predominantly pulmonary em-
Table 9-2. CORRELATION OF MORNING AND EARLY AFTERNOON OXIDANT LEVELS WITH OXYGEN CONSUMPTION
AND AIRWAY RESISTANCE OF 15 PATIENTS WITH CHRONIC RESPIRATORY DISEASE 12
Patient's
number
and
smoking
history6
102 S
1" 103 NS
1 104 NS
106 S
[107 S
108 S
110 S
[111 NS
112 S
[~113 NS
|_114 S
[115 S
116 S
Tin s
[ 118 NS
Number of
observations
Oxygen
consump-
tion
11
14
14
17
17
18
14
15
15
12
13
14
14
15
15
..z,,f
Airway
resis-
tance
17
14
14
17
17
18
16
17
15
12
13
14
15
15
15
Maximum
breathing
capacity,
liters/min.
—
88.4
88.4
99.4
69.1
117.7
52.9
181.5
65.3
26.3
96.1
38.6
37.4
Observed correlation coefficients
Oxygen consumption a | Airway resistance15
Resting conditions
a.m. oxidants
.282
.123
-.313
.473
.473
.489
.255
.434
.413
-.107
-.114
.423
.288
-
2.9919
p.m. oxidants
.405
.210
.007
.579
.579
.448
.136
.092
.209
.222
-.158
.290
-.094
.189
.345
2.7619
Exercise conditions
p.m. oxidants
.774
.251
.258
.521
.521
.409
-.172
-.459
-.348
.088
-.120
.130
.751
.456
.138
2.S379
a.m. oxidants
-.379
.717
.638
-.361
-.361
-.378
.431
.251
.339
.034
-.161
.217
.715
_
3.621h
p.m. oxidants
-.313
.567
.641
.146
.146
.656
.124
.354
.433
.006
.058
.557
.460
.609
.453
4.976h
a The first two correlations are with "resting" oxygen consumption, which was measured around 11 a.m.; the third correlation is
with "exercise" oxygen consumption, which was measured around 3 p.m.
b Airway resistance is "resting"; values given are averages of four measurements made throughout the day
c a.m. Oxidant was measured around 9:30 a.m.
dp.m. Oxidant was measured around 1:30 p.m.
e Smoking History: S = smoker, NS = nonsmoker, SS = stopped smoking when study began. [ - Indicates patients were tested
during the same period.
f "z" values were found by converting the individual correlations to t values, using the relationship
*i=ri [(nr2)/ (l-ii2)] % then summing the t values over all patients; the sums have variance
V(S tj) = S [(nj-2) / (nj-4)]. The "z" values shown are the ratio of
2 (t j) / VV2jti) which is approximately N(0,1).
S Significant at the 0.01 level.
h Significant at the 0.001 level.
9-10
-------
physema. Each subject underwent a series of
pulmonary function tests 4 times weekly; in
addition, functional residual capacity by the
helium dilution method was determined
monthly. Air pollution data were obtained
from a station about a quarter of a mile
upwind from the hospital. Statistical methods
of analysis were employed to detect associa-
tion between changes in pulmonary function
and air pollution levels. The results showed a
marked variability in the performance of
pulmonary function tests; the variability was
greater in the group of patients than in
normal subjects. A correlation between per-
formance and ambient carbon monoxide was
observed for some but not all of the subjects;
no such response was observed during major
smog episodes, and no seasonal pattern of
performance for the group was observed.
[This is in contrast to the findings of Mc-
Kerrow,14 who found yearly cycles in venti-
latory function tests in a group of ex-miners
with pneumoconiosis working in a car-assemb-
ly plant in South Wales.] The general level of
oxidant in the hospital area was not as high as
in some parts of the Los Angeles basin; the
mean oxidant was 120 /ig/m3 (0.06 ppm),
with a maximum of 820 Mg/m3 (0.42 ppm). It
is possible that the experiment did not detect
any effect of oxidant on simple respiratory
function tests because; (1) the group was too
ill to respond, (2) fluctuations in the subjects'
disease states or cigarette smoking habits were
the major determinants of test performance,
or (3) the subjects were exposed to a rela-
tively low level of oxidant.
Shoettlin15 studied the long-term effects
of community air pollution, occupational
exposure to air pollution, and smoking among
Armed Forces veterans living in the Domi-
ciliary Unit and Chronic Disease Annex of the
Los Angeles Veterans Administration Center.
Day to day variations in the physical status of
men with chronic respiratory disease were
studied in relation to changes in environ-
mental conditions in the coastal area of the
Los Angeles basin. Two groups of men were
selected. The first group, consisting of 528
veterans who had no positive signs or symp-
toms of respiratory disease, was used as a
control. The second group of 326 men was
selected on the basis of the presence of at
least 2 symptoms of respiratory disease (in-
cluding cough, sputum, shortness of breath,
and wheezing) for 2 or more years, and the
presence of abnormal breathsounds. Men
from these two groups were matched by age
and smoking history, and the resulting pairs
were studied weekly by means of repeated
pulmonary function tests and responses to a
respiratory symptom questionnaire. About 65
percent of the men selected cooperated in the
study. An air pollution monitoring station
was set up at the site, and a companion
program of observing vegetation damage was
established. Analysis of variance showed no
statistically significant effects of air pollution
on respiratory symptoms or functions. The
maximal oxidant values and oxidant precursor
values, however, consistently accounted for
more of the variation in frequency of symp-
toms and clinical signs for the diseased group
than for the control group (Table 9-3). For
example, the maximal oxidant precursor ac-
counted for 30 percent of the variation in
symptoms of the diseased group and 17
Table 9-3. PROPORTION OF VARIATION ASSOCIATED WITH ENVIRONMENTAL FACTORS IN
SYMPTOMS, SIGNS, AND VENTILATORY TESTS IN A DISEASED AND IN A CONTROL GROUP1
Environmental
factors
Mean oxidant
Maximal oxidant
Maximal oxidant precursor
Pollen count
Maximal temperature
Maximal relative humidity
Diseased group
Symptoms
0.11
0.17
0.30
0.02
0.05
0.05
Signs
0.13
0.16
0.17
0.05
0.03
0.05
Puff-
meter
0.04
0.10
0.17
0.05
0.12
0.10
Control group
Symp-
toms
0.08
0.04
0.04
0.07
0.09
0.23
Signs
0.06
0.03
0.07
0.02
0.06
0.08
Puffmeter
0.04
0.06
0.09
0.10
0.19
0.06
9-11
-------
percent of variations in the Puffmeter test,
whereas the proportion of the variation ac-
counted for in the control group was insignifi-
cant.
c. Discussion
A study of 137 patients with asthma
demonstrated a significant increase in the
number of asthma attacks on days when
photochemical oxidant levels exceeded 250
Mg/m3 (0.13 ppm) by the KI method. Using
the information presented in Chapter 3, sec-
tion B.I, the peak value of 250 ng/m3
oxidant might be expected to be associated
with a maximum hourly oxidant concentra-
tion of 100 to 120 Mg/m3 (0.05 to 0.06 ppm),
depending on localized conditions.
studied under usual conditions of ambient
oxidant exposure and then compared in a
clean, filtered room have shown improvement
in ventilatory function. The data are not
adequate for determining the threshold level
at which improved ventilatory function first
occurred. In a study performed an a location
with a mean oxidant concentration of 120
Mg/m3 (0.06 ppm), however, no association
between variations in oxidant concentration
and the performance of ventilatory function
tests by patients with chronic respiratory
disease was demonstrable. In another study,
no statistically significant association was
found between oxidant concentrations and
respiratory symptoms or functions in a se-
lected group of subjects with or without
chronic respiratory disease.
4. Impairment of Performance Associated
with Oxidant Pollution
a. Athletic Performance
Wayne16 et al. have studied the athletic
performance in 21 competitive meets of
student cross-country track runners at San
Marino High School, Los Angeles County,
from 1959 to 1964. Oxidant measurements
for the hour of the race, and 1, 2, and 3 hours
before the race were related to the running
time for each athlete. The effects of oxides of
nitrogen, temperature, relative humidity,
wind velocity, and wind direction were all
considered but did not reveal any relationship
to the running times. A significant relation-
ship was observed between oxidant levels and
the percent of team members whose per-
formance decreased compared to their per-
formance in the immediately previous home
meet, as is shown in Figure 9-5. The correla-
tions between performance and oxidant levels
were quite high but diminished as the interval
between the oxidant measurement and the
time of the meet increased. The authors
speculated as to possible mechanisms for this
association and pointed out that a direct
effect on oxygen utilization could occur or
that there might be detrimental effects of
discomfort from eye and respiratory irrita-
tion. The data provide convincing evidence
that some component of the air which was
measured as oxidant had a causal effect on
team performance. With increasing levels of
oxidant, there was a manifest impairment of
team performance in this study, conducted
LU
(J
•z.
o
LL
o:
Q
UJ
ct:
u
LU
Q
80
60
20
r = 0.945
^•O -1962-1964
r =0.945
0.0 0.10 0.20 0.30
OXIDANT LEVEL 1-hour BEFORE MEET, ppm
Figure 9-5. Relationship between oxidant
level in the hour before an athletic event
and percent of team members with de-
creased performance.16
9-12
-------
over a range of oxidant concentrations from
60 to 590 Mg/m3 (0.03 to 0.30 ppm). No
threshold level for this effect can be deter-
mined since the possibility always exists that
a team would always have a certain number of
individuals who would fail to improve their
previous performance.
b. Automobile Accidents
A study1 7 of the association of automobile
accidents with days of elevated oxidant levels
was performed because of the possibility that
oxidant pollution may impair performance
either directly, by interfering with oxygen
transport or utilization, or indirectly, by eye
discomfort and respiratory irritation. Ury
applied a sign-test and a non-parametric cor-
relation analysis to data for each daylight
hour of each weekday in the 3-month period
from August through October, for both 1963
and 1965. There was a total of 90 sets of data
for testing, covering 9 hours daily and 5 days
weekly. The sign-test results of each set were
obtained by taking successive pairs of weeks
(first week compared with second; third week
compared with fourth, etc.) and scoring a plus
(+) if the week with the higher oxidant had
more accidents for that set and a minus (-) if
it had fewer, and awarding a tie if the
accident frequency or the oxidant levels were
equal (Table 9-4). No particular pattern was
shown by hours of the day, but a pattern did
appear based on the day of the week.
Table 94. SIGN-TEST DATA FOR TESTING THE
ASSOCIATION OF OXIDANT LEVELS WITH ACCIDENTS,
LOS ANGELES, AUGUST THROUGH OCTOBER,
1963 AND 196517
Weekday
Monday
Tuesday
Wednesday
Thursday
Friday
Total
Total
Year
1963
1965
1963
1965
1963
1965
1963
1965
1963
1965
1963
1965
Plus
17
21
25
25
23
24
29
27
24
25
118
122
Minus
23
21
14
21
18
21
13
19
25
21
93
103
Tie
5
8
6
6
2
9
8
6
5
6
26
35
Total 24U lyb 01
The data from this study indicate a sta-
tistically significant relationship between
oxidant levels and automobile accidents. The
method of analysis employed in the study
does not lend itself to the determination of a
threshold level for this effect. Similar results
were obtained with the non-parametric cor-
relation test. Carbon monoxide, oxides of
nitrogen, or particulates, which would also
have been relatively increased during the
periods when oxidant was elevated, could also
have contributed to the observed results.
Furthermore, increased traffic density at cer-
tain times may have caused increases in both
oxidant levels and accident rates. Thus, addi-
tional statistical analyses are indicated.
c. Ventilatory Performance
The ventilatory performance, measured by
the Wright Peak Flow Meter, of two groups of
elementary schoolchildren living in the Los
Angeles basin was assessed twice monthly for
11 months by McMillan18 et al. One group of
50 children resided in an area exposed to
seasonally high photochemical oxidant con-
centrations. The other group of 28 children
lived in a less polluted area. During the 11
months of the study, no correlations were
found between acute changes in photo-
chemical oxidant pollution and ventilatory
performance. Contrary to expectation, per-
sistently higher ventilatory performance re-
sults were obtained from the children residing
in the more polluted of the two communities.
Several important differences existed, how-
ever, between these two groups of children.
The incidence of upper respiratory tract
illness was reported to be three times greater
in the children of the less polluted com-
munity, in which lower ventilatory per-
formance was measured. A significant ethnic
difference was also present; the majority of
children in the less polluted community were
from a single ethnic group, whereas the other
group of children were ethnically hetero-
geneous. Thus the expected impairment of
photochemical oxidant pollution on venti-
latory performance was not found either
because the group differences other than air
9-13
-------
pollution exposure had a ventilatory per-
formance effect opposite to that of oxidant
pollution, or because differences in oxidant
exposure of the magnitude found in this
study produced no functional impairment. In
either case, variations in photochemical oxi-
dant pollution, from daily averages of 100 to
550 Mg/m3 (0.05 to 0.28 ppm), had no
demonstrable effect on the ventilatory
performance of the 50 schoolchildren living in
the more polluted of the two communities.
d. Discussion
In a study of school athletic meets, it was
shown that team performance decreased as
hourly oxidant concentrations increased over
the range of 60 to 590 Mg/m3 (0.03 to 0.30
ppm). It has also been shown that there were
significantly more automobile accidents on
days of high oxidant concentration. A mini-
mum threshold level for the oxidant effect on
athletic performance or accident frequency
cannot be determined from the data available.
No acute or chronic effects on ventilatory
performance of elementary schoolchildren
were found in a study conducted during an 11
month period in Los Angeles basin when daily
average photochemical oxidant concentra-
tions varied from 100 to 550 Mg/m3 (0.05 to
0.28 ppm).
5. Eye Irritation in Relation
to Variations in Oxidant Levels
a. Panel Studies
A variety of individuals in various parts of
Los Angeles have been studied to determine
the occasions and the types of pollutants
responsible for eye irritation, one of the most
frequently reported symptoms associated
with exposure to oxidant pollution. The first
set of studies was conducted by the Air
Pollution Foundation in 1954.1 9
During the first period observers were
asked to report eye irritation on Tuesdays and
Fridays. This was later changed to just those
days for which eye-irritating levels of pollu-
tion were predicted. In general, the observers
were office and factory workers; one of the
panels consisted of a group of staff members
9-14
of the California Institute of Technology. The
eye irritation data were compared with in-
stantaneous values of oxidant concentrations
as measured by potassium iodide recorder.
The data are shown in Figures 9-6 and 9-7
and in Tables 9-5 and 9-6. The "expert" panel
(experienced scientists) and the other panel
did not significantly differ in the correlations
of eye irritation with oxidants, carbon
monoxide, particulates, and aldehydes. Dur-
ing the second period, August through No-
vember of 1955, similar panels observed eye
irritation effects during each day of the work
week. In this study maximum oxidant con-
centrations were compared with reported eye
irritation effects.
From the data provided by the Air Pollu-
tion Foundation studies, linear mathematical
relationships between maximum oxidant val-
ues and mean maximum eye irritation values
were derived. The data from these studies
demonstrated increasing eye irritation with
increasing concentrations of oxidant pollution
over the range of instantaneous values from
100 to 880 Mg/m3 (0.05 to 0.45 ppm),
although no clearly demarcated threshold
level for this effect is apparent (See Figure
9-6).
Other studies on eye irritation have been
performed, including one in which a panel of
Table 9-5. CORRELATION OF EYE IRRITATION WITH
SIMULTANEOUS OXIDANT CONCENTRATIONS, IN
ORDER OF DECREASING EYE IRRITATION SCORE,
FOR A NUMBER OF STATIONS IN THE
LOS ANGELES AREA 19
Station
5
8
4L
2
3
4E
11
Number
of daily
observa-
tions
25
29
24
30
67
66
344
Variance,
D (or i2)
0.88
0.68
0.76
0.06
0.56
0.65
0.18
Average
eye
irritation
score
26.2
22.0
21.9
21.3
18.2
13.0
18.8
Average
oxidant
concentra-
tion, ppm
0.13
0.10
0.21
0.11
0.15
0.17
0.14
-------
40
30
m
o:
UJ 20
Qi
o
(J
10
x'. "**"
STATION 3
STATION 4E
STATION 4L
STATION 5
STATION 8
ALL STATIONS
10
20 30
OXIDANT CONCENTRATION, pphm
40
50
Figure 9-6. Regression curves relating eye irritation and simultaneous oxidant concentrations
from a number of stations in the Los Angeles area."19
40
30
o
u
10
10 20 30 40 50 60 70
.MAXIMUM OXIDANT CONCENTRATION, pphm
80
90
Figure 9-7. Variation of mean maximum eye irritation, as judged by a panel of ".experts"
with maximum oxidant concentrations, Pasadena, August-November, 1955.
9-15
-------
Table 9-6. CORRELATION AS JUDGED BY A PANEL OF "EXPERTS" BETWEEN EYE
IRRITATION AND SIMULTANEOUS OTHER VARIABLES19
Variables
Oxidant
NOX
CO
Hydrocarbons
Visibility
Particulates
Aldehydes
Variance,
Dorr2
0.65
0.07
0.53
0.39
0.17
0.53
0.48
Average value of
variable, ppm
unless otherwise
noted
0.17
0.20
0.27
0.17
1.2 miles
21.1 Coh units
0.19
Average eye
irritation
score
13.0
13.1
14.2
14.0
13.3
13.7
14.0
Number of
observations
66
51
47
53
56
26
38
employees of the Los Angeles Air Pollution
Control District was queried during the period
1955-58.20 A group of environmental sanita-
tion workers in the San Francisco Bay Area
was also studied during the same period.
Neither of these panels reported anything
other than a tendency to experience in-
creasing occurrence of eye irritation with
increasing oxidant levels. As in all such
studies, there were some individuals who
reported eye irritation even when there was
no oxidant present.
b. Student Nurse Study
Hammer2 l et al. reported on respiratory
and eye symptoms among two groups of
student nurses studied during a 24-day period
from October 29 through November 25,
1962, in Santa Barbara and Los Angeles. In
general, the symptoms were more frequent
among the Los Angeles students than among
those in Santa Barbara. The choice of period
for study was intended to obviate the effect
of season or of major respiratory and in-
fectious disease. The relationships between
the mean frequency of symptom by day as
measured by eye irritation, coughing, and
sneezing, and the daily maximum oxidant
level is shown for the Los Angeles students in
Figure 9-8. Unfortunately, a complete set of
oxidant measurements was not available. This
accounts for the gap in the distribution
shown. It is of interest that on 1 day in which
an oxidant level of 450 jug/m3 (0.23 ppm)
was observed in Santa Barbara, no unusual
symptom frequency was reported by the
students. Data plotted in Figure 9-8 again
show a relationship between increasing eye
irritation and maximum daily photochemical
oxidant concentrations over the range of 200
to SSO/xg/m3 (0.10 to 0.55 ppm).
c. Evaluation of Filters for Removing Eye
Irritants from Polluted Air
A study was conducted to evaluate the
sensory effectiveness of air-filter media for
removing eye irritants from polluted air in
downtown Los Angeles.2 2 >2 3 Eye irritation
in two groups of 20 female telephone com-
pany employees, similar with respect to age
and job characteristics and employed in iden-
tical adjacent rooms, was evaluated each
work-day (123 study days) from May to
November of 1956. Active and dummy filter
units were switched periodically between the
two rooms so that the groups were alternately
exposed to test and control conditions. The
sensory response of the subjects was measured
daily at 11:00 a.m. by means of a question-
naire; simultaneous measurements of oxi-
dants, particulate matter, and nitrogen diox-
ide were obtained within each of the two
rooms and immediately outside the building.
9-16
-------
o
LL.
o
u
Q
UJ
I
O
O
(J
o
X
UJ
N
UJ
UJ
DAILY MEAN FREQUENCY OF SYMPTOM
DAILY MAXIMUM OXIDANT LEVEL
8 10 12 14 16 18 20 22 24
10 —
DAY OF MONTH
Figure 9-8. Relationship between oxidant concentrations and selected symptoms in
Los Angeles, October 29 through November 25, 1962.21
9-17
-------
The differences in eye irritation between
the activated-carbon-filtered and non-filtered
test situations were in all cases highly signifi-
cant (Table 9-7). A statistically significant
correlation between eye irritation and oxidant
concentrations occurred in the non-filtered
room (Table 9-8). The scatter diagram of
results (see Figure 9-9) suggests an eye irrita-
tion threshold' as the concentration of oxi-
dants exceeded 200 jug/m3 (0.10 ppm). The
index of eye irritation for the study groups
increased progressively as oxidant concentra-
tions exceeded the 200 Mg/m3 (0.10 ppm)
level.
Nitrogen dioxide concentrations were re-
duced by the activated-carbon filters during
their early use but, after a period of time,
nitrogen dioxide concentrations in the filtered
atmosphere increased. No significant correla-
tions between eye irritation and nitrogen
dioxide levels were observed, nor were signifi-
cant correlations found between eye irritation
and concentrations of particulate matter.
d. Photochemical Oxidant and Eye Irritation
in Locations Other Than California
Oxidant measurements at levels likely to be
associated with eye irritation have been re-
Table 9-7. EFFECT OF FILTER UPON SENSORY IRRITATION AND CHEMICAL MEASUREMENTS
22
Test condition
0.0323 Activated carbon filter
Mean, non-filtered room
Mean, filtered room
Difference between means
Probability that the difference
could have occurred by chance
0.016 Activated carbon filter
Mean, non-filtered room
Mean, filtered room
Difference between means
Probability that the difference
could have occurred by chance
0.0075 Activated carbon filter
Mean, non-filtered room
Mean, filtered room
Difference between means
Probability that the difference
could have occurred by chance
0.0030 Activated carbon filter
Mean, non-filtered room
Mean, filtered room
Difference between means
Probability that the difference
could have occurred by chance
Particulate filter
Mean, non-filtered room
Mean, filtered room
Difference between means
Probability that the difference
could have occurred by chance
Eye
irritation
index
1.99
1.01
0.98
<0.01
2.95
1.41
1.54
<0.01
5.45
2.35
3.10
<0.05
2.35
1.19
1.16
<0.01
2.13
1.91
0.22
c
Oxidants,
pphmb
9.8
0.49
9.4
«0.01
8.4
1.8
6.7
«0.01
13.9
4.9
9.0
<0.01
7.3
3.6
3.7
<0.01
5.7
3.4
2.3
<0.01
NO2,
pphm
1.5
0.41
1.1
«0.01
3.4
1.6
1.8
«0.01
2.7
5.7
3.0
c
4.7
4.9
0.2
c
6.3
5.5
0.8
<0.02
a Refers to air detention time in seconds
b Measured by the KI method.
c
Difference not significant.
9-18
-------
ported from a number of other cities (Chapter
3). Circumstantial evidence of increased eye
irritation has been reported in Washington,
D.C., Denver, New York City, and St. Louis.
An epidemiologic study of eye irritation was
carried out by McCarroll2 4 et al. on a
population living in midtown Manhattan. The
investigators established a system of weekly
health reports by families, based on the
presence or absence of certain symptoms. In
October 1963, there were substantial in-
creases in the frequency of new reports of eye
irritation (increasing from about 2 to nearly 5
percent of the population). Oxidant measure-
ments, made at some distance away, had
increased during the period under study.
Unfortunately, clear conclusions from these
data cannot be drawn; there were high levels
of sulfur oxide pollution, of particulate pol-
lution, and of carbon monoxide. It is quite
possible that eye irritation symptoms in New
York City result from mixed pollution of
both the oxidizing and reducing type.
e. Discussion
From these data, it can be only concluded
that eye irritation in relation to increased
"SEVERE" IRRITATION
I = 0.577 0K| - 3.23
MODERATE" IRRITATION
BARELY NOTICEABLE" IRRITATION
15 20 25
OXIDANT CONCENTRATION, pphm
Figure 9-9. Mean index of eye irritation versus oxidant concentration.22
9-19
-------
levels of air pollution can occur elsewhere
than in California. It is of great importance
that this impression is documented and quan-
tified by additional panel studies.
Several studies in California have shown
that the incidence of eye irritation increases
progressively when the ambient oxidant levels
exceed 200 Mg/m3 (0.10 ppm). Using the
information presented in Chapter 3, section B.
1, the instantaneous value of 200 MS/m3 (0.10
ppm) oxidant, which is related to eye irrita-
tion, might be expected to be associated with
a maximum hourly average oxidant concen-
tration of 50 to 100 Mg/m3 (0.025 to 0.50
ppm), depending on localized conditions. Eye
irritation in a group of subjects in downtown
Los Angeles was diminished significantly in a
room with an activated-carbon air-filter when
compared simultaneously with results ob-
tained in a non-filtered room.
When interpreting implied relationships as-
sociating eye irritation and ambient oxidant
levels, care must be exercised in conclusions
regarding cause and effect. Experimental stud-
ies have shown that ozone, the principal
contributer to ambient oxidant levels, is not
an eye irritant, as discussed in Chapter 8,
Section E. Peroxyacyl nitrates have been
shown to be powerful eye irritants; even more
irritating is peroxybenzoyl nitrate. Formal-
dehyde and acrolein, also products of the
photochemical system, have been shown to
produce eye irritation. A postulated explana-
tion for the relationship between ambient
oxidant levels and eye irritation is that "oxi-
dant" is a measure of the photochemical
activity which produces the aforementioned
eye irritants.
C. CHRONIC EFFECTS OF
PHOTOCHEMICAL OXIDANTS
To define the chronic effects of prolonged
exposure to photochemical oxidant pollution,
investigators have contrasted health character-
istics of populations living in clean and
polluted communities. Results from these
studies must be interpreted with caution, for
the populations of two communities are often
different in many respects other than air
pollution exposure. In carefully designed
epidemiologic studies, the principal deter-
minants of the disease condition being in-
vestigated are identified, and population
samples from each study area are matched on
these determinants. Thus, information on
socio-economic status, climate, cigarette
Table 9-8. PEARSON PRODUCT-MOMENT CORRELATION COEFFICIENTS BETWEEN EYE
IRRITATION AND ENVIRONMENTAL FACTORS IN A NONFILTERED
ROOM22
Irritation
Irritation
Irritation
Irritation
Irritation
Irritation
Temperature
Temperature
vs
vs
vs
vs
vs
vs
vs
vs
Oxidants concentration, by
Phenolphtalein method
Oxidants concentration, by
KI method
NO2 concentrations
Particulate
Temperature
Relative Humidity
Relative Humidity
Oxidants concentration, by
0.81
0.81
0.05
0.15
0.49
-0.24
-0.38
0.29
Oxidants concentration,
by Phenolphtalein
method
KI method
Oxidants concentration, by
KI method
0.88
NO2 concentrations
Oxidants concentration, by
KI method
-0.15
9-20
-------
smoking habits, and occupation must usually
be obtained in two-community air pollution
studies, and the similarity in these character-
istics of the study population must be docu-
mented. When differences other than air
pollution exposure -are present in the study
areas, demonstration of the same air pollu-
tion—health effect association in studies of
other communities is usually required before
the association can be firmly accepted.
In general, epidemiologic identification of
the chronic effects of air pollution requires
replicated studies of large, well-defined popu-
lations over relatively long periods of times by
competent investigators producing consistent
results. These requirements are not ade-
quately met in this section. Although the
results of the reported studies are therefore
only suggestive, they are an essential part of
air quality criteria because they can caution
the public about hazardous substances in the
atmosphere. To prove or disprove the ex-
istence of a long-term effect may require an
excessively long or hazardous period of ex-
posure and measurement. Studies which
strongly suggest that a pollutant may be a
health hazard are sufficient to warrant pre-
ventive action until such time as the pol-
lutant—health effect association is convincing-
ly proved or disproved.
1. Mortality in Areas of High and
Low Oxidant Pollution
a. Lung Cancer Mortality
It is known that active chemical car-
cinogens are found in polluted atmospheres2 s
and that ozone, a principal component of
photochemical oxidant pollution, has radio-
mimetic properties. Beginning in 1957, a
prospective study of lung cancer among
69,160 members of the California Depart-
ment of the American Legion was under-
taken. This represented between 50 and 60
percent of the membership mailing list of
eligible individuals. This population under-
represents those with chronic illness of long
duration, since they may not have been
eligible for military service; it probably over-
represents those who are cigarette smokers.
The cooperating subjects reported, by postal
questionnaire, their residence, occupation,
and smoking histories. It thus became possible
to carry out a reasonably economical, longi-
tudinal study and to contrast, according to
lung cancer experience, short-term with long-
term residents of the major metropolitan
areas of California. Buell26 et al. have re-
ported on the first 5 years of followup of this
population. Identifying data for each indi-
vidual were maintained on a roster against
which were checked the death certificates for
the 5-year period 1958 to 1963 from the
California Department of Public Health. Data
for mortality from other chronic lung condi-
tions were also available. A total of 336,571
man-years of observation were included in the
report.
As is shown in Table 9-9, long-term resi-
dents of Los Angeles County have slightly
lower age-smoking adjusted lung cancer rates
than residents of the San Francisco Bay area
counties and San Diego County. These urban
groups have higher rates than the population
residing in the rest of the state. The relative
risk of lung cancer for heavy smokers, or
more than one pack a day, is greater in Los
Angeles County than in other areas of Cali-
fornia (Table 9-10). For non-smokers, the rate
in the two metropolitan groups is substan-
tially greater than in the rest of the state. The
San Francisco—San Diego rates, however, are
higher than in Los Angeles. The duration of
exposure necessary to induce lung cancer
might possibly exceed the duration of obser-
vation for these populations. Hence, it ap-
pears worthwhile to continue the observation.
From these data, it is not possible to
demonstrate any effect of oxidant pollution
on lung cancer mortality. In view of the
radiomimetic properties of ozone reported in
the previous chapter, the possibility of a
carcinogenic effect by photochemical oxi-
dants must be studied in greater depth.
9-21
-------
b. Chronic Respiratory Disease Mortality
Mortality rates for other chronic respira-
tory diseases as reported in the above Ameri-
can Legion Study2 6 were somewhat higher in
Los Angeles than in San Francisco and San
Diego Counties, particularly among persons
resident for 10 or more years in their respec-
tive counties (Table 9-11). Studies by Winkle-
stein2 7 '2 8 et al., however, have demonstrated
the strong effect of socioeconomic level on
chronic respiratory disease mortality. For this
reason, the reported relationship between
chronic respiratory disease mortality and area
of residence in California should be con-
sidered as tenuous until the possible effect
of differences in socioeconomic level among
Table 9-9. TOTAL LUNG CANCER MORTALITY IN AN AMERICAN LEGION STUDY
POPULATION, CALIFORNIA, 1958-1962
26
Age-adjusted*3
Age-smoking
adjusted
Resident0
At least 10 yr
Less than 10 yr
Unknown
Los Angeles
County
Mortality
rate2
95.9
95.4
96.6
76.7
123.4
Total
deaths
n/a
n/a
79
27
12
San Francisco
Bay Area and
San Diego Counties
Mortality
rate3
104.5
102.0
106.3
69.1
215.3
Total
deaths
n/a
n/a
58
13
10
All other
Calif, counties
Mortality
rate3
75.3
75.5
79.9
68.5
65.2
TotaT
deaths
n/a
n/a
69
30
6
Deaths per 100,000 man-years.
Age-adjusted by the direct method to the total study population.
Age and smoking adjusted.
Table 9-10. LUNG CANCER DEATHS AND RELATIVE RISKS PER 100,000 MAN-YEARS
OF AN AMERICAN LEGION STUDY POPULATION, BY EXTENT OF CIGARETTE SMOKING
AND RESIDENCE, CALIFORNIA, 1958-196226
Cigarette smoking
lifetime history3
None
Less than one pack
About one pack
More than one pack
Los Angeles
County
Rate
28.1
63.6
126.0
241.3
More than one pack
R i ti n • • " ft
none
Relative
risk
2.5
5.7
11.3
21.5
S.F. Bay Area and
San Diego Counties
Rate
43.9
77.1
134.5
226.0
Relative
risk
3.9
6.9
12.0
20.2
All other
counties'1
Rate
11.2
61.0
124.9
137.5
Relative
risk
1.0
5.4
11.2
12.3
-6 5.1 12.3
a Age-adjusted by the direct method to the total study population.
Nonsmokers in all other counties taken as unit risk.
9-22
-------
Table 9-11. TOTAL CHRONIC RESPIRATORY DISEASE MORTALITY IN AN AMERICAN
LEGION STUDY POPULATION, CALIFORNIA, 1958-1962a
Residency
Resident 10 yrs.
Resident less than 10 yrs.
Unknown
TOTAL
Los Angeles County
Mortality
rateb
38.4
41.2
139.1
46.7
Total
deaths
31
14
12
57
San Francisco Bay
Area and San Diego
Counties
Mortality
rateb
28.3
45.6
59.8
34.0
Total
deaths
15
8
3
26
All other
Counties
Mortality
rateb
45.6
41.3
39.7
44.4
Total
deaths
40
17
4
61
a Age and smoking adjusted by the direct method to the total study population.
b Per 100,000 man-years.
these study areas is documented or ruled out.
The data clearly should be substantiated by
studies in depth, considering these and other
variables.
c. Discussion
No obvious effect of prolonged exposure to
photochemical oxidants on lung cancer mor-
tality rates was evident. A relationship be-
tween chronic respiratory disease mortality
and photochemical oxidant pollution was
suggested in an isolated study in which data
on other important variables were not ob-
tained. A considerable amount of further
epidemiologic study is needed to test this
association.
2. General Morbidity in Areas of
High and Low Oxidant Pollution
a. State of California Health Survey
In 1954, weekly studies were initiated to
estimate the total morbidity among the general
population of California throughout the
year.1 In addition, the population aged 65
years and over was studied separately. As
shown in Figures 9-10 and 9-11, a significant
association of morbidity with periods of high
air pollution within Los Angeles County was
lacking, even when selected conditions (colds,
asthma, hay fever, and respiratory conditions)
were considered. The data in Figure 9-10,
however, show that the incidence of illness
and injury is consistently greater for the
population age 65 years and older in Los
Angeles than in the remainder of California.
The average weekly incidence was about 7
percent for the non-Los Angeles population
and about 10.4 percent for the Los Angeles
population, approximately 50 percent greater.
These data are only suggestive of an air
pollution effect, since differences in popula-
tion density, race, socioeconomic level and
other important factors are known to exist
between Los Angeles and the remainder of
California.
A general health survey was again under-
taken in 1956, with one goal being the
evaluation of photochemical air pollution in
Los Angeles, in the San Francisco Bay Area,
and in the rest of the state.2 9 Because of the
widespread public interest in air pollution,
special precautions were taken to emphasize
that this study was undertaken as a general
health survey. Special efforts were made to
prevent the household interviewers from sug-
gesting the air pollution objective of the study
to the subject. The study was designed to
explore the following four questions:
1. How extensive is the air pollution
problem in Los Angeles in relation to
the rest of the state?
2. Does air pollution affect a few
people much of the time and many
people occasionally?
9-23
-------
3. Is air pollution a serious source of
discomfort?
4 Does air pollution cause dissatisfac-
tion with living conditions in residen-
tial communities or in places of
employment?
A probability sample of 3,545 households
was selected as representative of all the people
in the state, in the ratio of 1 to 1,055. The
only populations not included were those in
institutions and service camps. Interviewing
took place during May and June of 1956 on
the basis of a sample designed by the United
States Census Bureau. In each household
sampled, one adult was randomly chosen and
predesignated for a personal interview. These
sub-samples were appropriately weighted.
From the survey data presented in Table
9-12, it can be seen that asthma, cough, and
nose and throat complaints were somewhat
more frequent in Los Angeles, Orange, and
San Diego Counties than in the San Francisco
Bay area counties or the rest of the state.
Differences, though statistically significant,
were small. Bronchitis was reported by an
equal proportion of sampled persons in the
Los Angeles area and in the rest of the state.
Sinus conditions and hay fever were most
common in the rest of the state. Those
persons who admitted to suffering from
chronic conditions during the previous year
were asked whether they felt worse on some
days and, if so, why. The interviewers made
no mention of smog or air pollution; the
answers which referred to air pollution were
considered spontaneous. In Figure 9-12, the
responses obtained from residents of Los
Angeles County and the San Francisco Bay
area are compared. The proportion of the
population who attributed a worsening of
50
o
CO
LLJ
Q.
OL
LJJ
CL
30
LOS ANGELES COUNTY
CALIFORNIA LESS
LOS ANGELES COUNTY
HIGH SMOG PERIODS
WEEK ENDING
Figure 9-10. Relationship of high smog periods to incidence of illness and injury,
persons 65 years and over, August 2-November 28, 1954.1
9-24
-------
CO
Z
o
ts>
Qi
a:
LLI
Q.
LU
i-
<
LOS ANGELES COUNTY
CALIFORNIA LESS
LOS ANGELES COUNTY
WEEK ENDING
Figure 9-11. Relationship of high smog periods to incidence of selected conditions
for persons of all ages, August 2-November 28, 1954.1
Table 9-12. SELECTED RESPIRATORY CONDITIONS REPORTED BY GENERAL POPULATION SAMPLE,
CALIFORNIA, MAY 1956
29
Conditions
reported
Bronchitis
Asthma
Cough
Sinus
Hay fever
Nose complaints
Throat complaints
Number of persons
interviewed1-
California
Frequency
309
188
1,341
1,202
695
751
848
6,939
Percent"
4
3
19
17
10
11
12
100
Los Angeles, Orange, and
San Diego Counties
Frequency
156
104
746
576
265
445
505
3,450
Percent
5
3
22
17
8
13
15
100
San Francisco Bay
Area Counties*
Frequency
71
45
323
302
221
186
192
1,846
Percent
4
2
17
16
12
10
10
100
Rest of State
Frequency
82
39
272
324
209
120
151
1,643
Percent
5
2
17
20
13
7
9
100
aSan Francisco, Alameda, Contra Costa, San Mateo, Santa Clara, Marin, Napa, Solano, and Sonoma Counties.
''Percentages will not add to 100 due to reports of multiple conditions or of no conditions.
general sample of 6,939 persons was drawn from the State's civilian, non-institutional population, age 18 years or older.
9-25
-------
WORSENING EFFECTS, percent
AIR POLLUTION
CONDITION
ASTHMA
NOSE
COMPLAINTS
THROAT
COMPLAINTS
SINUS TROUBLE
HAYFEVER
BRONCHITIS
51
50
1
44
I
41
30
22
1
OTHER FACTORS°'b
49
fiSSS^-Jiysi^^
50
56
59
70
78
LOS ANGELES
SAN FRANCISCO BAY AREA
alncludes the "don't know" responses.
Includes specific foods, overeating, working
too hard, not getting enough sleep, emotional
upsets, smoking, and presence of other con-
ditions.
Figure 9-12. Air pollution responses for
selected conditions obtained from volun-
teers in Los Angeles and San Francisco
Bay areas.3U
their condition to air pollution was much
greater in Los Angeles than in San Francisco.
The respondents who reported either
chronic or repeated attacks of bronchitis,
asthma, or cough in the 1956 health survey
were selected for a longitudinal study.30 To
eliminate youthful allergic asthmatics, the
panel was limited to those age 30 years and
older. They were reinterviewed on four occa-
sions, twice in 1957, once in 1958, and once
in 1959. Data were obtained as to the relative
severity and the consequences of illness from
respiratory conditions. No patterns of mor-
tality of changes in morbidity were discovered
which would indicate significant differences
in diverse areas of the state and hence might
be attributed to exposure to air pollution.
b. Chronic Respiratory Disease Survey
of Telephone 'Workers
In comparative studies on outdoor tele-
phone workers, Deane31 et al., used stand-
ardized respiratory survey techniques to study
a group of West Coast workmen whose
general occupation, medical status, and social
status were similar to workmen on the East
Coast and in the United Kingdom. In the
older group (age 50-59 years), respiratory
symptoms were more frequent in the Los
Angeles than in the San Francisco population.
Persistent cough and phlegm in the 50-59 year
age-group were reported by 31.4 percent of
the group in Los Angeles, compared with 16.3
percent in San Francisco. The differences
between these two groups could not be
accounted for by differences in smoking
habits. There were not important differences
in the results of pulmonary function tests. In
the younger group (age 40-49 years), the
frequencies of various respiratory symptoms
were not consistently different between Los
Angeles and San Francisco residents.
Questions regarding eye irritation were also
included. The 40-49 age group in San
Francisco reported eye irritation about 10
percent of the time; the 50-59 age group,
about 4 percent. The comparable figures for
Los Angeles were 30 percent and 29 percent
respectively. Perhaps more important is the
fact that over 50 percent of those in both age
groups in San Francisco had never ex-
perienced eye irritation, while the correspond-
ing figure for Los Angeles was less than 10
percent.
9-26
-------
c. Discussion
Several surveys suggest a higher incidence
of both chronic respiratory disease symptoms
and of other symptoms, including asthma and
nose and throat complaints, among residents
of Los Angeles than in other areas of Cali-
fornia, including the San Francisco Bay area.
3. Effects of Photochemical Oxidant Pollu-
tion on Community Satisfaction
a. State of California General Health Survey
At the end of the general health survey
undertaken in California in 1956 and pre-
viously described,2 9 direct questions con-
cerning the effects of air pollution were
asked. Seventy-five percent of the surveyed
population from Los Angeles County was
"bothered" by air pollution, in contrast to 24
percent in the San Francisco Bay area, and 22
percent in the rest of the state. These con-
trasts were also reported for the working
populations from these areas (Table 9-13). Of
the total number who were bothered by air
pollution, 17 percent in Los Angeles con-
sidered moving because of it, in contrast to 4
percent in San Francisco. Of the same total
number, 9 percent in Los Angeles considered
changing jobs because of air pollution, in
contrast to 3 percent in San Francisco (Table
9-14). About 20 percent of the state's resi-
dents who had moved out of an air-polluted
area said the pollution had some influence on
their decision to move; 4 percent gave air
pollution as their sole reason for moving.
Among those who had moved from California
communities because of air pollution, 75
percent had moved out of Los Angeles
County, 8 percent had moved out of the San
Francisco Bay area, and 17 percent had
moved out of other areas of the state. The
reasons given for all of these moves are listed
in Table 9-15. Air pollution was given as the
Table 9-13. PERCENT OF SURVEY RESPONSES OF GENERAL AND WORKING POPULATIONS "BOTHERED"
BY AIR POLLUTION, BY MAJOR GEOGRAPHIC AREAS IN CALIFORNIA, MAY 1956
29
Responses
General population sample
Not bothered by air pollution
Bothered by air pollution
Either at home or work
Both at home and at work
At home only
At work only
Total at home
Total at work
Working Population Sample
Not bothered by air pollution
Bothered by air pollution
Either at home or work
Both at home and at work
At home only
At work only
Total at home
Total at work
California
6,939
Los Angeles
County
2,892
San Francisco
Bay area
1,846
Rest of State
2,210
Percent*
55
45
14
24
7
38
21
3,732
24
75
27
39
8
66
35
1,577
76
24
4
14
6
18
10
1,028
78
22
4
13
5
17
9
1,127
Percent2
51
49
25
12
12
37
38
20
80
49
16
15
66
65
71
29
7
11
11
18
18
73
27
9
8
10
17
18
aPercents are rounded independently.
9-27
-------
Table 9-14. PERCENT OF SURVEY RESPONSES OF GENERAL AND WORKING POPULATIONS,
"BOTHERED" BY AIR POLLUTION, WHO HAVE CONSIDERED MOVING OR CHANGING
THEIR JOBS FOR THIS REASON, BY MAJOR GEOGRAPHIC AREAS IN CALIFORNIA,
MAY 19562 9
Responses
General population sample,
bothered by air pollution
Have given serious considera-
tion to moving
Have not given serious
consideration to moving
Total
Working population, sample
workers bothered by air
pollution at work
Have given serious considera-
tion to changing jobs
Have not given serious
consideration to changing
jobs
Total
California
2,616
Los Angeles
County
1,904
San Francisco
Bay Area
326
Rest of State
386
Persons bothered, percent
15
85
100
1,410
17
83
100
1,012
4
96
100
190
12
88
100
208
Persons bothered, percent
8
92
100
9
91
100
3
97
100
3
97
100
Table 9-15. REASONS FOR MOVING FROM THREE AREAS OF CALIFORNIA,
IN RESPONSE TO GENERAL POPULATION SURVEY, MAY 195629
Reason for moving
from area
Financial
Personal
Health
Air Pollution
Weather
Total percent
Los Angeles
County, percent
Prior to
1947
62
32
4
2
100
1947-56
51
27
3
13
6
100
San Francisco
Bay Area, percent
Prior to
1947
52
32
6
10
100
1947-56
51
39
2
8
100
Rest of State,
percent
Prior to
1947
64
27
2
7
100
1947-56
60
28
5
1
6
100
9-28
-------
reason for 13 percent of the moves from Los
Angeles County since 1947, compared with 2
percent prior to 1947. For other areas of the
state, the proportion of moves attributed to
air pollution was negligible.
Eye irritation appeared to be the most
frequently reported effect of air pollution; in
some instances, this symptom was accom-
panied by nasal irritation (Table 9-16). About
20 percent of the respondents expressed a
dissatisfaction with the communities in which
they lived. Air pollution had not been men-
tioned at this point in the interview. The
reasons for community dissatisfaction are
shown in Table 9-17. A far greater proportion
of dissatisfied Los Angeles residents (32 per-
cent) attributed their dissatisfaction to air
pollution than residents of the San Francisco
Bay area (1 percent) or for the rest of the
state (6 percent).
b. Survey of Los Angeles Physicians
A joint committee of the Los Angeles
County Medical Association and the Tuber-
culosis and Health Association of Los Angeles
County carried out a survey of Los Angeles
physicians in December, I960.32 A l-in-16
sample of the physicians registered in practice
in the county during 1958 was drawn, result-
ing in a sample of 526 from a total of 9,228
physicians. A pretested questionnaire was
mailed with a letter signed by the chairman of
the air pollution subcommittee. A followup
was also mailed, and telephone calls were
made to the offices of those physicians who
had not responded.
Three-hundred fifty of the questionnaires
were returned. Of those, 307 (58 percent)
were completed and tabulated. The words
"air pollution" did not appear in the ques-
tionnaire, although bias could have been intro-
duced by the fact that the chairman of the air
pollution subcommittee attached a letter to
the questionnaire. Seventy-seven percent of
the physicians believed that air pollution
adversely affected the health of their patients.
Two-thirds of the responding physicians felt
that air pollution was a factor adversely
Table 9-16. AIR POLLUTION EFFECTS
REPORTED IN GENERAL POPULATION SURVEY, BY TYPE OF COMMUNITY AND
BY MAJOR GEOGRAPHIC AREAS IN CALIFORNIA, MAY 1956 2 9
Air pollution effects
General population sample
Respondents bothered by air
pollution
Percent bothered by air
pollution
Air pollution effects cited:
Eyes, effects
Eye irritation
Eye and nasal irritation
Eye irritation and annoying
Eye, nasal irritation, and
annoying
Nasal irritation, eye not
mentioned
Nasal irritation
Nasal irritation and annoying
Annoying only
Other effects, only
No effects reported
— , £ • •
Total percent
California
At home
6,939
2,616
38
At work
3,732
1,410
37
Los Angeles
County
At home
2,892
1,904
66
At work
1,577
1,012
64
San Francisco
Bay Area
At home
1,846
326
18
At work
1,028
190
18
Rest of State
At home
2,201
386
17
At work
1,127
208
19
Persons bothered, percent
75
44
23
5
3
10
8
2
5
5
5
100
76
46
24
3
3
9
8
1
7
2
6
100
89
54
26
6
3
5
4
1
2
2
2
100
88
53
27
4
4
4
3
1
3
1
4
100
38
17
15
4
2
22
19
3
17
5
18
100
39
18
14
3
4
23
19
4
26
5
7
100
41
23'
14
3
1
22
18
4
10
17
10
100
51
30
19
2
21
21
8
4
16
100
9-29
-------
Table 9-17. EFFECTS OF AIR POLLUTION ON COMMUNITY SATISFACTION,
REPORTED IN GENERAL POPULATION SURVEY, BY MAJOR GEOGRAPHIC AREA,
CALIFORNIA, MAY 1956 26
Reason volunteered for dis-
satisfaction with community
Dissatisfied, total number
Climatic
Air pollution
Weather
Nonclimatic
Miscellaneous
Total percent
California
1,345
30
16
14
64
6
100
Los Angeles
County
612
41
32
9
54
5
100
San Francisco
Bay area
327
18
1
17
74
8
100
Rest of
state
406
27
6
21
69
4
100
affecting chronic respiratory disease. One-
third of the physicians had advised one or
more of their patients to leave the Los
Angeles area for health reasons; air pollution
was a factor mentioned in two-thirds of these
instances. By extrapolation from the sample,
assuming it to be representative, it was esti-
mated that physicians had advised over
10,000 patients to move; it was reported that
approximately 25 percent of the patients had
done so. Nearly one-third of the physicians
had themselves considered moving from the
Los Angeles area because of air pollution.
Among other environmental factors men-
tioned were overcrowding and traffic conges-
tion, but these were of very small magnitude
in relation to the reported difficulties with air
pollution.
c. Discussion'
A significantly large proportion of Los
Angeles residents were subjectively bothered
by air pollution when compared with resi-
dents of the San Francisco Bay area and the
rest of the state. A larger proportion of
residents who were so bothered had consi-
dered moving or had moved from Los Angeles
than residents of other areas of California.
Eye irritation, at times accompanied by
nasal irritation, was the most frequently
reported nuisance effect of air pollution,
according to the California Health Survey.
One-third of sampled physicians in the Los
Angeles area advised one or more of their
patients to leave the area for health reasons,
and nearly one-third of the physicians had
themselves considered moving from the Los
Angeles area because of air pollution.
9-30
D. SUMMARY
Epidemiologic studies have been conducted
relating photochemical air pollution with
mortality, hospital admissions, aggravation of
respiratory diseases, impairment of human
performance, and eye irritation. The effects
of prolonged oxidant exposure on mortality,
morbidity, ventilatory function, and com-
munity satisfaction have also been studied.
1. Review of Results from Cited Studies
No convincing relationship was observed
b&tween short-term variations in photo-
chemical oxidants and (1) daily mortality or
(2) hospital admissions.
A study of 137 patients with asthma
demonstrated significantly more asthma at-
tacks on days when photochemical oxidant
concentrations exceeded 250 jui/m3 (0.13
ppm). Such a peak oxidant value might be
expected to be associated with a maximum
hourly average oxidant concentration of 100
to 120 jug/m3 (0.05 to 0.06 ppm), depending
on localized conditions.
Chronic respiratory disease patients re-
moved from an ambient atmosphere of eleva-
ted oxidant concentrations to a room from
which pollutants were filtered have shown
improvement in ventilatory function. In two
other studies, no significant association was
found between variations in ambient oxidant
levels and changes in respiratory symptoms or
function in patients with chronic respiratory
disease.
The team performance of high school
cross-country track runners was impaired on
days of elevated oxidant concentrations mea-
-------
sured 1 hour before the commencement of
each race; hourly oxidant concentrations
ranged from 60 to 590 ng/m3 (0.3 to 0.30
ppm), although no threshold for this effect
can be determined from the available data.
Significantly more automobile accidents have
also occurred on days of high oxidant concen-
trations.
Eye irritation appears to increase progres-
sively when oxidant concentrations exceed
200Mg/m3 (0.10 ppm). This oxidant value,
related to eye irritation might be expected to
be associated with a maximum hourly average
oxidant concentration of 50 to 100 Mg/m3
(0.025 to 0.50 ppm), depending on localized
conditions. Eye irritation, at times accompa-
nied by nasal irritation, was the most frequent-
ly reported nuisance effect of air pollution in
California. A postulated explanation for the
relationship between ambient oxidant levels
and eye irritation is that the level of oxidantsis
a measure of the photochemical activity which
produced the eye irritants.
Lung cancer mortality rates were similar
among California residents studied in both
high-and low-oxidant pollution areas. A rela-
tionship between noncancerous chronic res-
piratory disease mortality and long-term pho-
tochemical oxidant exposure has been sugges-
ted in an isolated study in which other
important variables were not analyzed. Fac-
tors other than oxidant exposure could well
have accounted for these observations, and
considerable documentation from other epi-
demiologic studies is required to substantiate
these findings. Several surveys have also re-
ported a higher incidence of both chronic
respiratory disease symptoms and of other
respiratory symptoms, including asthma and
nose and throat complaints, among residents
of Los Angeles than in other areas of Cali-
fornia.
A significantly larger proportion of Los
Angeles residents have been subjectively both-
ered by air pollution than residents of the San
Francisco Bay area and the rest of the state. A
larger proportion of residents who were both-
ered by air pollution have considered moving
or have moved from Los Angeles than resi-
dents of other areas of California. One-third
of the physicians sampled in the Los Angeles
area had advised one or more of their patients
to leave the area for health reasons, and
nearly one-third of the physicians had them-
selves considered moving from Los Angeles
because of air pollution.
2. Future Research Needs
Relatively scanty information has been
gathered on community health effects of
photochemical oxidants. The relatively local-
ized nature of the oxidant problem accounts
for this gap in knowledge. Data reported in
this chapter need to be augmented, particular-
ly with regard to lung cancer mortality and
the prevalence of chronic respiratory disease.
The known irritant potential of ozone, a major
component of photochemical pollution,
should be explored to establish more exactly
how exacerbations of illness in subjects with
asthma and chronic bronchitis on days of
elevated oxidant concentrations may be re-
lated to the presence of ozone. Studies to
date suggest that this portion of the popula-
tion may be more sensitive to oxidant varia-
tions. Studies of the acute effects of oxidant
pollution could be further refined by careful
selection of comparison communities in
which differences in exposure to photochemi-
cal oxidant levels are maximized. Both chron-
ic and acute effects associated with air pollu-
tion exposure can be identified more readily
through such studies.
Systemic effects of oxidant exposure were
suggested in the athletic performance study
and in the study on accident frequency.
Replication and extension of these studies are
clearly indicated. Physiologic and psycho-
motor tests to elucidate pathological mecha-
nisms for these effects v/ould add important
confirmatory evidence and point the way to
the development of dose-response relation-
ships.
Well-designed prevalence studies in clean
and polluted communities would provide use-
ful quantitative data on the prevalence of
chronic respiratory disease, heart disease, and
9-31
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possibly chronic eye pathology in relation to
prolonged oxidant exposure. The effect of
oxidant exposure on growth and development
in the first years of life is a clearly feasible
prospective study. Such a study may provide
important information on the action of this
pollutant during a period of life when man is
highly sensitive to environmental influences.
The impairment by oxidant pollution of
immune mechanisms of response to infectious
agents, suggested in animal studies, has not
been explored in community studies. Classical
epidemiologic and laboratory methods to
study acute respiratory illness rates in popula-
tions could be applied profitably to the
photochemical oxidant problem.
3. Discussion
Accumulated studies reviewed in this chap-
ter reveal an inadequacy of epidemiologic
information on the health effects of photo-
chemical oxidant pollution. Consistent results
for some effects, obtained by various investi-
gators under varying conditions of exposure,
are lacking. The few demonstrated associa-
tions between oxidant exposure and health
effects, such as asthma, pulmonary function,
or athletic performance, are inadequate to
establish minimum threshold levels for each
effect.
Reported studies do suggest, however, that
photochemical oxidants are potentially hazar-
dous environmental contaminants. Subjects
with chronic respiratory disease seem to be
the most threatened by such exposure, but
virtually all segments of the population may
experience eye irritation at levels of oxidants
frequently present in the ambient air. Hazards
to normal respiratory function, optimum ath-
letic performance, and safe automobile driv-
ing have also been suggested. An association,
although not necessarily a cause-effect rela-
tionship, has been shown between ambient
levels of photochemical oxidants and eye
irritation. Since one of the objectives of air
pollution control is to promote good health
and minimize exposures to potentially hazar-
dous pollutants, the information provided by
reported studies can not be discounted.
E. REFERENCES
1. Clean Aii for California. California Dept. of Public
Health. Berkeley. Initial Report. March 1955. Second
Report. March 1956. Third Report 1957.
2. Oechsli, F.W. and R.W. Buechley. Mortality During Hot
Spells in Los Angeles and Orange Counties, 1939-1963.
PHS Contract 85-65-20. 1965.
3. Massey, F.J., E. Landau, and M. Deane. Air Pollution
and Mortality in Two Areas of Los Angeles County.
Presented at the Joint Meeting of the American Statisti-
cal Association and the Biometric Society (ENAR). New
York City. December 27, 1961.
4. Hechter, H.H. and J.R. Goldsmith. Air Pollution and
Daily Mortality. Amer. J. Med. Sci. 247:581-588, May
1961.
5. Mills, C.A. Respiratory and Cardiac Deaths in Los
Angeles Smogs. Amer. J. Med. Sci.233:379-386, April
1957.
6. Brant, J.W.A. Human Cardiovascular Diseases and Atmo-
spheric Air Pollution in Los Angeles, California. Int. J.
Air Water Pollution. P(4):219-231, April 1965.
7. Brant, J.W.A. and S.R.G. Hill. Human Respiratory
Diseases and Atmospheric Air Pollution in Los Angeles,
California. Int. J. Air Water Pollution. 5:259-277, May
1964.
8. Sterling, T.D. et al. Urban Morbidity and Air Pollution:
A First Report. Arch. Environ. Health. 13(21): 158-170,
August 1966.
9. 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.
10. Schoettlin, C.E. and E. Landau. Air Pollution and
Asthmatic Attacks in the Los Angeles Area. Public
Health Repts. 75:545-548, 1961.
11. Motley, H.L., R.H. Smart, and C.I. Leftwich. Effect of
Polluted Los Angeles Air (Smog) on Lung Volume
Measurements. J. Amer. Med. Assoc. 777:1469-1477,
November 1959.
12. Remmers, J.E. and O.J. Balchum. Effects of Los Angeles
Urban Air Pollution Upon Respiratory Function of
Emphysematous Patients: The Effect of the Micro-
Environment on Patients with Chronic Respiratory
Disease. Presented at Air Pollution Control Association
Meeting. Toronto, June 1965.
13. Rokaw, S.N. and F. Massey. Air Pollution and Chronic
Respiratory Disease. Amer. Rev. Respirat. Diseases.
S<5(5):703-704, November 1962.
14. McKerrow, C.B. Chronic Respiratory Disease in Great
Britain. Arch. Environ. Health. 5:174-179, January
1964.
15. Schoettlin, C.E. The Health Effect of Air Pollution on
Elderly Males. Amer. Rev. Respirat. Diseases.
S<5(6):878-897, December 1962.
16. Wayne, W.S., P.P. Wehrle and R.E. Carroll. Oxidant Air
Pollution and Athletic Performance. J. Amer. Med.
Assoc. 799(12):901-904, March 20, 1967.
17. Ury, H. Photochemical Air Pollution and Automobile
Accidents in Los Angeles. Arch. Environ. Health.
7 7(3):334-342, September 1968.
18. McMillan, R.S., D.H. Wiseman, B. Hanes and P.P.
Wehrle. Effects of Oxidant Air Pollution on Peak
9-32
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Expiratory Flow Rates in Los Angeles School Children.
Arch. Environ. Health, 18:94-99, 1969.
19. Renzetti, N.A. and V. Gobran. Studies of Eye Irritation
Due to Los Angeles Smog 1954-1956. Air Pollution
Foundation. San Marino, Calif. July 1957.
20. Goldsmith, J.R. and M. Deane. Outdoor Workers in the
United States and Europe. The Millbank Memorial Fund
Quart. 45:107-116, 1965.
21. Hammer, D.I. et al. Los Angeles Pollution and Respir-
atory Symptoms. Relationship During a Selected 28-day
Period. Arch. Environ. Health. 70:475-480, March 1965.
22. Richardson, N.A. and W.C. Middleton. Evaluation of
Filters for Removing Irritants from Polluted Air. Univer-
sity of California, Dept. of Engineering. Los Angeles.
Report Number 57-43. June 1957.
23. Richardson, N.A. and W.C. Middleton. Evaluation of
Filters for Removing Irritants from Polluted Air. Heat-
ing, Piping Air Conditioning. 50:147-154, November
1958.
24. McCarroll, J.R. et al. Health and the Urban Environ-
ment. Air Pollution and Family Illness: I. Design for
Study. Arch. Environ. Health. 70:357-363, February
1965.
25. Sawicki, E. Airborne Carcinogens and Allied Com-
pounds. Arch. Environ. Health. 74:46-53, January 1967.
26 Buell, P., J.E. Dunn, Jr., and L. Breslow. Cancer of the
Lung and Los Angeles Type Air Pollution: Prospective
Study. Cancer. 20:2139-2147, December 1967.
27. Winklestein, W. et al. The Relationship of Air Pollution
and Economic Status to Total Mortality and Selected
Respiratory System Mortality in Men: I. Suspended
Particulates. Arch. Environ. Health. 74:162-171, January
1967.
28. Winkelstein, W., Jr. et al. The Relationship of Air
Pollution and Economic Status to Total Mortality and
Selected Respiratory System Mortality in Men. II.
Oxides of Sulfur. Arch. Environ. Health. 7(5:401-405,
March 1968.
29. Hausknecht, R. Air Pollution Effects Reported by
California Residents (from the California Health Survey).
California Dept. of Public Health. Berkeley. 1960.
30. Hausknecht, R. Experiences of a Respiratory Disease
Panel Selected From a Representative Sample of the
Adult Population. Amer. Rev. Respirat. Diseases.
S6(6):858-866, December 1962.
31. Deane, M., J.R. Goldsmith, and D. Tuma. Respiratory
Conditions in Outside Workers: Report on Outside Plant
Telephone Workers in San Francisco and Los Angeles.
Arch. Environ. Health. 70:323-331, February 1965.
32. Physicians Environmental Health Survey: A Poll of
Medical Opinion. Los Angeles County Medical Associa-
tion and Tuberculosis and Health Association. Los
Angeles, Calif. May 1961.
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Chapter 10.
SUMMARY AND CONCLUSIONS
A. INTRODUCTION
This document is a consolidation and
assessment of the current state of knowledge
on the origin and effects of the group of air
pollutants known as photochemical oxidants
on health, vegetation, and materials. The
purpose of this chapter is to provide a concise
picture of the information contained in this
document, including conclusions which are
believed reasonable to consider in evaluating
concentrations of photochemical oxidants
which are known to have an effect on either
health or welfare. Although nitrogen dioxide
is considered one of the photochemical
oxidants, it is to be subject of a separate
report. Consequently, nitrogen dioxide is
discussed in this document only to the extent
that it participates in the formation and reac-
tions of other photochemical oxidants. The
information and data contained in this docu-
ment comprise the best available bases, and
provide the rationale for development of
specific levels of standards of photochemical
oxidants in the ambient air for protection of
public health and man's environment.
B. NATURE OF PHOTOCHEMICAL
OXIDANTS
Photochemical oxidants result from a com-
plex series of atmospheiic reactions initiated
by sunlight. When reactive organic substances
and nitrogen oxides accumulate in the atmo-
sphere "and are exposed to the ultraviolet
component of sunlight, the formation of new
compounds, including ozone and peroxyacyl
nitrates, takes place.
Absorption of ultraviolet light energy by
nitrogen dioxide results in its dissociation into
nitric oxide and an oxygen atom. These
oxygen atoms for the most part react with air
oxygen to form ozone. A small portion of the
oxygen atoms and ozone react also with
certain hydrocarbons to form free radical
intermediates and various products. In some
complex manner, the free radical intermedi-
ates and ozone react with the nitric oxide
produced initially. One result of these reac-
tions is the very rapid oxidation of the nitric
oxide to nitrogen dioxide and an increased
concentration of ozone.
The photochemical system generally is ca-
pable of duplication in the laboratory. For
various reasons, however, laboratory results
cannot be quantitatively extrapolated to the
atmosphere. Theoretically generation of an
atmospheric simulation model should be feasi-
ble, enabling the prediction of ambient oxi-
dant concentrations from a knowledge of
emission and meteorological data. The devel-
opment of such a model, however, is depen-
dent on the acquisition of more reliable and
applicable quantitative information derived
from direct atmospheric observations, as well
as on the refinement of results obtained from.
irradiation chamber studies.
C. ATMOSPHERIC PHOTOCHEMICAL
OXIDANT CONCENTRATIONS
The presence of photochemically formed
oxidants has been indicated in all of the major
U.S. cities for which aerometric data have
been examined. On a concentration basis,
ozone has been identified as the major com-
ponent of the oxidant levels observed. Diffi-
culties arise, however, in interpreting data
obtained by the most commonly used oxidant
measuring method; this method is nonspecific
and subject to several interferences. Adjusted
oxidant concentrations, obtained by correc-
ting potassium iodide oxidant measurements
10-1
-------
for known interferences, have been found to
be relatively close to concurrent measure-
ments of ozone alone.
Since photochemical oxidants are the pro-
ducts of atmospheric chemical reactions, the
relationship between precursor emissions and
atmospheric oxidant concentrations is much
less direct than is the case for primary
pollutants. A further complicating situation is
the dependence of these photochemical reac-
tions on intensity and duration of sunlight,
and on temperature.
In an analysis of oxidant concentration
data for 4 years and 12 stations, the daily
maximum 1-hour average concentration was
equal to or exceeded 290 ng/m3 (0.15 ppm)
up to 41 percent of the time; maximum
1-hour average concentrations ranged from
250 to 1,140 Mg/m3 (0.13 to 0.58 ppm);
short-term peaks were as high as 1,310 Mg/m3
(0.67 ppm). Yearly averages, commonly app-
lied to other pollutants, are not representative
of air quality with respect to oxidant pollu-
tion, because 1-hour average ozone concentra-
tions will necessarily be at or about zero for
approximately 75 percent of the time when
photochemical reactions are minimal.
Peroxyacyl nitrates, through not routinely
measured, have been identified in the atmo-
sphere of several cities. These compounds
may be assumed to be present whenever
oxidant levels are elevated.
D. NATURAL SOURCES OF OZONE
Ozone can be formed naturally in the
atmosphere by electrical discharge, and in the
stratosphere by solar radiation, by processes
which are not capable of producing signifi-
cant urban concentrations of this pollutant.
Maximum instantaneous ozone levels of from
20 to 100 jug/m3 (0.01 to 0.05 ppm) have
been recorded in nonurban areas.
E. MEASUREMENT OF PHOTOCHEMICAL
OXIDANTS
The most widely used technique for the
analysis of atmospheric total oxidants is based
on the reaction of these compounds with
potassium iodide to release iodine. The iodine
may then be measured by either colorimetric
or coulometric methods. Calibrating the oxi-
dant measurement method used against a
known quantity of ozone provides a measure-
ment of the net oxidizing properties of the
atmosphere in terms of an equivalent concen-
tration of ozone. Most oxidant measurements
are currently being made by the colorimetric
method, although coulometric analyzers are
used in a number of laboratory and field studies.
In order to generate comparable data, it is
essential that all measurements be made by
techniques which have been calibrated against
the same standard or reference method. Since
at the present time there is no standard
method for the determination of total oxi-
dants, the National Air Pollution Control
Administration recommends use of the neu-
tral-buffered 1 percent potassium iodide col-
orimetric technique as the method against
which all instruments and other methods
should be compared. In addition to serving as
a manual procedure for determining oxidants,
the reference method may be used in conjunc-
tion with a "dynamic calibration" technique
for instrumental methods.
Reducing agents such as sulfur dioxide
produce a negative interference in oxidant
determination. Such interference can be re-
duced, however, by passing the air stream
through a chromium trioxide scrubber prior
to measurement. Unfortunately, a portion of
the nitric oxide which may be present in the
air stream is oxidized to nitrogen dioxide by
the scrubber. This results in an apparent
increase in the oxidant measurement of about
11 percent of the concentration of nitric
oxide. Moreover, a portion of the atmospher-
ic nitrogen dioxide concentration will also
contribute to the oxidant measurement. Per-
oxyacyl nitrate concentrations are usually
small and contribute only a very slight
amount to the oxidant reading.
There are several means for the specific
measurement of atmospheric ozone. Instru-
mental methods include chemiluminescent
analysis based on the reaction of ozone with
Rhodamine B, gas phase olefin titration, and
10-2
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ultraviolet and infrared spectroscopy. A semi-
quantitative method for ozone measurement
is based on its ability to produce cracks in
stretched rubber. Peroxyacyl nitrates can be
measured in the atmosphere by gas chromato-
graphy with the use of an electron-capture
detector.
For a better evaluation of the results of
research on the effects of photochemical
oxidants, it is essential that data be obtained
for individual oxidants such as nitrogen diox-
ide, ozone, PAN, formaldehyde, acrolein, and
organic peroxides. These data would either
replace or complement data on total oxidants.
Instrumentation currently available permits
the accurate measurement of atmospheric
ozone, nitrogen dioxide, and PAN. There
exists, however, a further need to develop
instruments capable of measuring other indi-
vidual gaseous pollutants which have the
properties of oxidants. Photochemical reac-
tions and problems derived from oxidants can
be much better defined using specific meth-
ods for measurement in preference to the
traditional total oxidants determination.
F. EFFECTS OF PHOTOCHEMICAL
OXIDANTS ON VEGETATION
AND MICROORGANISMS
Injury to vegetation is one of the earliest
manifestations of photochemical air pollu-
tion, and sensitive plants are useful biological
indicators of this type of pollution. The
visible symptoms of photochemical oxidant
produced injury to plants may be classified
as: (1) acute injury, identified by cell collapse
with subsequent development of necrotic
patterns; (2) chronic injury, identified by
necrotic patterns with or without chlorotic or
other pigmented patterns; and, (3) phsyiologi-
cal effects, identified by growth alterations,
reduced yields, and changes in the quality of
plant products. The acute symptoms are
generally characteristic of a specific pollutant;
though highly characteristic, chronic injury
patterns are not. Ozone injury to leaves is
identified as a stippling or flecking. Such
injury has occurred experimentally in the
most sensitive species after exposure to 60
Aig/m3 (0.03 ppm) ozone for 8 hours. Injury
will occur in shorter time periods when low
levels of sulfur dioxide are present. PAN-pro-
duced injury is characterized by an under-sur-
face glazing or bronzing of the leaf. Such
injury has occurred experimentally in the
most sensitive species after exposure to 50
Mg/m3 (0.01 ppm) PAN for 5 hours. Leaf
injury has occurred in certain sensitive species
after a 4-hour exposure to 100 Mg/m3 (0.05
ppm) total oxidant. Ozone appears to be the
most important phytotoxicant in the photo-
chemical complex.
There are a number of factors affecting the
response of vegetation to photochemical air
pollutants. Variability in response is known to
exist between species of a given genus and
between varieties within a given species; varie-
tal variations have been most extensively
studied with tobacco. The influence of light
intensity on the sensitivity of plants to damage
during growth appears to depend on the phy-
totoxicant. Plants are more sensitive to PAN
when grown under high light intensities, but
are more sensitive to ozone when grown under
low light intensities. Reported findings are in
general agreement that sensitivity of green-
house-grown plants to oxidants increases with
temperature, from 10° to 38° C (40° to 100°
F), but this positive correlation may result
from the overriding influence of light intensi-
ty on sensitivity. The effects of humidity on
the sensitivity of plants has not been well
documented. General trends indicate that
plants grown and/or exposed under high
humidities are more sensitive than those
grown at low humidities. There has been little
research in this direction, but there are
indications that soil factors such as drought
and total fertility influence the sensitivity of
plants to phytotoxic air pollutants. The age of
the leaf under exposure is important in de-
termining its sensitivity to air pollutants.
There is some evidence that oxidant or ozone
injury may be reduced by pretreatment with
the toxicant.
10-3
-------
Identification of injury to a plant as being
caused by air pollution is a difficult undertak-
ing. Even when the markings on the leaves of
a plant may be identified with an air pollut-
ant, there is the further difficulty of evaluat-
ing the injury in terms of its effect on the
intact plant. Additional problems arise in
trying to evaluate the economic impact of
air pollution damage to a plant.
The interrelations of time and concen-
tration (dose) as they affect injury to plants
are essential to air quality criteria. There are,
however, only scant data relating concen-
trations and length of photochemical oxi-
dant exposure to chronic injury and effects
on reduction of plant growth, yield, or
quality. There is also a dearth of infor-
mation relating concentrations to acute
injury. A larger body of information exists
on the acute effects of ozone, but even in
this instance, the information is far from
complete. Sufficient data do exist, however,
to tabularly present ozone concentrations
which will produce 5 percent injury to sensi-
tive, intermediate, and resistant plants after
a given short-term exposure, as shown in
Table 10-1. Information available lists 20
species and/or varieties as sensitive, 55 as
intermediate in sensitivity, and 64 as rela-
tively resistant.
Bacteriostatic and bacteriocidal properties
of photochemical oxidants in general have
been demonstrated. The growth suppression
of microorganisms by ozone is a well-known
phenomenon, although the ozone concen-
trations for this activity are undesirable from
a human standpoint. The bacteriocidal
activity of ozone varies with its concen-
tration, the relative humidity, and the
species of bacteria.
G. EFFECT OF OZONE ON MATERIALS
The detailed, quantitative extent of damage
to materials caused by atmospheric levels of
ozone is unknown, but generally any organic
material is adversely affected by concentrated
ozone. Many polymers are extremely sensitive
to even very small concentrations of ozone,
this sensitivity increasing with the number of
double bonds in the structure of the polymer.
Economically, rubber is probably the most
important material sensitive to ozone attack,
particularly styrene-butadiene, natural, poly-
butadiene, and synthetic polyisoprene. Anti-
ozonant additives have been developed and
are capable of protecting elastomers from
ozone degradation; synthetic rubbers with
inherent resistance to ozone are also available.
These additives are expensive, however, and
add to the cost of the end product; in
addition, increasing amounts of antiozonants
are required as the amount of ozone which is
to be encountered increases, and sometimes
only temporary protection is provided.
Ozone attacks the cellulose in fabrics
through both a free radical chain mechanism
and an electrophilic attack on double bonds;
light and humidity appear necessary for ap-
preciable alterations to occur. The relative
susceptibility of different fibers to ozone
attack appears to be, in increasing order,
cotton, acetate, nylon, and polyester.
Table 10-1. PROJECTED OZONE CONCENTRATIONS WHICH WILL PRODUCE, FOR
SHORT-TERM EXPOSURES, 5 PERCENT INJURY TO ECONOMICALLY
IMPORTANT VEGETATION GROWN UNDER SENSITIVE CONDITIONS
Time,
hi
0.2
0.5
1.0
2.0
4.0
8.0
Ozone concentrations producing injury in three types of plants, ppm
Sensitive
0.35-0.75
0.15-0.30
0.10-0.25
0.07-0.20
0.05-0.15
0.03-0.10
Intermediate
0.70-1.00
0.25-0.60
0.20-0.40
0.15-0.30
0.10-0.25
0.08-0.20
Resistant
0.90 and up
0.50 and up
0.35 and up
0.25 and up
0.20 and up
0.15 and up
10-4
-------
Certain dyes are susceptible to fading during
exposure to ozone. The rate and extent of fad-
ing is also dependent upon other environmental
factors such as relative humidity and the
presence of air pollutants other than ozone, as
well as the length and concentration of ozone
exposure and the type of material exposed.
H. TOXICOLOGICAL STUDIES OF
PHOTOCHEMICAL OXIDANTS
1. Effects of Ozone in Animals
The major physiological effects of ozone
are on the respiratory system. Inhalation of
ozone at concentrations greater than about
5,900 Mg/m3 (3 ppm) for several hours pro-
duces hemorrhage and edema in the lungs.
This reaction can be fatal to animals. Rats and
mice appear to be more sensitive than rabbits,
cats, and guinea pigs. The toxicity is greater
for young animals and for exercising animals.
It is abated by intermittency of exposure, by
prophylactic administration of chemical re-
ducing agents, or by introducing agents into
the diet which reduce the activity of the
thyroid gland. At exposures less than those
which produce edema in the lungs, changes in
the mechanical properties of the lung occur.
These are accompanied by increased breathing
rates and increased oxygen consumption. Re-
peated non-fatal exposures to concentrations
greater than 15,700 ng/m3 (8 ppm) for 30
minutes have produced fibrosis in the respira-
tory tract of rabbits, with the damage increas-
ing in severity over the length of the respira-
tory tract from the trachea to the bronchioles.
Short-term exposures to ozone also pro-
duce chemical changes in the lung tissue ele-
ments of animals. A study conducted on a
small number of rabbits showed that inhala-
tion of 1,960 to 9,800 jug/m3 (1 to 5 ppm)
ozone for 1 hour can produce denaturation of
the structural lung proteins. Ozone also ap-
pears to oxidize the sulfhydryl groups of
amino acids in the lung.
Short-term exposures to ozone also pro-
duce changes in organs other than the lung.
Concentrations of 5,900 Mg/m3 (3 ppm) for
20 hours can stimulate some adaptive liver
enzymes. Inhalation of 390 to 490
(0.2 to 0.25 ppm) ozone for 30 to 60 minutes
makes the red blood cells of mice, rabbits,
rats, and man more sensitive to the shape-al-
tering effects of' irradiation. Exposure of
blood to ozone in vitro produces interference
with the release of oxygen from red blood
cells; this suggests that ozone exposure could
impair the delivery of oxygen to the tissues.
Ozone exposures at concentrations from
1,310 to 7,800/zg/m3 (0.67 to 4.0 ppm) have
been shown to reduce the in vitro phagocytic
abilities of the pulmonary alveolar macrophag-
es. A 3-hour exposure to 9,800 /ig/m3 (5
ppm) ozone has been shown to reduce the
activity of bactericidal enzyme, presumably
due to in vivo oxidation of the enzyme.
Ozone inhalation increases the vulnerability
of animals to other agents. A single exposure
to ozone at a concentration of 160 Mg/m3
(0.08 ppm) for 3 hours has increased the
mortality among mice from inhalation of
pathogenic bacteria. This occurred when the
bacteria were administered both before and
after exposure to ozone. Ozone also increases
the toxicity of histamine in guinea pigs.
Long-term effects of ozone exposure in-
clude, in some species, the development of
tolerance to biological effects of ozone,
production of fibrotic changes in the lungs,
and a possible increase in the rate of aging.
While tolerance has been shown in rodents, it
has not been shown in chickens, and it is not
certain whether or not it occurs in man. In
species where tolerance to ozone exposure has
been demonstrated, information is not avail-
able concerning the duration and mechanism
of tolerance following repeated exposure. The
aging effect may be similar to the changes
produced by exposure to free radicals or by
irradiation.
2. Effects of Ozone in Humans
Some studies of human exposures to ozone
have focused on the determination of the
threshold level at which odor can be detected,
and on the occurrence of changes in pulmo-
nary function. Nine out of 10 subjects ex-
posed to 40 Mg/m3 (0.02 ppm) ozone were
able to detect the odor immediately, and it
10-5
-------
persisted for an average of 5 minutes. Thir-
teen of 14 subjects exposed to 100 Mg/m3
(0.05 ppm) ozone indicated the odor is
considerably stronger at this concentration,
and the odor persisted for an average of 13
minutes.
Occupational exposure of humans to ozone
concentrations of up to 490 jug/m3 (0.25
ppm) has not produced detectable changes in
pulmonary function. Respiratory symptoms
and a decrease in vital capacity in three out of
seven smokers who had been occupationally
exposed to ozone have occurred at concentra-
tions greater than 590 ng/m3 (0.3 ppm).
Experimental exposures of humans have
been carried out at concentrations ranging
from 200 to 7,800 Mg/m3 (0.1 to about 4
ppm) for periods of up to 2 hours. Exposure
to 390 Mg/m3 (0.2 ppm) for 3 hours daily, 6
days a week, for 12 weeks has not produced
any change in ventilatory function tests.
Similar exposure to 980 Mg/m3 (0.5 ppm)
produced a decrease in the forced expiratory
volume during the last 4 weeks of exposure,
with recovery taking place in a subsequent
6-week period. In each of 11 subjects, expo-
sure to 1,180 to 1,570 Mg/m3 (0.6 to 0.8
ppm) for 2 hours resulted in an impairment of
the diffusing capacity of the lung. Small
decreases in vital capacity and forced expira-
tory volume were observed in some of these
subjects. Resistance to flow of air in the
respiratory tract increased slightly in some sub-
jects after exposure to 200 to 1,180 jug/m3
(0.1 to 0.6 ppm) for 1 hour, and increased con-
sistently in each of four subjects after exposure
to 1,960 jug/m3 (1 ppm) for 1 hour.
Data obtained from animal experimenta-
tion cannot be used directly to define the
ozone concentrations above which human
health will be affected. Animal mortality
studies, however, can be useful in determining
the factors involved in toxicity. While the
concentrations of ozone used in the deter-
mination of short-term non-fatal effects in
animals are rarely found in ambient air, the
changes in pulmonary function observed dur-
ing and after exposure to these concentrations
call attention to the possibility that similar
effects may be observed in humans.
When interpreting the research conducted
thus far using human subjects, it must be
noted that occupational exposures differ from
experimental exposures, because it is difficult
in an occupational environment to define the
exact nature and dose of the pullutants
present.
3. Effects of Peroxyacetyl Nitrate
Experimental studies with peroxyacetyl ni-
trate (PAN) in animals indicate that mortality
may be delayed for 7 to 14 days after
exposure; however, the exposure levels requir-
ed to produce this mortality never occur in
ambient atmospheres.
A single experimental study of healthy
human subjects exposed to 1,485 Mg/m3 (0.3
ppm) peroxyacetyl nitrate indicated only that
there may be a small increase in oxygen
uptake with exercise. Sensitive pulmonary
function tests were not obtained.
The data from animal and human studies
are sparse and inadequate for determining the
toxicological potential of peroxyacetyl ni-
trate. It would appear, however, that at the
concentrations of this compound known to
occur in ambient atmospheres, PAN does not
present any recognized health hazard.
4. Effects of Mixtures Containing Photo-
chemical Oxidants on Animals
Studies have been conducted on animals
exposed to both synthetic and natural photo-
chemical smog. Synthetic smog has been
produced by the irradiation of diluted motor
vehicle exhaust or by irradiation of air mix-
tures containing nitrogen oxides and certain
hydrocarbons. Exposures to irradiated motor
vehicle exhaust are complicated by the simul-
taneous presence of carbon monoxide and
other non-oxidant substances which include
high concentrations of formaldehyde. Guinea
pigs show increased respiratory volume during
a four-hour exposure to irradiated exhaust
containing 1,570 jug/m3 (0.8 ppm) total
oxidant.
10-6
-------
Exposure of mice to both natural and
synthetic smog for 3 hours, at concentrations
greater than 780 jug/m3 (0.4 ppm) oxidants
have produced changes in the fine structure of
the lung. The nature and extent of the
damage was the same after exposure to either
type of smog with the same oxidant levels.
The severity of the damage increased with age
and became irreversible at age 21 months.
Chronic exposure of guinea pigs to ambient
air with an average oxidant concentration of
from 40 to 140 Mg/m3 (0.02 to 0.07 ppm)
leads to a significant increase in flow resist-
ance when the peak oxidant concentrations
exceed 980 Mg/m3 (0.5 ppm).
When male mice, prior to mating, were
given long-term exposures to irradiated auto
exhaust containing from 200 to 1,960 Mg/m3
(0.1 to 1.0 ppm) oxidant, a decrease in
fertility and an increase in neonatal mortality
of their offspring resulted; the irradiated
mixture also contained varying concentrations
of carbon monoxide, nitrogen oxides, and
hydrocarbons. Similar exposures also cause a
reduction in spontaneous running activity,
which results in an adaptation response.
Thus a number of experimental studies
have demonstrated that changes in lung tissue
or lung function occur when animals are
exposed for several hours to photo-oxidized
mixtures containing 980 Mg/m3 (0.5 ppm) or
more of oxidants.
5. Effects of Mixtures Containing Photo-
chemical Oxidants on Humans
Laboratory studies of human exposure to
photochemical smog have involved primarily
the measurement of eye irritation. Based on
the existing data, it appears that: (1) the
effective eye irritants are the products of
photochemical reactions; (2) although oxi-
dant concentrations may correlate with the
severity of eye irritation, a direct cause-effect
relationship has not been demonstrated since
ozone, the principal contributor to ambient
oxidant levels is not an eye irritant; (3) the
precursors of the eye irritants are organic
compounds in combination with oxides of
nitrogen, the most potent being aromatic
hydrocarbons; (4) the chemical identities of
the effective irritants in synthetic systems are
known as being formaldehyde, peroxybenzoyl
nitrate (PBzN), peroxyacetyl nitrate (PAN),
and acrolein, although the latter two contri-
bute to only a minor extent; and (5) the
substances causing eye irritation in the atmo-
sphere have not been competely defined.
I. EPIDEMIOLOGICAL STUDIES OF PHO
TOCHEMICAL OXIDANTS
Several studies have examined daily mortal-
ity rates in localities where photochemical air
pollution occurs, to determine if a relation-
ship exists with increased levels of oxidant.
Such an association has not been shown.
These studies, however, pose a number of
unresolved questions. One of these is, what is
the effect of temperature, either alone or in
combination with oxidants? In some of the
most severe episodes, there has been an
associated increase in environmental tempera-
ture, sufficient to cause excess mortality by
itself. Several studies of mortality among resi-
dents in nursing homes in Los Angeles showed
such excess mortality. In recent heat wave
and air pollution episodes, however, large
proportions of the elderly and ill persons in
nursing homes have been protected by air
conditioning.
Evidence of increased morbidity has been
sought through study of general hospital
admissions, but no unequivocal association
between photochemical air pollution and in-
creased morbidity has been shown. Additional
studies are indicated for improved definition.
Peak oxidant values of 250 Mg/m3 (0.13
ppm), which might be expected in relation to
maximum hourly average levels of 100 to 120
Mg/m3 (0.05 to 0.06 ppm), have been associa-
ted with aggravation of asthma. No associa-
tion between ambient oxidant concentrations
and changes in respiratory symptoms or func-
tion was shown, however, in two separate
studies of subjects with preexisting chronic
respiratory disease. Non-smoking subjects
with chronic respiratory disease did, however,
demonstrate less airway resistance when they
were studied in a room where the ambient air
10-7
-------
of Los Angeles was filtered before entry. No
acute or chronic effects of oxidant pollution
on ventilatory performance of elementary
schoolchildren were demonstrated in a study
conducted in two communities within the Los
Angeles basin.
Impairment of performance by high school
athletes has been observed when photochemi-
cal oxidants ranged from 60 to 590 [J-g/m3
(0.03 to 0.3 ppm) for 1 hour immediately
prior to the start of activities. Significantly,
more automobile accidents have also occurred
on days of high oxidant concentrations, but
no threshold level for this effect could be
determined from the analysis.
Among the general community, eye irrita-
tion is a major effect of photochemical air
pollution. In Southern California, it has af-
fected more than three-fourths of the popula-
tion. Eye irritation under conditions prevalent
in Los Angeles is likely to occur in a large
fraction of the population when oxidant
concentrations in ambient air increases to
about 200 jug/m3 (0.10 ppm). This oxidant
value might be expected to be associated with
a maximum hourly average oxidant concen-
tration of 50 to 100 Mg/m3 (0.025 to 0.50
ppm), depending on localized conditions.
According to survey data gathered in 1956,
asthma, cough, and nose and throat com-
plaints were more frequent in Los Angeles,
Orange, and San Diego counties than in the
San Francisco Bay area or in the rest of the
State.
Casual reports of the presence of the
symptoms of eye irritation have been record-
ed in many cities in the United States.
Epidemiologic studies have been inadequate,
however, to relate these symptoms clearly to
measured exposures to photochemical oxi-
dants. In fact, one of the major photochemi-
cal oxidants, ozone, is not an eye irritant.
That eye irritation is experienced whenever
the oxidant level exceeds a certain value is an
indication that oxidant concentrations corre-
late well with other aspects of the photo-
chemical complex; oxidant levels are probably
a measure of the photochemical activity
which produces the eye irritants. On the other
hand, it must be recognized that reactions of
ozone with hydrocarbons do lead to hydro-
carbon fragments which are eye irritants. Nor
can the possibility be discounted that ozone
in the photochemical complex may exert a
synergistic effect on eye irritation. Because
the oxidant reading measured only the net
oxidizing property of the atmosphere, how-
ever, the same amount of eye irritation
experienced in two different geographical
locations from identical irritants could be
associated with different levels of oxidant, if
other pollutants differed in their concentra-
tion.
J. AREAS FOR FUTURE RESEARCH
1. Environmental Aspects of Photochemical
Oxidants
1. Research should be conducted to further
identify the substance(s) which cause
eye irritation.
2. The nature of the photochemical aero-
sol, its behavior at different pressures of
water vapor, and the nature of the
surface layer of the particulates remains
to be determined.
3. The role of sulfur dioxide in the forma-
tion of photochemical aerosols and in
the impairment of visibility should be
investigated.
4. Mechanisms of photochemical oxidant
formation should be explained.
2. Toxicity of Ozone, Photochemical
Oxidants, and Peroxyacyl Nitrates
1. The effect of ozone and PAN in
combination with other pollutants found
in ambient air should be investigated.
Considerable information is available on
the separate effects of ozone, nitrogen
dioxide, and sulfur dioxide, but data on
the combined effects of defined concen-
trations of these gases are sparse. The
effect of particulates (dust, saline drop-
lets, oil, soots, etc.) should be deter-
mined alone and in combination with
the gases. Additional variables such as
10-8
-------
humidity and temperature should be
controlled and recorded. These experi-
ments should be carried out with materi-
als, vegetation, animals, and, under ap-
propriate conditions, in man.
2. Experiments with human exposures to
gas mixtures should include a compari-
son between the respiratory effects
shown in healthy subjects and those
shown in patients with chronic respira-
tory disease, care being taken to respect
the rights of experimental subjects.
3. Existing data demonstrate that tolerance
occurs only in rodents. Indices other
than mortality are required to demon-
strate tolerance in animals. If such in-
dices can be developed, then a study is
needed to see if a similar phenomenon
occurs in man.
4. The mechanisms of systemic effects of
ozone (headache, fatigue, impaired oxy-
gen transport by hemoglobin, inability
to concentrate, etc.) have yet to be
explained.
5. The rate and site of uptake of ozone and
its fate following uptake should be deter-
mined in vegetation and animals.
6. The mechanism for the production of
ozone-induced pulmonary edema re-
mains unexplained.
7. Additional research in needed to define
the role of peroxyacyl nitrates in the
production of eye irritation.
3. Epidemiology of Photochemical Oxidants
1. Of high priority is the need to study eye
and respiratory irritation in metropolitan
areas outside of California. Studies
should be supplemented by pulmonary
function tests.
2. Although the effects of episodes of high
pollution levels have been studied with
respect to mortality, morbidity, impair-
ment of performance, etc., additional
studies are needed at different sites and
for different effects. These should in-
clude congenital malformations, still-
births, hospitals admissions for miscar-
riage, and alterations in the sex ratio of
newborns.
3. The examination of children has received
insufficient attention in epidemiologic
studies of the health effects of air
pollution. This should be undertaken
with respect to the effects of photo-
chemical oxidants using simple pulmon-
ary function tests. Emphasis should be
placed on further studies of the inci-
dence of asthma attacks during episodes
of high pollution.
K. CONCLUSIONS
Derived from a careful evaluation of the
studies cited in this document, the conclu-
sions given below represent the best judgment
of the scientific staff of the National Air
Pollution Control Administration of the ef-
fects that may occur when various levels of
photochemical oxidants are reached in the
ambient air. The more detailed information
from which the conclusions were derived, and
the qualifications that entered- into the con-
sideration of these data, can be found in the
appropriate chapter of this document.
1. Human Exposure
a. Ozone
(1) Long-term exposure of
human subjects.
(a) Exposure to a concentration of up to
390 ME/m3 (0-2 ppm) for 3 hours a
day, 6 days a week, for 12 weeks, has
not produced any apparent effects
(Chapter 8, section B.2.)
(b) Exposure to a concentration of 980
jug/m3 (0.5 ppm) for 3 hours a day,
6 days a week, has caused a decrease
in the 1-second forced expiratory
volume (FEVi_o) after 8 weeks
(Chapter 8, section B.2)
(2) Short-term exposure of
human subjects.
(a) Exposure to a concentration of 40
Mg/m3 (0.02 ppm) was detected
immediately by 9 of 10 subjects.
10-9
-------
After an average of 5 minutes expo-
sure, subjects could no longer detect
ozone (Chapter 8, section E.2).
(b) Exposure to a concentration of 590
Mg/m3 (0.3 ppm) for 8 hours appears
to be the threshold for nasal and throat
irritation (Chapter 8, section E.2.)
(c) Exposure to concentrations of from
1,180 to 1,960 Mg/m3 (0.6 to 1.0
ppm) for 1 to 2 hours may impair
pulmonary function by causing in-
creased airway resistance, decreased
carbon monoxide diffusing capacity,
decreased total capacity, and de-
creased forced expiratory volume
(Chapter 8, section B.2'.)
(d) Exposure to concentrations of from
1,960 to 5,900 Mg/m3 (1.0 to 3.0
ppm) for 10 to 30 minutes is in-
tolerable to some people (Chapter 5,
section B.2.)
(e) Exposure to a concentration of
17,600 Mg/m3 (9.0 ppm) produces
severe illness (Chapter 5, section B.2.)
b. Oxidan ts
(1) Long-term exposure of human
subjects.
Exposure to ambient air containing an
oxidant concentration of about 250
Mg/m3 (0.13 ppm) (maximum daily
value) has caused an increase in the
number of asthmatic attacks in about 5
percent of a group of asthmatic patients.
Such a peak value would be expected to be
associated with a maximum hourly average
concentration of 100 to 120 Mg/m3 (0.05
to 0.06 ppm) (Chapter 9, section B.3.)
(2) Short-term exposure of
human subjects.
(a) Exposure to an atmosphere with peak
oxidant concentrations of 200 Mg/m3
(0.1 ppm) and above has been asso-
ciated with eye irritation. Such a peak
concentration would be expected to
be associated with a maximum hourly
average concentration of 50 to 100
Mg/m3 (0.025 to 0.05 ppm) (Chapter 9,
section B.3.)
(b) Exposure to an atmosphere with aver-
age hourly oxidant concentrations
ranging from 60 to 590 Mg/m3 (0.03 to
0.30 ppm) has been associated with
impairment of performance of stu-
dent athletes (Chapter 9, section B.4.)
2. Other Exposures
a. Photochemical Oxidants
(1) Effects on vegetation and
laboratory animals.
(a) Exposure to concentrations of about
60 Mg/m3 (0.03 ppm) ozone for 8
hours or to 0.01 ppm peroxyacetyl
nitrate for 5 hours has been associa-
ted with the occurence of leaf lesions
in the most sensitive species, under
laboratory conditions (Chapter 6, sec-
tion E.)
(b) Exposure to ambient air containing
oxidant concentrations of about 100
Mg/m3 (0.05 ppm) for 4 hours has
been associated with leaf injury to the
most sensitive species (Chapter 6,
section E.)
(c) Experimental exposures of laboratory
animals to ozone concentrations of
from 160 to 2,550 Mg/m3 (0.08 to
1.30 ppm) for 3 hours has resulted in
increased susceptibility to bacterial
infection (Chapter 8, section B.I.)
b. Ozone Effects on Susceptible Materials
(1) Polymers.
(a) Many polymers, especially rubber, are
extremely sensitive to very small con-
centrations. To provide protection,
/\
antiozonant additives are used, but are
expensive and add to the cost of the
end product (Chapter 7).
(2) Cellulose and dyes.
(a) The cellulose in fabrics is attacked by
ozone, with subsequent weakening of
the fabric. Similarly, certain dyes are
susceptible to fading during exposure
to ozone (Chapter 7). Tables 10-2
10-10
-------
Table 10-2. EFFECTS OF OZONE
Effect
Vegetation damage3
Cracking of stretched rubber
Odor detection
Increased susceptibility of
laboratory animals to
bacterial infection
Respiratory irritation (nose
and throat), chest constriction
Changes in pulmonary function:
Diminished FEVj Q after
8 weeks
Small decrements in VC, FRC,
and DL(->Q in, respectively, 3,
2, and 1 out of 7 subjects
Impaired diffusion
capacity (DL^,O
Increased airway resistance
Reduced VC, severe cough,
inability to concentrate
Acute pulmonary edema
Exposure
ppm
0.03
0.02
0.02
0.08
to
1.30
0.30
0.50
0.20
to
0.30
0.60
to
0.80
0.10
to
1.00
2.00
9.00
Mg/m3
60
40
40
160
to
2,550
590
980
390
to
590
1,180
to
1,570
200
to
1,960
3,900
17,600
Duration
8 hours
1 hour
-------
Table 10-3. EFFECTS ASSOCIATED WITH OXIDANT CONCENTRATIONS IN PHOTOCHEMICAL SMOG
Effect
Vegetation damage
Eye irritation
Aggravation of respiratory
diseases-asthma
Impaired performance of stu-
dent athletes
Exposure,
ppm
0.05
Exce
0.1
0.13a
0.03
to
0.30
jug/m
100
eding
200
250
60
to
590
Duration
4 hours
Peak values
Maximum daily
value
1 hour
Comment
Leaf injury to sensitive species
Result of panel response.
Such a peak value would be expected
to be associated with a maximum
hourly average concentration of
50 to 100 Mg/m3 (0.025 to 0.05 ppm)
Patients exposed to ambient air. Value
refers to oxidant level at which number
of attacks increased
Such a peak value would be expected to
be associated with a maximum hourly
average concentration of 100 to 120
Mg/m3 (0.05 to 0.06 ppm).
Exposure for 1 hour immediately prior
to race
Reference
MacDowall et al
Renzetti and Gobran
Schoettlin and
Landau
Wayne et al.
Calculated from a measured value of 0.25 ppm (phenolphthalein method) which is equivalent to 0.13 ppm by the Kl method.
-------
and 10-3 present these conclusions in
tabular form.
L. RESUME'
Under the conditions prevailing in the areas
where studies were conducted, adverse health
effects, as shown by impairment of perfor-
mance of student athletes, occurred over a
range of hourly average oxidant concentra-
tions from 60 to 590 ng/m3 (0.03 to 0.3
ppm). An increased frequency of asthma
attacks in a small proportion of subjects with
this disease was shown on days when oxidant
concentrations exceeded peak values of 250
jug/m3 (0.13 ppm), a level that would be
associated with an hourly average concentra-
tion ranging from 100 to 120Mg/m3 (0.05 to
0.06 ppm). Adverse health effects, as mani-
fested by eye irritation, were reported by
subjects in several studies when photochemi-
cal oxidant concentrations reached instan-
taneous levels of about 200 Mg/m3 (0.10
ppm), a level that would be associated with an
hourly average concentration ranging from 60
to 100 Mg/m3 (0.03 to 0.05 ppm).
Adverse effects on sensitive vegetation were
observed from exposure to photochemical
oxidant concentrations of about 100 ng/m3
(0.05 ppm) for 4 hours. Adverse effects on
materials from exposure to photochemical
oxidants have not been precisely quantified,
but have been observed at the levels presently
occurring in many urban atmospheres.
It is reasonable and prudent to conclude
that, when promulgating ambient air quality
standards, consideration should be given to
requirements for margins of safety that would
take into account possible effects on health,
vegetation, and materials that might occur
below the lowest of the above levels.
10-13
-------
APPENDIX
CONVERSION BETWEEN VOLUME
AND MASS UNITS OF CONCENTRATION
The physical state of gaseous air pollutants
at atmospheric concentrations generally may
be described 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 = unival gas constant
T = absolute temperature
The number of moles (n) may be calculated
from the weight of pollutant (w) and its
molecular weight (m) by:
n =
w
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).
1 ppm =
106V
(4)
Substituting equation (3) into equation (4)
yields:
ppm =•
w
RT
V pmlO6
(5)
Using the appropriate values for variables in
equation 5 a conversion from volume to mass
units of concentration for 03 may be derived
as shown below.
T = 298° K(25° C)
p = 1 atm
m = 48 g/mole
R = 8.21 x 10'2 e-atm/mole0 K
nmn _ w(g) x 106 Qzg/g)
PP V(C) x 1(T3 (m3/C)
8.21 x 1C)'2 (£-atm/mole0K) x 298(°K)
l(atm) x 48 (g/mole) x 106
1 ppm = 1,960 jug/m3
3 =0.51 x 10'3 ppm
A-l
-------
Subject Index
Adjusted oxidant, 3-7-3-11
Age
correlated with mortality and
oxidant levels, 9-1
Animal data
mechanisms of ozone toxicity,
8-15-8-16
ozone interaction with other
agents, 8-12-8-15
ozone toxicity, 8-1—8-18
prolonged exposure to ozone,
8-10-8-12
sensory irritation, 8-37-8-40
toxicity of peroxyacyl nitrates,
8-35
toxicological effects of oxidants,
8-25-8-35
Asthma
aggravation of, 9-8
Automobile accidents
related to oxidant levels, 9-13
B
Biochemical changes due to effect of
ozone, 8-5-8-8
Bronchitis
aggravation of, 9-8-9-12
California
health surveys, 9-23-9-26,
9-27-9-30
Cardiac diseases
oxidant levels and mortality,
9-5-9-6
Chemical and biochemical change
in pulmonary organs from ozone,
8C O O
-J— 0-6
Chronic effects of oxidants
community satisfaction, 9-27—9-30
general, 9-20-9-21
lung cancer mortality, 9-2 1
mortality, 9-21-9-23
respiratory disease mortality,
9-22-9-23
Chronic respiratory diseases
mortality and oxidant levels,
9-22--9-23
Community satisfaction
effect of pollution on, 9-27-9-30
state of California health survey,
9-27-9-29
survey of Los Angeles physicians,
9-29-9-30
Criteria
development of, 1-1-1-2
D
Daily mortality
acute effects of oxidants, 9-1 -9-7
oxidants-two-community study,
9-4-9-5
Diurnal variations
of oxidant concentrations, 3-4—3-6
Dose injury relationships
to pollutants on plants, 6-7—6-12
Dyes
ozone fading, 7-4— 7-6
Emphysema
aggravation of, 9-8—9-12
Epidemiological appraisal
of photochemical oxidants,
9-1-9-32
Epidemiological studies
acute effects of oxidant,
9-1-9-20
chronic effects of oxidants,
9-20 9-30
Experimental exposure
to ozone, 8-19-8-24
Eye irritation
among student nurses, 9-16
control filters, 9-16-9-18
in animals, 8-35-8-38
in humans, 8-38-8-39
panel studies, 9-14-9-16
related to oxidant levels,
9-14-9-20
Fabrics
effect of ozone on, 14
Fading
of dyes by ozone, 74—7-6
Filters
removal of eye irritants, 9-16—9-18
Formation Processes
hydrocarbon reactivity, 2-8—2-10
nitric oxide, 2-3-2-6, 2-10.-2-11
nitrogen dioxide, 2-3—2-6,
2-10-2-11
nitrogen dioxide photolytic cycle,
2-3-2-6
ozone, 2-3—2-6
H
Health surveys
morbidity and oxidants,
9-23-9-26, 9-27-9-30
Heat waves
oxidant levels and mortality,
9-1 9-3
Hospital admissions
Los Angeles county, 9-7
Los Angeles metropolitan area,
9-7-9-8
related to oxidant levels, 9-7-9-8
Human data
experimental studies of eye irrita-
tion, 8-38-8-39
olfactory effects from pollutants,
8-38
ozone exposure, 8-18—8-19
peroxyacyl nitrate toxicity, 8-35
sensory irritation, 8-35-8-40
toxicological effects of ozone,
8-18-8-25
Hydrocarbons
interaction with nitrogen dioxide
photolysis, 2-6-2-8
reactivity, 2-8-2-10
I
Immunology and exposure to
ozone, 8-8-8-9
1-1
-------
Impairment of performance
associated with oxidant levels,
9-12-9-14
Interferences
in oxidant measurement, 3-6—3-7
Los Angeles
survey of physicians, 9-29—9-30
Los Angeles Basin
transport of pollutants, 3-15—3-17
Los Angeles County
hospital admissions, 9-7
Los Angeles metropolitan area
hospital admissions, 9-7—9-8
Lung cancer
mortality and oxidant levels, 9-2 1
Lung tumors from exposure to
oxidants, 8-32-8-33
M
Materials deterioration
ozone attack mechanisms, 7-1
Measurement methods
ozone, 5-5—5-6
peroxyacetyl nitrate, 5-6—5-7
total oxidants, 5-3—5-5
Mechanisms
of ozone toxicity, 8-15—8-16
Meterological effects
sunlight, 2-11-2-13
temperature, 2-13
Microorganisms
effects of ozone on, 6-12—6-18
effects of photochemical oxidants,
6-12
Monitoring programs, 3-1—3-2
Monitoring stations
location as related to oxidant
concentration, 3-17
Morbidity
related to oxidant levels,
9-23-9-27
respiratory disease survey,
telephone workers, 9-26
State of California health survey,
9-23-9-26
Mortality
chronic effects of oxidants,
9-21-9-23
chronic respiratory diseases, 9-22
heat waves and oxidant levels,
9-1-9-3
of nursing home residents, 9-4
related to age, 9-1
related to cardiac and respiratory
diseases, 9-5—9-6
related to lung cancer, 9-21
related to oxidant levels, 9-1—9-7
9-21-9-23
N
Nitric oxide
interference in oxidant
measurement, 3-7
Nitrogen dioxide
formation processes, 2-3—2-6,
2-10-2-11
interference in oxidant
measurement 3-6—3-7
Nitrogen dioxide photolytic cycle,
2-3-2-6
hydrocarbon interactions, 2-6—2-8
Non-urban areas
ozone concentrations, 4-1 —4-3
o
Occupational exposure to ozone,
8-18-8-19
Olfactory effects
of photochemical oxidants, 8-38
Oxidant concentrations
as related to location of monitoring
station, 3-17
diurnal variations, 3^t—3-6
in urban atmospheres, 3-1—3-7
meteorological factors, 3-14—3-17
patterns, 3-2-3^
seasonal variations, 3^—3-6
transport, 3-15-3-17
Oxidant concentration
transport, 3-15-3-17
Oxidant levels
heat waves and mortality, 9-1—9-3
re'ated to automobile accidents,
9-13
related to daily mortality,
9-1-9-7
related to hospital admissions,
9-7-9-8
related to morbidity, 9-23-9-27
related to mortality, 9-21-9-23
related to mortality of nursing
home residents, 9-4
Oxidant measurement—see
Total oxidants measurement
Oxidants
acute effects of, 9-1 -9-20
adjusted, 3-7-3-11
effect on microorganisms, 6-12
effects on pulmonary tissues,
8-25-8-33
measurement interferences,
3-6-3-7
toxicological effects of,
8-25-8-35
Oxidant toxicity
animal data, 8-25-8-35
changes in fertility and neonatal
mortality, 8-33
changes in pulmonary function,
8-25-8-28
development of lung tumors,
8-32 8-33
pathological changes in pulmonary
tissues, 8-28-8-32
stress response, 8-33
systemic effects, 8-33
Ozone
damage to textile fabrics, 7-4
effects on materials, 7-1—7-7
effects on microorganisms,
6-12-6-18
effects of prolonged exposure,
8-10-8-12
effects on dyes, 7^—7-6
effects on rubber, 7-1-7-4
injury to plants, 6-2—6-3,
6-13-6-17
natural sources, 4-1
physical properties, 2-2
reaction mechanisms of attack on
materials, 7-1
sensitivity of plants, 6-13—6-17
1-2
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transfer mechanisms, 4-1 -4-3
Ozone concentration
adjusted oxidants, 3-7-3-11
correlation with oxidant
concentration, 3-7-3-11
non-urban areas, 4-1—4-3
patterns of, 3-11
upper atmosphere, 4-1
urban atmospheres, 3-7—3-11
Ozone exposure
aging, 8-10-8-11
development of tolerance,
8-11-8-12
long term pulmonary effects, 8-10
lung tumor acceleration, 8-10
related to increased
susceptibility to bacterial
infection, 8-12-8-14
bacterial infection, 8-12—8-14
related to increased susceptibility
to histamine, 8-14-8-15
histamine, 8-14-8-15
Ozone measurement methods
chemiluminescence, 5-5
rubber cracking, 5-6
ultraviolet photometry, 5-6
Ozone toxicity
effects on pulmonary organs ,
8-3-8-8
effects on the heart, liver, and
brain, 8-9-8-10
immunology, 8-8—8-9
mechanisms in animals, 8-15—8-16
systemic effects, 8-8-8-10
Pathological changes
from acute ozone exposure, 8-5
Patients
oxidant levels and mortality of, 9-4
Performance impairment
athletic performance, 9-12-9-13
automobile drivers, 9-13
ventilatory performance,
9-13-9-14
Peroxyacetyl nitrate
formation of, 2-9-2-10
physical properties, 2-3
Peroxyacetyl nitrate concentrations
measurement of, 3-11—3-14
urban atmospheres, 3-11—3-14
Peroxyacetyl nitrate measurement
gas chromatography, 5-7
long path infrared spectroscopy,
5-6-5-7
Peroxyacyl nitrates toxicity
human data, 8-35
Peroxyacyl nitrates
injury to plants, 6-2—6-3
lethality, 8-35
toxicological appraisal, 8-35
Physicians
Los Angeles morbidity studies,
9-29-9-30
Phytotoxicants
general discussion of, 6-1
Plant damage
diagnosis of, 6-6—6-7
Plant indicators
general discussion of, 6-1.
Plant injury
caused by peroxyacyl nitrate,
6-2-6-3
diagnosis of, 6-6—6-7
ozone effects, 6-2
threshold levels for ozone,
6-7-6-12
Plant response
environmental factors, 64—6-5
general, 6-5—6-6
genetic factors, 6-3—6-4
Plants
dose injury relationships, 6-7—6-12
response to photochemical
pollutants, 6-1-6-6
sensitivity to ozone, 6-13—6-17
Potassium iodide colorimetric
method, 5-1-5-3
Public attitudes
see community satisfaction
Pulmonary function
effects of peroxyacyl nitrates on,
8O Of Q T C
-j — o-j , o-o J
effects of oxidants on, 8-25-8-28
effects of ozone exposure on,
8-3-8-8,8-18,8-19-8-25
Pulmonary Organs
chemical and biochemical changes,
8-5-8-8
pathological changes, 8-5
toxicological effects of ozone on,
8-3
Pulmonary tissues
effects of oxidant exposure on,
8-25-8-33
R
Reactant concentration studies
atmospheric, 2-15-2-17
environmental chambers,
2-13-2-15
Reaction mechanisms
of ozone attack on materials, 7-1
Reference method
use in measurement of total
oxidants, 5-1—5-3
Respiratory diseases
aggravation by oxidants, 9-8—9-12
asthma, 9-8
bronchitis, 9-8-9-12
emphysema, 9-8—9-12
oxidant levels and mortality,
9-5-9-6,9-22-9-23
Rubber
effects of ozone, 5-6, 7-1 -7-4
Seasonal variations
of oxidant concentrations, 3-4—3-6
Sensitivity
of plants to ozone, 6-13—6-17
Sensory irritation
by photochemical oxidants,
8-35-8-40
human data, 8-35-840
olfactory effects, 8-38
Sulfur dioxide
interference in oxidant
measurement, 3-6
1-3
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Sunlight
effect on oxidant formation,
2-11-2-13
Surveys
chronic respiratory disease, 9-26
community satisfaction, 9-27—9-30
morbidity oxidants, 9-23-9-26,
Symptoms
plant injury by photochemical
pollution, 6-2—6-3
Systemic effects
oxidant exposure, 8-33
Telephone workers
chronic respiratory disease survey,
9-26
Temperature
effect on oxidant formation, 2-13
Thresholds
plant injury from ozone, 6-7—6-12
Time-concentration relationship
plant injury, 6-7—6-12
Tolerance
development of to ozone exposure,
8-11 8-12
Total oxidants
discussion of measurement, 5-1
stratospheric ozone, 4-1—4-2
Total oxidants measurement
alkaline KI method, 5-5
colorimetric methods, 5-3—5-5
coulometric methods, 5-3—5-5
ferrous ammonium sulfate, 5-5
phenolphthalein method. 5-5
Toxicity of ozone on animals,
8-1-8-17
Toxicological effects
of exposure to oxidants, 8-25—8-35
of exposure to ozone, 8-1—8-25
of ozone on pulmonary organs,
8-3-8-8
of peroxyacyl nitrates exposure,
8-35
sensory irritations, 8-35—8-40
Transport
as related to oxidant
concentrations, 3-15—3-17
u
Urban atmospheres
oxidant concentration, 3-1—3-7
ozone concentrations, 3-7—3-11
peroxyacetyl nitrate concentration,
3-11-3-14
Vegetation
diagnosis of pollution effects on,
6-6-6-7
economic impact of photochemical
pollution on, 6-6—6-7
sensitivity to photochemical
pollutions, 6-1 —6-6
symptoms of pollution effects,
6-2-6-3
ventilatory performance related to
oxidant levels, 9-13-9-14
14
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