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

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 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

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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

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 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

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      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

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                                      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

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 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

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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

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    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

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     (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

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 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

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                                      NITROGEN
                                       DIOXIDE
                                         (N02)
                 HYDROCARBON
                 FREE RADICAL
                      (R02)
Figure 2-3.  Interaction of hydrocarbons with atmospheric nitrogen dioxide photolytic cycle.
                                                                                      2-7

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 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

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                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.

I.  REFERENCES
 l.Aii Quality Criteria for Sulfur Oxides. U.S. DHEW, PHS,
  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
                                                                                         2-19

-------
    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-
    tion  of Organic Compound-Nitric Oxide Mixtures in Air.
    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-
   ature on Photochemical  Smog Reactions. Intern.  J. Air
   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

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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

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                                     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

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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

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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

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 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.
5-8

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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

-------
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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    by Damage to Vegetation. In: Proceedings of the 3rd
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 67. Taylor, O.C.  and  D.   Maclean.  Recognition  of Air
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 68. Feder, W.A. and F.J. Campbell. Influence of Low levels
    of  Ozone  Flowering of Carnations.  Phytopathology.
    55:1038-1039, July 1968.
 69. Menser, H.A.  et  al. Air Filtration of "Hidden" Air       87.
    Pollution  Injury  to Tobacco  Plants.  Plant Physiol.
    39-.LVU1,  1964.
 70. Taylor, O.C. Air Pollution with Relation to Agronomic        88.
    Crops: IV. Plant Growth  Suppressed  by Exposure to
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    September 1958.
 71. Hill, A.C., and N. littlefield. Ozone: Effect on Apparent        89.
    Photosynthesis, Rate of Transpiration, and Stomatal
    Closure in  Plants.  Environ.  Sci. Technol. 5:52-56,
    January 1969.
 72. Dugger, W.M., Jr., J. Koukol, and R.L.  Palmer. Physio-        90.
    logical  and  Biochemical Effects  of Atmospheric Oxi-
    dants  on  Plants.  J.  Air  Pollution  Control  Assoc.
    76:467471, September 1966.
 73. Heck, W.W.  Factors Influencing Expression of Oxidant        91.
    Damage  to  Plants.  In:   Annual  Review  of  Phy-
    topathology,  Vol.  6, Horsfall, J.G. and  K.F.  Baker
    (eds.).  Palo Alto,  Annual  Reviews,   Inc.,  1968. p.        ^2.
    165-188.
 74. Berry, C.R. and H.G. Hepting.  Injury to Eastern White
    Pine by Unidentified Atmospheric Constituents. Forest        93
    Sci. .70:2-13,1964.
 75. Feder,  W.A. et  al. Varietal Responses of Petunia to
    Several Air Pollutants.  Plant Dis. Reptr. 55:506-510,        94
    1969.
 76. Menser, H.A., Jr. Effects of Air Pollution  on Tobacco
    Cultiuars Grown  in  Several States.  Tobacco. 20-25,
    1969.                                                     95
 77. Reinert, R.A.,  D.T. Tingey, and H.C. Carter. Varietal
    Sensitivity of Tomato and Radish to Ozone. Horticul-        96
    turalSci. 4:106,1969.
 78. Tingey, D.T., R.A. Reinert, and  H.C. Carter. Differential

6-22
 Sensitivity  of  Soybean  Varieties to  Ozone.  Agron.
 Abstr. 1969. p. 34.
 Engle, R.L., W.H. Gableman, and R.R. Romanowski, Jr.
 Tipburn, an Ozone Incited Response in Onion, Allium
 cepa L.  Proc. Amer. Soc. Horticultural Sci. 56:468474,
 1965.
 Engle, R.L. and W.H.  Gableman. Inheritance and Mech-
 anism for Resistance to Ozone Damage in Onion, Allium
 cepa L. Proc. Amer. Horticultural Sci. 59:423, 1966.
 Feder, W.A. Reduction in Tobacco Pollen Germination
 and Tube Elongation, Induced by Low Levels of Ozone.
 Science. 760(3832):! 122, June 7, 1968.
 Dugger,  W.M., Jr. et  al. The  Effect  of light  on
 Predisposing Plants to Ozone and PAN Damage. J. Air
 Pollution Control Assoc. 18: 423428, September 1963.
 Heck, W.W. and J.A. Dunning. The Effects of Ozone on
 Tobacco and  Pinto Bean  as  Conditioned by  Several
 Ecological  Factors. J.  Air Pollution  Control Assoc.
 77:112-114, February 1967.
 Ting, I.P. and W.M. Dugger, Jr. Factors Affecting Ozone
 Sensitivity and Susceptibility of Cotton  Plants. J. Air
 Pollution Control Assoc. 75:810-813, December 1968.
 Heck, W.W., J.A. Dunning,  and I.J.  Hindawi. Inter-
 actions of Environmental Factors on the Sensitivity of
 Plants to Air Pollution. J. Air Pollution Control Assoc.
 75:511-515, November 1965.
 Menser,  H.A.,  Jr.  The  Effects  of  Ozone and  Con-
 trolled-Environment Factors on Four Varieties of To-
 bacco (Nicotiana  tabacum L.). University of Maryland.
 College Park. Ph. D. Thesis,  1962.
 Otto, H.W.  and  R.H.  Daines.  Plant  Injury by» Air
 Pollutants;  Influence  on  Stomatal Apertures to Plant
 Response on Ozone. Science. 760:1209-1210, 1968.
 Heggestad, H.E. et al.  Leaf Injury on Tobacco Varieties
 Resulting from Ozone, Ozonated Hexen-1, and Ambient
 Air of Metropolitan Areas. Int. J. Air Water Pollution.
 5:1-10, January 1964.
 Heck, W.W. Plant  Injury  Induced  by Photochemical
 Reaction Products of  Propylene-Nitrogen Dioxide Mix-
 tures. J. Air Pollution Control Assoc. 74:255-261, July
 1964.
 Guderian, R.,  H.  van Haut, and H. Stratmann. The
 Estimation  and Evaluation of  the Effects of Atmos-
 pheric Gas Pollutants  Upon Vegetations.  Z. Pflanzenk.
 Pflanzenschutz. 67(5):257-264,1960.
. Hill, G.R., Jr. and M.D. Thomas.  Influence  of Leaf
 Destruction by  Sulfur Dioxide and by Clipping on Yield
 of Alfalfa. Plant Physiol. 5:223-245, 1933.
. Dugger,  W.M.,  Jr. et al. Effect of Peroxyacetyl Nitrate
 on C  02 Fixation by Spinach Chloroplasts and Pinto
 Bean Plants. Plant Physio. 55(4):468472, July 1963.
.Thomson, W.W.,  W.M. Dugger, Jr., and  R.L. Palmer.
 Effects of Peroxyacetyl Nitrate on the Ultrastructure of
 Chloroplasts. Botan. Gaz.  726(l):66-72, March 1965.
. O'Gara,  P.J. Sulfur Dioxide and  Fume Problems and
 Their Solutions. In: The 14th  Semiannual Meeting of
 the American  Institute of Chemcial Engineers. J. Ind.
 Eng. Chem. 74:744-745. August 1, 1922.
. Heggestad,  H.E. Ozone as a Tobacco Toxicant.  J. Air
 Pollution Control Assoc.  76:691-694, December 1966.
. Heck, W.W., J.A.  Dunning, and I.J. Hindawi. Ozone:
 Non-Linear  Relation  of Dose and  Injury in  Plants.
 Science. 757(3710):577-578, February 4,1966.

-------
 97. Menser, H.A., H.E.  Heggestad, and  O.E. Street. Re-
    sponse of Plants to Air Pollutants. II.  Effects of Ozone
    Concentration and Leafy Maturity on Injury to Nico-
    tiana  tobacum. Phytopathology.  55:1304-1308,  Nov-
    ember 1963.
 98. Hill,  A.C.  et al. Plant Injury  Induced  by  Ozone.
    Phytopathology. 51 :356-363, June 1961.
 99. Menser, H.A. and G.H. Hodges. Varietal Tolerance of
    Tobacco to Ozone Dose Rate. Agron. J. 60(4):349-352,
    July-August 1968.
100. Ledbetter, M.C., P.W. Zimmerman, and A.E. Hitchcock.
    The  Histopathological  Effects  of  Ozone on  Plant Fo-
    liage.  Contributions from  Boyce  Thompson  Institute.
    20(4):275-282, October-December 1959.
101. Taylor,  O.C.  and  J.T. Middleton.  Susceptibility to Air
    Pollutants: Spermatophytes. In: Environmental Biology,
    Altaian, P.L.  and D.S. Dittmer (eds.). Washington,  D.C.,
    Federation  of American  Societies for Experimental
    Biology, 1966. p. 310-316.
102. Miller, P.R. et al.  Ozone Injury to the  Foliage of Pinus
    ponderosa. Phytopathology. 55:1072-1077, September
    1963.
103. Taylor,  O.C. and J.D. Mersereau. Smog  Damage  to
    Cotton. Calif. Agr. 1 7:2-3, November 1963.
104. Goetz, A. and N.  Tsuneishi. A Bacteriological Irritation
    Analogue    for   Aerosols.   Arch.  Ind.   Health.
    20(2):167-180, August  1959.
105. Hill, L.H. and M. Flack. The Physiological Influence of
    Ozone.  Proc.   Roy.  Soc.   (London),   Series  B.
    S4(B573):404-415, December 28, 1912.
106. Sawyer, W.A., H.L. Beckwith, and E.M. Skolfield. The
    Alleged Purification  of Air by  the Ozone  Machine. J.
    Amer. Med.  Assoc. 61 (13): 1013-1015, September 27,
    1913.
107. Kendall, A.I. and A.U. Walker. The Effects  of Ozone
    upon Certain Bacteria  and  Their Respective  Phages:
    Studies in  Bacterial  Metabolism. J.  Infectious Dis.
    55:204-214, March-April 1936.
108. Hibben, C.R. Sensitivity of  Fungal Spores to Sulphur
    Dioxide and  Ozone.  Phytopathology. 5(5:880-881, Au-
    gust 1966.
109. Rich,  S. And H. Tomlinson.  Ozone  Injury to  Con-
    diophores ofAltemaria solani. Phytopathology. 56:896,
    August 1966.
110. Christensen, E. and A.C. Giese. Changes in Absorption
    Spectra of Nucleic  Acids and Their  Derivatives Fol-
    lowing Exposure to Ozone and Ultraviolet Radiations.
    Arch. Biochem. Biophys. 51:208-216, July 1954.
111.  Scott, D.B.M. and E.C. Lesher. Effect of Ozone  on
     Survival  and Permeability of Escherichia coli.  J. Bac-
     teriol. 55:567, 1963.
112. Fetner, R.H.  and R.S. Ingols. A Comparison of the
     Bactericidal Activity  of Ozone and Chlorine  Against
     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

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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

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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
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                                      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

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                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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    Pollution Control Assoc. 70(1):17-20, February 1960.
88. Mettier,  S.R., Jr. et al. A  Study of the Effects  of Air
    Pollutants on the  Eye. Arch.  Ind. Health. 27:1-6,
    January  1960.
89. Witheridge, W.N. and Cf. Yaglou. Ozone in Ventilation:
    Its  Possibilities  and Limitations. Trans.  Amer. Soc.
    Heating Ventilation Eng. 45:509-520, July 1939.
90. Henschler, D. et  al. The  Odor  Threshold of Some
    Important Irritant Gases (Sulfur  Dioxide, Ozone, Nitro-
    gen Dioxide) and  the Manifestations of the Effect of
    Small Concentrations on Man  [Geruchsschwellen einiger
    Wichtiger Reizgase  (Schwefeldioxyd, Ozon,  Stickstoff-
    dioxyd)  und Erscheinungen bei der Einwirkung Geringer
    Konzentrationen a u f den Menschen]. Arch. Gewerbe-
    pathol. Gewerbehyg. 77:547-570, 1960.
91. Schuck,  E.A. and G.J. Doyle. Photooxidation of Hydro-
    carbons  in Mixtures Containing Oxides of Nitrogen and
    Sulfur Dioxide.  Air Pollution Foundation Report Num-
    ber 29. San Marino, California, October 1959. 104 p.
92. Stephens, E.R. et al. Photochemical Reaction Products
    in  Air   Pollution.  Air  Water   Pollution  Intern.  J.
    4(]/2):79-100, June 1961.
93. Heuss, J.M. and W.A. Glasson. Hydrocarbon Reactivity
    and Eye Irritation.  Environ.Sci.  Technol. 2:1109-1116,
    December 1968.
94. Hamming, W.J.,  W.G. MacBeth, and  R.L. Chass. The
    Photochemical Air Pollution Syndrome. Exhibited by
    Attack  of  October 1965.   Arch.  Environ.  Health.
    74:137-149, January 1967.
8-44

-------
                                     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
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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

-------
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
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   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.
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   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:
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   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
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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-
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    1965.
25. Sawicki, E.  Airborne  Carcinogens  and Allied Com-
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26  Buell, P., J.E. Dunn, Jr., and L. Breslow. Cancer of the
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    Study. Cancer. 20:2139-2147, December 1967.
27. Winklestein, W. et al. The Relationship of Air Pollution
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28. Winkelstein,  W.,  Jr. et  al.  The  Relationship of Air
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    Selected  Respiratory  System  Mortality in Men.  II.
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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
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    Adult  Population.   Amer.  Rev.  Respirat.  Diseases.
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31. Deane, M., J.R. Goldsmith,  and D.  Tuma. Respiratory
    Conditions in Outside Workers: Report on Outside Plant
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32. Physicians  Environmental Health Survey:  A  Poll  of
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    Angeles, Calif. May 1961.
                                                                                                              9-33

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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

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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

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  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

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  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

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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

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   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

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 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

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     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

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                                                    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


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                    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.

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        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

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                                     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

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                                               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

-------
 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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