ponpr,,'-} v • •
            VT.\ .. _ n US           t PA - 450/3 - 78 -005
•
.Diagnosing  Vegetation
I    Injury Caused   By
•       Air, Pollution
•     PROPER™ OF
_      DIVISION
I        OF
_     METEOROLOGY
I                 BY
          APPLIED SCIENCE ASSOCIATES, INC.
_            VALENCIA, PA. 16059
            CONTRACT NO. 68 - 02 - 1344
I

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         EPA PROJECT OFFICER: DAVID R. HICKS
         AIR POLLUTION TRAINING INSTITUTE
           PREPARED FOR

   U.S. ENVIRONMENTAL PROTECTION AGENCY
   OFFICE OF AIR AND WASTE MANAGEMENT
OFFICE OF AIR QUALITY PLANNING AND STANDARDS
  CONTROL PROGRAMS DEVELOPMENT DIVISION
    RESEARCH TRIANGLE PARK, N. C.  27711
           FEBRUARY 1978

 For sale by the Superintendent of Documents, U.S. Government Printing Office, Washington, D.C. 20402
           Stock No. 055-003-00088-2

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USEPA
                 SELF INSTRUCTIONAL

            TRAINING COURSE AVAILABLE
   A Self-Instructional Training Course # Sl:448 "Air Pollution Effects
on Vegetation" has been developed by EPA and compliments this
Handbook. Sl:448 consists of 35 mm. slides, booklets, audio cassette
tapes and quizzes with answers at the end of each unit. Tests required
for receipt of a certificate of completion may be obtained from the
Registrar, Air Pollution Training Institute, MD-20, Research Triangle
Park, North Carolina 27711.

   The SI Course may be purchased from the National Audiovisual
Center, Washington, D.C., ATTN. Order Section. Price of the Course
has not been established at this printing.
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   This is not an official policy and standards document. The opin-
ions, findings, and conclusions are those of the authors and not
necessarily those of the  United States  Environmental Protection
Agency. Every attempt has been made to represent the present state
of the art as well as the subject areas still under evaluation. Any men-       •
tion of products, or organizations, does not constitute endorsement       H
by the United States Environmental  Protection Agency.
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                              FOREWORD



     This handbook was written for the Environmental Protection Agency

                      by the following individuals.

              The EPA gratefully acknowledges their assistance.


Editors:
   Dr. Norman L. Lacasse	 Spring Mills, Pennsylvania
   Dr. Michael Treshow	 University of Utah

Contributors:
   Dr. Charles E. Anderson	 North Carolina State University
   Mr. Neil W. Blahut  	 Applied Science  Associates, Inc.
                                       Valencia, Pennsylvania
   Dr. Robert H. Daines  	 Rutgers University
   Dr. Donald D. Davis	 Pennsylvania State University
   Dr. William A. Feder	 University of Massachusetts
   Mr. Reid P. Joyce	 Applied Science  Associates, Inc.
                                       Valencia, Pennsylvania
   Dr. Norman L. Lacasse	 Spring Mills, Pennsylvania
   Dr. David C. MacLean	 Boyce Thompson Institute for
                                       Plant Research
   Dr. Delbert C. McCune	 Boyce Thompson Institute for
                                       Plant Research
   Dr. John M. Skelly	 Virginia Polytechnic Institute

Advice and assistance provided by:
   Dr. Walter W. Heck	 ARS, USDA, Raleigh, N.  C.
   Dr. David T. Tingey  	 NERL, EPA, Corvallis, Oregon
   Dr. Donald Gillette	 HSL, NERC, EPA, Research
                                       Triangle Park, N. C.
   Mr. Stanley F. Sleva	 Chief, L&SS, APTI, NERC, EPA,
                                       Research Triangle Park,  N. C.
   Mr. James L. Dicke	 Chief, AQMS, APTI, NERC, EPA,
                                       Research Triangle Park,  N. C.
   Ms. Anne S. Rampacek	 IDS, APTI, NERC, EPA,  Research
                                       Triangle Park, N. C.
   Mr. Robert Wood  	 IDS, APTI, NERC, EPA,  Research
                                       Triangle Park, N. C.

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Color prints were contributed by the following institutions:

   Arizona State University

   Boyce Thompson Institute for Plant Research

   Michigan State University

   National Ecological Research Laboratory

   North Carolina State University

   Phytotoxicology Laboratory, Department of Health, Ontario, Canada

   Pennsylvania State University

   Rutgers University

   University of California (Riverside)

   University of Utah

   United States Department of Agriculture

   United States Environmental Protection Agency

   Virginia Polytechnic Institute
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                       TABLE OF CONTENTS
Chapter 1.  Introduction to Diagnosis of Air Pollution
           Damage to Vegetation ...............................  1-1
Selected References ..........................................  1-6

Chapter 2.  Structure and Function of Plants in Relation
           to Air Pollution Injury ...............................  2-1
Introduction ................................................  2-1
Plant Cell Ultrastructure .......................................  2-1
Plant Organs ................................................  2-3
Roots [[[  2-3
Stems [[[  2-6
Leaves  [[[  2-8
Flowers, Fruits and Seeds ......................................  2-12
Selected References ..........................................  2-13

Chapter 3.  The Photochemical Oxidants ..........................  3-1
Introduction ................................................  3-1
   SECTION 1 .  OZONE ......................................  3-2
   Sources  .................................................  3-2
   Atmospheric Chemistry .....................................  3-4
   Monitoring Data  ..........................................  3-7
   Symptomatology ..........................................  3-8
   Factors Affecting Plant Response  .............................  3-1 1
   Injury Threshold Doses .....................................  3-12
   Air Quality Standards ......................................  3-13
   Relative Sensitivity of Plants to Ozone .........................  3-14
   Leaf Tissue Analysis  .......................................  3-1 6
   SECTION 2.  PAN .........................................  3-17
   Introduction .............................................  3-17
   Symptomatology ..........................................  3-17
   Factors Affecting Plant Response  .............................  3-19
   Injury Threshold Doses .....................................  3-19
   Air Quality Standards ......................................  3-19
   Relative Sensitivity of Plants to PAN ...........................  3-19
   Leaf Tissue Analysis  .......................................  3-2 1
   SECTION 3.  OXIDES OF NITROGEN ........................  3-22
   Introduction .............................................  3-22

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                                                                     Page

   Symptomatology	  3-26
   Factors Affecting Plant Response  	  3-27
   Injury Threshold Doses	  3-28
   Air Quality Standards 	  3-29
   Relative Sensitivity of Plants to NO2	  3-29
   Leaf Tissue Analysis  	  3-31
Selected References   	  3-31

Chapter 4.  Sulfur Dioxide	  4-1
Introduction	  4-1
Sources	  4-1
Atmospheric Chemistry	  4-2
Monitoring Data	  4-2
Symptomatology	  4-4
Factors Affecting Plant Response	  4-6
Injury Threshold Doses  	  4-8
Air Quality Standards	  4-10
Relative Sensitivity of Plants to SO2  	  4-10
Leaf Tissue Analysis	  4-11
Selected References	  4-11

Chapter 5.  Fluorides	  5-1
Introduction	  5-1
Sources	  5-1
Atmospheric Chemistry  	  5-3
Monitoring Data	  5-4
Symptomatology	  5-4
Factors Affecting Plant Response	  5-10
Injury Threshold Doses  	  5-1 3
Air Quality Standards	  5-17
Relative Sensitivity of Plants to HF	  5-17
Leaf Tissue Analysis	  5-17
Selected References	  5-18

Chapter 6.  Minor Pollutants  	  6-1
Introduction	  6-1
   SECTION 1.  CHLORINE	  6-2
   Introduction  	  6-2
   Sources  	  6-2
   Atmospheric  Chemistry	  6-2
   Monitoring Data 	  6-3
   Symptomatology	  6-3
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                                                                  Page

Factors Affecting Plant Response  	  6-4
Injury Threshold Doses	  6-4
Air Quality Standards  	  6-4
Relative Sensitivity of Plants to Chlorine	  6-4
Leaf Tissue Analysis  	  6-5
SECTION 2.  HYDROGEN CHLORIDE	  6-6
Introduction  	  6-6
Sources  	  6-6
Atmospheric Chemistry	  6-6
Monitoring Data 	  6-7
Symptomatology	  6-7
Factors Affecting Plant Response  	  6-7
Injury Threshold	  6-8
Air Quality Standards  	  6-8
Relative Sensitivity of Plants to Hydrogen Chloride  	  6-8
Leaf Tissue Analysis  	  6-9
SECTION 3.  ETHYLENE	  6-10
Introduction  	  6-10
Sources  	  6-10
Atmospheric Chemistry	  6-10
Monitoring Data 	  6-11
Symptomatology	  6-11
Factors Affecting Plant Response  	  6-13
Air Quality Standards  	  6-13
Relative Sensitivity of Plants to Ethylene 	  6-14
Leaf Tissue Analysis  	  6-14
SECTION 4.  AMMONIA  	  6-15
Introduction  	  6-15
Sources  	  6-15
Atmospheric Chemistry	  6-15
Monitoring Data 	  6-15
Symptomatology	  6-16
Factors Affecting Plant Response  	  6-16
Injury Threshold	  6-17
Air Quality Standards  	  6-17
Relative Sensitivity of Plants to Ammonia	  6-17
Leaf Tissue Analysis  	  6-17
SECTION 5.  HYDROGEN SULFIDE	  6-18
Introduction  	  6-18
Sources  	  6-18
Atmospheric Chemistry	  6-18
Monitoring Data 	  6-18
Symptomatology	  6-18

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                                                                    Page

   Factors Affecting Plant Response 	  6-19
   Injury Threshold	  6-19
   Air Quality Standards 	  6-19
   Relative Sensitivity of Plants to Hydrogen Sulfide	  6-19
   Leaf Tissue Analysis 	  6-19
   SECTION 6. CARBON MONOXIDE  	  6-21
   Introduction  	  6-21
   Sources  	  6-21
   Symptomatology	  6-21
   SECTION 7. HEAVY METALS	  6-23
   Introduction  	  6-23
   Lead  	  6-23
   Zinc, Cadmium and Copper	  6-24
   Mercury Vapors	  6-24
   Relative Sensitivity of Plants to Mercury Vapors	  6-25
   Leaf Tissue Analysis 	  6-26
   SECTION 8. PARTICULATE MATTER  	  6-27
   Introduction  	  6-27
   Sources  	  6-27
   Atmospheric Chemistry	  6-27
   Symptomatology	  6-27
   Air Quality Standards  	  6-28
   SECTION 9. PESTICIDES 	  6-29
   Introduction  	  6-29
   Sources  	  6-29
   Symptomatology	  6-30
   Relative Sensitivity of Plants to Pesticides	  6-30
   Leaf Tissue Analysis 	  6-30
Selected References	  6-32

Chapter 7.  Interactions Between Pollutants and Between
           Pollutants and Pathogens	  7-1
Pollutant — Pollutant Interactions	  7-1
Pollutant — Pathogen Interactions	  7-5
Selected References	  7-6

Chapter 8.  Mimicking Symptoms 	  8-1
Abiotic Agents	  8-1
Biotic Agents	  8-5
Teratogenic Agents	  8-7
Summary	  8-7
Selected References	  8-8
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                                                                     Page

Chapter 9.  Meteorology and Air Pollution Injury
           to Vegetation	  9-1

Sources of Air Pollution	  9-1
Meteorological Aspects of Air Pollution	  9-2
Effects of Topography on Dispersion	  9-7


Chapter 10.  Diagnosis of Suspected Air Pollution
            Injury to Vegetation	10-1

Diagnosis — Basic Procedure	10-1
Diagnosis — Systematic Approach  	10-5
Diagnostic Routine	10-8


Appendix A.   Conversion Factors  	A-l


Appendix B.   National Primary and Secondary Air
              Quality Standards  	  B-l


Appendix C.   Composite Sensitivity Chart and Scientific
              Names of Plants	C-l


Appendix D.   Bio-Indicators  	D-l


Appendix E.   Glossary of Air Pollution and Botanical Terms 	E-l

Index	Index-!

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                           LIST OF TABLES
Table No.                                                             Page
   3-1      Data Showing Long-term Trends in Oxidant
           Concentrations  Recorded at CAMP Sites from 1964
           to 1967 in Four Large Urban Areas	  3-7
   3-2      Threshold Doses of Ozone Needed to Cause Injury
           to Plants Grown Under Sensitive Conditions	  3-13
   3-3      Relative Sensitivity of Various Plants
           to Ozone	  3-14
   3-4      Relative Sensitivity of Various Plants to PAN	  3-20
   3-5      Relative Sensitivity of Various Plants to NO2  	  3-29
   4-1      Estimated Total Nationwide SO2 Emissions
           Levels, 1940-1970	  4-2
   4-2      Nationwide Estimates of SO2  Emissions from
           Various Sources During  1970  	  4-3
   4-3      Sulfur Dioxide Annual Average Concentration
           of Four Air Quality Control Regions for 1964 and
           1971,injug/m3  	  4-3
   4-4      Relative Sensitivity of Various Plants to SO2  	  4-9
   5-1      Estimated Total Fluoride Emissions from Major
           Industrial Sources in  the United States in 1968	  5-3
   5-2      Relative Sensitivity of Various Plants to F	  5-15
   6-1      Threshold Concentrations for Acute Chlorine Injury	  6-4
   6-2      Relative Sensitivity of Various Plants to Chlorine	  6-5
   6-3      Relative Sensitivity of Various Plants to
           Hydrogen Chloride 	  6-8
   6-4      Dose Response  of Plants to Ethylene	  6-13
   6-5      Relative Sensitivity of Various Plants to Ethylene	  6-14
   6-6      Relative Sensitivity of Various Plants to Ammonia	  6-17
   6-7      Relative Sensitivity of Various Plants to
           Hydrogen Sulfide	  6-20
   6-8      Relative Sensitivity of Various Plants to
           Mercury Vapors	  6-25
   6-9      Relative Sensitivity of Various Plants to 2,4-D  	  6-31
   7-1      Selected Examples of Effects of Sulfur Dioxide
           and Ozone Mixtures on Foliar Injury	  7-2
   7-2      Selected Examples of Effects of Sulfur Dioxide
           and Nitrogen Dioxide Mixtures on Foliar Injury	  7-3

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Table No^                                                            Page
   7-3      Selected Examples of Effects of Sulfur Dioxide and
           Hydrogen Fluoride Mixtures on Foliar Injury	  7-4
   7-4      Selected Examples of Pollutant-Pathogen
           Interaction	  7-5
   8-1      List of Agents That Can Induce Plant Diseases  	  8-1
   8-2      Cross-Reference of Symptoms Which May be Confused
           for Air Pollution Injury by the Layman	  8-7
   D-l      Distribution of Epiphytic Lichens in Various
           IAP Zones	  D-2
   D-2      List of Common Bio-indicators and Pollutant(s)
           to Which They Are Sensitive	  D-4
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                          LIST OF FIGURES

Figure No.                                                           Page

   3-1      Atmospheric NO2 Photolytic Cycle	   3-3

   3-2     Photolytic Cycle with Hydrocarbons	   3-3

   3-3     Monthly Variation of Mean Daily Maximum One-Hour
           Average Oxidant Concentrations for Three Selected Cities  . . .   3-4

   3-4     Average Daily One-Hour Concentrations of Selected
           Pollutants in Los Angeles, July 19, 1965	   3-5

   3-5     Diurnal Variations of Mean Hourly Average Oxidant
           Concentrations in Philadelphia, August 6-8, 1966	   3-6

   3-6     Diurnal Variation of Mean Hourly Average Oxidant
           Concentrations in Los Angeles and St. Louis	   3-6

   3-7     Weekday  and Weekend One-Hour Average NO
           Levels in Chicago, 1962 through 1964	   3-24

   3-8     Average and Standard Deviation of Daily Maximum
           Oxides of Nitrogen and Nitrogen Dioxide Concentrations
           for Seven Locations in  Los Angeles Basin, 1962	  3-24

   3-9     Trend Lines for NOX Annual Averages in
           Five CAMP Cities	   3-25

   3-10     Approximate Thresholds for Death, Leaf Injury, and
           No Effect, as Related to NO2 Concentration and
           Duration  of Exposure  	   3-28

   5-1      Composite Picture of Environmental Fluoride	   5-2

   5-2     The Relationship of Concentration of Atmospheric
           Fluoride and Duration  of Exposure to the
           Threshold for Foliar Symptoms for Sensitive,
           Intermediate,  and Tolerant Species of Plants	   5-14

   6-1      Trend Lines for CO Annual Averages in Five CAMP Cities  . . .   6-22

   9-1      Temperature Variations with Altitude	   9-4

   9-2     Temperature Variation with Altitude Illustrating a
           Temperature Inversion Based at the Earth's Surface 	   9-4

   9-3     Temperature Profile Illustrating Two Inversion Layers  	   9-5

   9-4     Conditions of Figure 9-3 in a Different Perspective	   9-6

  10-1      Topographical Features of the Hypothetical Example	10-6

  10-2     The One Pathway Followed to Solve a Particular Problem  ...  10-9
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                      LIST OF PHOTOGRAPHS

Plate No.                                                            Page

  2-1       Leaf Cells of Spartina alterniflora (Smooth Cord
           Grass) Showing Cell Organelles 	  2-14

  2-2       Portion of Root Meristem Cell of Chrysanthemum
           Showing Cell Organelles	  2-15

  2-3       Section Through Chloroplasts of a Chrysanthemum
           Leaf Cell Showing Details of Grana and Lamella	  2-16

  2-4       Cross Section of a Ranunculus sp. (Buttercup) Root	  2-17

  2-5       Cross Section Showing the Stele Area of a
           Ranunculus sp. (Buttercup) Root  	  2-18

  2-6       Longitudinal Section Through the Apical Meristem
           of Strophostyles helvola (Beach Pea) Root
           Showing Area Where Primary Growth Occurs	  2-19

  2-7       Cross Section of the Root of Nicotiana
           tobaccum (Tobacco) Showing Secondary Growth
           and Lateral  Root Formation	  2-20

  2-8       Cross Section of the Herbaceous Dicot Stem of
           Medicago sativa (Alfalfa)	  2-21

  2-9       Cross Section of the Woody Dicot Stem of
           Liriodendron tulipifera (Tulip Poplar)	  2-22

  2-10     Cross Section of the Gymnosperm Stem of Pinus sp. (Pine) ..  2-23

  2-11     Cross Section of the Outer Area of the Gymnosperm
           Stem of Pinus sp. (Pine) Showing Sites of
           Secondary Growth	  2-24

  2-12     Cross Section of the Monocot Stem of Zea mays (Corn)	  2-25

  2-13     Longitudinal Section of the Shoot Tip of Spartina
           alterniflora (Smooth Cord Grass) Showing the Apical
           Meristem, Young Leaves and Intercalary Meristems	  2-26

  2-14     Cross Section of the Broad-leaved Leaf of
           Glycine max (Soybean)	  2-27

  2-15     Cross Section of the Narrow-leaved Leaf of
           Zea mays (Corn) 	  2-28

  2-16     Cross Section of the Needle-like  Leaf of
           Pinus sp. (Pine)  	  2-29

  2-17     Surface View of a Stoma of Zebrina sp.
           (Wandering  Jew) 	  2-30

  2-18     Cross Section of the Outer Bark of Liriodendron
           tulipifera (Tulip Poplar) Showing a Lenticel  	  2-31

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Plate No.                                                            Page

  3-1       Example of Initial Water-Soaked Appearance on
           Broccoli Immediately after Exposure. This Plant
           was Fumigated with 10 pphm O3 and 0.5 ppm SO2	 3-33

  3-2       Bel W-3 Tobacco Injured by Ambient Oxidant
           in St. Louis, MO, Showing Both Fleck and
           Bifacial Necrosis 	 3-33

  3-3       Ozone Injury (Flecking) to White Ash	 3-34

  3-4       Ozone Injury to Swiss Chard	 3-34

  3-5       Ozone Injury to Tobacco	 3-35

  3-6       Ozone Injury to Radish	 3-35

  3-7       Ozone Injury to Radish and Subsequent
           Reduced Yield on Right	 3-36

  3-8       Cucumber Injured by Ambient Oxidant Near
           Cincinnati, Ohio	 3-36

  3-9       Oxidant Injury to Squash  	 3-37

  3-10     Tomato Leaflet Showing Oxidant Injury
           (Probably  Ozone)  	 3-37

  3-11     Safflower Leaf Showing Oxidant Injury
           (Probably  Ozone)  	 3-38

  3-12     Soybean Leaves Showing Various Stages of Oxidant
           Injury (Normal Leaf in Center; Leaflet on Right
           is Secondary Response to Oxidants)  	 3-38

  3-13     Tempo Bean Leaves Showing Oxidant Injury
           (Probably  Ozone)  	 3-39

  3-14     Bronzing of White Bean Leaves Caused by Oxidant
           (Probably  Ozone)  	 3-39

  3-15     Severe Ozone Injury and Bifacial Necrosis of
           Browallia Leaves  	 3-40

  3-16     Severe Grape Stipple Caused by Ozone	 3-40

  3-17     Pinto Bean Injured by Ambient Oxidant Near
           Cincinnati, Ohio, Showing Stipple Symptom 	 3-41

  3-18     Ozone Stipple of White Ash as Observed in the Field  	 3-41

  3-19     Bluegrass Injured by Ambient Oxidant in the
           Los Angeles Basin  	 3-42

  3-20     Severe Oxidant  Injury to Ponderosa Pine	 3-43

  3-21     Chronic Ozone Injury of Ponderosa Pine. Note
           Difference in Tolerance Between Trees and
           Tufted Appearance of Foliage	 3-44
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Plate No.                                                            Page
  3-22     Tipburn of Onion Caused by Ozone  	  345

  3-23     Eastern White Pine Displaying Oxidant Injury
           (Probably Ozone)  	  3-45

  3-24     Comparison of Ozone and PAN Injury on Alfalfa.
           Upper row:  Ozone Injury; Lower row: PAN Injury	  3-46

  3-25     PAN Injury to a Bean Leaflet. Left, Upper Leaf
           Surface; Right, Lower Leaf Surface Showing
           Silvering or Glazing Due to PAN	  3-46

  3-26     Young Primary Leaf of Pinto Bean Injured by PAN
           After Exposure to Irradiated Auto Exhaust	  347

  3-27     Escarole Showing Oxidant Injury
           (Probably Due to PAN)	  3-47

  3-28     PAN (Ambient) Injury to Swiss Chard 	  3-48

  3-29     Petunia with PAN or Ozone Injury 	  348

  3-30     PAN Injury to Oats	  3-49

  3-31     Injury on Broccoli One Week After Exposure to NO2.
           Leaves Show Some Recovery from Initial Water-
           Soaking and also Some Marginal and
           Interveinal Necrosis	  349

  3-32     Marginal and Interveinal Injury on Periwinkle
           Fumigated with 19.3 ppm of NO2 for 0.5 Hours	  3-50

  3-33     Marginal and Interveinal Injury on Cherry
           Belle Radish Fumigated with 7.7  ppm NO2
           for Four Hours  	  3-50

  4-1       Acute Sulfur Dioxide Injury to Bracken Fern,
           Typically Orange-Red; Occurs on Margins
           of Fronds	  4-12

  4-2       Typical Sulfur Dioxide Injury to Fox Grape.
           Light Brown, Occurs Between Veins; Top
           Leaves Show Upper Surface; Bottom Leaves
           Show Undersurface  	  4-12

  4-3       Acute Sulfur Dioxide Injury to White Birch Foliage  	  4-13

  4-4       Acute Sulfur Dioxide Injury to Trembling
           Aspen Leaves. Injured Areas are Reddish-
           Brown and Darken with Age	  4-14

  4-5       Typical Acute Sulfur Dioxide Injury to the
           Garden Pea   	  4-15
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Plate No.

  4-6       Corn Foliage Exhibiting Acute Sulfur Dioxide
           Injury (Injured Areas are Composed of White-to-
           Ivory Colored  Collapsed Cells)	  4-15
  4-7       Light Acute Sulfur Dioxide Injury to Alfalfa	  4-16
  4-8       Severe Acute Sulfur Dioxide Injury to Alfalfa
           Leaves. Injury Ivory Colored, Marginal with
           Intercostal Spotting	  4-16
  4-9       Acute Sulfur Dioxide Injury on Blackberry
           Growing Within Five Miles of the Source	  4-17
  4-10     Typical  Acute Sulfur Dioxide Injury to Hickory.
           Reddish-Brown; Frequently Extends from Near
           Midrib to Near Edge of Leaf	  4-17
  4-11     Acute Sulfur Dioxide Injury to Eggplant
           Leaves (Ivory-to-Light Tan)	  4-18
  4-12     Acute Sulfur Dioxide Injury to Quince Foliage
           (Colorful Brownish-Red)	  4-18
  4-13     Acute Sulfur Dioxide Injury to Careless Weed
           (Ivory-Colored; Note Little or No Injury on
           Young Expanding Leaves)	  4-19
  4-14     Chronic Sulfur Dioxide Damage to Cotton Foliage
           in Palm  of Hand.  Note Injured Areas are Chlorotic
           But Not Collapsed; Veins Usually Remain Green	  4-19
  4-1 5     Acute Sulfur Dioxide Injury to Sonora Wheat
           (Ivory-Colored)	  4-20
  4-16     Suspected Sulfur  Dioxide Injury on Virginia
           Pine Growing  1.5 Miles from a Source	  4-21
  4-17     Typically Acute Sulfur Dioxide Injury to
           Loblolly Pine  Needles  	  4-22
  4-18     Acute Sulfur Dioxide Injury to Yellow Summer
           Squash. Acute Injury to all Squash and Pumpkin
           Plants Is White or Ivory-Colored  	  4-22
  4-19     Acute Sulfur Dioxide Injury to Tulip. Note  Ivory-
           Colored Injury Occurs at Leaf Tips and Margins 	  4-23
  5-1       Citrus Foliage with the Typical Fluoride-
           Induced Pattern of Chlorosis	  5-19
  5-2      Blueberry Leaves Showing the Kind of Injury
           Induced by Atmospheric Fluoride	  5-19
  5-3      Marginal and Intercostal Necrosis of a Grape Leaf	  5-20
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5-4       Hydrogen Fluoride Injury to Poplar (Field Exposure) .......  5-20
5-5       Oregon Grape with Symptoms Mimicking Fluoride
          Injury, Cause Not Known ............................  5-21
5-6       Lamb's Quarters Showing HF-Induced Injury  .............  5-21
5-7       Leaves of Sweet Corn Showing HF-Induced
          Symptoms and Varietal Differences in Tolerance.
          From Top (Tolerant) to Bottom (Sensitive) the
          Varieties are: Surecross, Golden Cross Bantam,
          Gold Rush, Spancross, and Marcross ....................  5-22
5-8       Injury Due to HF on Gladiolus, Pine, and
          Tulip Fumigated Together ............................  5-22
5-9       Fluoride-Induced Injury on Gladiolus Foliage  .............  5-23
5-10      Fluoride-Induced  Injury on Fir; Note
          Several Uninjured Needles ............................  5-23
5-1 1      Slash Pine Displaying the Reddish-Brown
          Discoloration of Needles  Injured by Fluoride  ............  5-24
5-1 2      Suture Red Spot Syndrome of Peach Fruit
          Induced by HF on Dwarf Elberta  ......................  5-24
5-1 3      Fluoride Injury to Ponderosa Pine. Note That
          Only One Tree Exhibits Injury. This is an
          Illustration of the Natural Differences in
          Tolerance Found in the Field  .........................  5-25
6-1       Chlorine Injury to Sassafras Showing Reddish-
          Brown Interveinal Necrosis ...........................  6-33
6-2       Chlorine Injury to Witch  Hazel Showing
          Necrotic Lesions Along Veins and a Portion
          of the  Leaf Margins .................................  6-33
6-3       Chlorine Injury to Italian Prune Showing
          Upper Leaf Surface Flecking ..........................  6-34
6-4       Chlorine Injury on Wild Mustard Showing
          Bleaching Effect  ...................................  6-34
6-5       Chlorine Injury on Pine Showing Reddish-
          Brown Discoloration ................................  6-35
6-6       Chlorine Injury on Larch from Chemical Plant
          Spill. Note Chlorotic Mottle  ..........................  6-35
6-7       Hydrogen Chloride Injury to Norway Maple
          Showing Marginal Necrosis ...........................  6-36
6-8      Hydrogen Chloride Injury to European Black Alder
         Showing Interveinal Necrosis ..........................  6-36

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Plate No,                                                          Page

  6-9      Hydrogen Chloride Injury to Black Cherry
          Showing Leaf Spotting	  6-37
  6-10     Hydrogen Chloride Injury on Norway Spruce
          Showing Tip Necrosis  	  6-37
  6-11     Ethylene Injury on Orchid Showing "Dry Sepal"
          on Flower at the Left  	  6-38
  6-12     Azalea Fumigated  with 2 ppm Ethylene for Seven
          Days. Note Heavy  Leaf Drop and Loss of Flowers.
          Control Plant is on Right	  6-38
  6-13     Ammonia Injury on Poison Ivy Showing Blackened Appearance. .  6-39
  6-14     Ammonia Injury on Cotton	  6-39
  6-15     Cement Dust  Deposit on Fir Branch  	  6-40
  6-16     Lime Dust Deposit on Spruce Twigs on the Right	  6-40
  6-17     2,4-D Injury to Oak Leaves Showing "Lacy"
          Appearance of Leaves  	  6-41
  6-18     Atrazine Injury on Soybeans. Grain Sorghum was
          Sprayed with Atrazine During Previous
          Growing Season	  6-41
  7-1      Bel W-3 Tobacco Exhibiting Injury from
          Fumigation with .05 ppm 03 and .10 ppm of SO2.
          Note the Similarity to Ozone Injury  	  7-7

  7-2      Injury to Bel W-3 Tobacco Fumigated with .05 ppm
          of O3 and .50 ppm of SO2. In This Case the
          Injury More Closely Resembles SO2 Injury	  7-7
  7-3      Pinto Bean Fumigated with .15 ppm of O3  and .50 ppm
          of SO2. Note the Almost Complete Absence of
          Bleaching and the  Slight Purplish Discoloration	  7-8
  7-4      Bleaching of Tomato Leaf as a Result of Fumigation
          with .05 ppm of O3 and .25 ppm of SO2   	  7-8
  7-5      Lower Surface of Soybean Leaf Fumigated with .10
          ppm of O3  and .50 ppm of SO2. Note the
          Difference in  Symptoms from Plate 7-6	  7-9
  7-6      Soybean Leaf Fumigated with .10 ppm of O3
          and .50 ppm of SO2  	  7-9
  7-7      Bel W-3 Tobacco Fumigated with .10 ppm of SO2                           H
          and .10 ppm of NO2  	  7-10          •
  7-8      Lower Leaf Surface of Pinto Bean Leaf Fumigated
          with .05 ppm of SO2 and .10 ppm of NO2  	  7-10
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Plate No.                                                            Page
  8-1       Heat Injury to Roadside Trees Caused by
           Street Paving	  8-9
  8-2       Winter Injury to Boxwood and Deodora Cedar. Many
           Different Agents Could Cause Similar Damage  	  8-10
  8-3       Roadside Maples Affected by De-Icing Salts.
           Position of the Trees and the History
           of Salt Application are Keys to
           Proper Diagnosis  	  8-11
  8-4       Roadside Shrubs Affected by Salt Spray from
           Passing Vehicles Following Use of De-Icing
           Salts	  8-12
  8-5       Injury to Oaks Caused by Grade Changes
           in Landscaping. Bronzing of Foliage and
           Leaf Drop  Preceded Death	  8-12
  8-6       Frost Injury to White Oak. Note Similarity of
           Damage Symptoms to SO2 or F-Induced Injury	  8-13
  8-7       Nitrogen Deficient Corn Leaves, Showing Symptoms
           That Could Readily Be Confirmed Through a Soil
           or Foliage Test	  8-13
  8-8       Manganese Deficient Grape Leaves Showing
           Symptoms Similar to Those Induced by Ozone	  8-14
  8-9       Miticide (Kelthane) Injury on Soybean Leaves.
           Note Similarity to Air Pollution Injury	  8-14
  8-10      Needlecast of Scotch Pine. Similar Initial
           Symptoms Could be Caused by SO2, O3> or F  	  8-15
  8-11      Bluegrass Injured by Thrips (center); Normal
           Leaves (right); 03 Injured Leaves (left)  	  8-15
  8-12      Pine Sawfly Damage to Loblolly Pine Stand.
           Close Examination Would Easily Indicate This
           Cause Unless the Insect Was Not Present	  8-16
  8-13      Mite Injury to Tomato Leaflets Grown in the
           Field. Note Similarity to Ozone Injury  	  8-16
  8-14      Soybean Leaves. Left, Oxidant Injury (Probably
           Ozone); Center, Normal Leaflet; Right, Mite Injury	  8-18
  8-15      Dogwood with Lacewing Injury. Note Similarity
           of Insect Damage to Air Pollution Injury	  8-17
           Eastern  White Pine with Oyster Scale Insect Injury.
           Note Similarity to Air Pollution Injury	8-18
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                                Chapter 1

     INTRODUCTION TO  DIAGNOSIS OF AIR  POLLUTION
                    DAMAGE TO VEGETATION

A Brief History
   Natural sources of air pollution have been with us for a long time, but they
did not achieve the status of a major social problem until the 1300's. The intro-
duction of coal  as a source of energy polluted the air  of populated areas with
sulfur  dioxide and particulates, irritating the mucous membranes  and esthetic
senses of rich and poor alike.*
   As technology grew,  various industries added their own brands of pollutants
to the  air. The metallurgical industry contributed contaminants associated with
metal processing such as sulfur dioxide, flouride, and heavy metals. The chemical
industry  donated hydrochloric acid, chlorine, ammonia, hydrogen sulfide, nitro-
gen  oxides, and  others.  Each major industry  has  added  its  own  particular
complex of pollutants,  making  the problem  of control  progressively more
difficult.
   In recent  decades, automobile exhaust  has become a massive, widespread
problem. Petroleum  components in  the exhaust  react  with atmospheric com-
ponents  in the presence  of sunlight to  form photochemical smog,  which is
responsible for many respiratory problems.

Air Pollution and the Public
   To  the  public, the most obvious effects of air pollution are the effect on
visibility, and the effect  it has on them — burning eyes, raw throats,  and the like.
The next most obvious effect is  the "dirtying" of the public's environment —
unpleasant air, smog, damaged paint and metal surfaces,  etc.  The damage that air
pollution causes  in plants is less visible. City dwellers may note the dirty leaves
of the  Norway maples in the park, but when they travel, the countryside looks
clean and beautiful by comparison, and so many people are quite unaware of the
increasing seriousness of air pollution damage to plants, particularly to crops.

Economic Importance and Assessment of Air Pollution Damage to Vegetation
   A 1969 Stanford Research Institute study estimated that vegetation damage
due to photochemical pollutants ran to nearly $113 million, including losses on
ornamentals, non-commercial forests, parks, roadways, and residential plantings.
While this is only 0.6 percent of the total crop value, it is a sizeable loss, and a
loss that  is growing annually. It should be noted,  however,  that these estimates
were derived from 1969 census data. The estimate assumes that average climatic
conditions  prevailed during the  growing season. Climate and growing conditions
vary considerably from  year  to year and one would expect variations in crop
"The earliest known air-pollution regulation was a royal proclamation by Queen Elizabeth I
 in the 16th century, prohibiting the burning of coal in London when Parliament was in
 session.
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losses accordingly. Current losses from air pollution damage to vegetation would
amount to approximately $200 million based on more recent agricultural prices
and  production figures. Air pollution standards aimed at protecting vegetation
are being  adopted to arrest  the  trend,  but here a problem arises: Are  the
standards based on good data, and are they realistic? The first order of business
is to obtain good data, and that is what assessment is all about.
   In an industrialized society, it is customary to base  decisions of economic
consequence  on benefit/cost analyses.  Dollar values often need to be placed on
problems before resources can  be  allocated  to solve them.  The  problem of
pollution damage  to plants has not escaped this custom. The  "benefit" side of
the argument says that pollution injury is so undesirable that it  should  not be
permitted, regardless  of the cost of control.  The "cost" side of the argument
says that pollution control equipment is very expensive, not only in terms of
capital  costs  but  also  in  terms of  the additional  human and management
resources needed, and so enthusiasm for returning the environment to its pristine
quality  should be tempered by  realism. But regardless of one's viewpoint, one
thing is  clear: to  intelligently deal with the benefit/cost problems of pollution
damage, we must first have a good way to assess the damage.
   Air quality standards  have  been established  to  protect vegetation, but it is
possible  that some factors may have been overlooked or insufficiently studied,
and that conditions may change over time, so that the standards may prove to be
inadequate. Past surveys conducted in the various states have for  the  most part
been limited  in scope or breadth, and have been conducted with varying degrees
of experience and  knowledge, using a diversity of methods. A uniform system of
data collection and interpretation would be useful in comparing the intrastate
and  interstate quality of the air, and more  specifically, would be valuable in
evaluating local losses that might or might not be associated with air pollution.
We need a system  for evaluating air pollution effects on  vegetation that  clearly
determines the extent of damage, and identifies which pollutant is  the culprit.
   Air pollution survey techniques have ranged from the systematic to the guess.
At  one   end  of the scale, a systematic sampling of crops in  affected fields is
conducted, and the amount of leaf area injured on individual plants is calculated
and used to determine reductions in yield. At the other extreme, damaged crops
are simply inspected  in the field, and  a "guesstimate" is made  of loss  to the
farmer.  A number of states have conducted statewide surveys by simply enlisting
the help of county agents or agricultural field inspectors to locate damage.
   More recently,  a systematic method of estimating and predicting losses was
developed by the Stanford  Research Institute. This model basically predicts the
amount  of injury  on a  county-by-county basis, based on the amount of fuel
consumed, the presence of sensitive crops, and weather parameters. The  model
offers a simple approach to a complex problem, but it has not been field-tested
extensively, and until additional ground surveys are conducted to determine
whether refinements in the model are needed, its value will be limited. Compari-
sons have been made of the S. R. I. estimates and estimates from states that have
conducted surveys, and although there is reasonable agreement in the  estimates,
a more refined model and better field assessment techniques are needed.
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Direct Losses
   For the most part, air pollution surveys have centered on direct losses. These
are defined as tangible losses which are easily estimable. For example, a direct
loss to a farmer would  consist of damage that reduces the quality or quantity of
his crops.  Foliar injury to tobacco that downgrades the leaf from cigar-wrap
grade to cut-tobacco  grade is an example of reduction in quality. Leaf injury to
potato vines resulting in smaller yields is an example of reduction in quantity.
Direct losses may also take other forms — for example, processing costs may be
increased if spinach or lettuce leaves are injured and have to be sorted to remove
the unmarketable leaves before packaging.
   Losses of this type  are not restricted to food producers. Homeowners may
experience  losses  with  their garden  crops  or ornamental  plants.  A  severely
damaged white pine on someone's front lawn may have  to be  replaced because
of its unsightliness.  In  this case, the direct loss would include the value of the
tree, plus the labor involved in replacing it.

Indirect Losses
   Indirect losses are  less tangible, more difficult to assess, and have not  received
focus in the  air pollution  surveys. Indirect losses  are  those generated  by or
related to direct losses. For example, if a farmer can no longer grow a given crop
on his land because of its sensitivity to ambient air pollution levels,  he has little
choice but to switch  to  another crop. The new crop may bring a lesser return to
the farmer for his investment, or he may have to buy new or different machin-
ery, or the new crop may not be as well adapted to the soil type. Although there
is no pollution damage  to the new  crop, the farmer has still sustained a loss. On
the other  hand,  the  new crop  may be better adapted  and worth  more, thus
increasing a farmer's return on his investment.
   Pollutants  may  predispose plants  to  insect or disease injury,  forcing the
farmer to spray or take other precautionary measures.  Again, although the air
pollutants  have not in themselves caused direct, visible damage, the farmer has
incurred a financial loss.
   Perhaps  the most serious indirect loss  is that involving  the  reduction  of
property value. If farm  land  in an area becomes unproductive, or if production
becomes economically unfavorable to the farmer, the land may be  diverted to
other uses.  Indeed, it may  be taken out of production  and permanently com-
mitted to other uses. The general public is  affected by such losses because the
increased  cost of  production and  processing  are passed on to the  consumer.
Crops that can no longer be  grown in one area may have  to be transported from
a more distant area.
   Indirect losses may also affect the homeowner by  decreasing the  value of his
property if ornamentals are injured or deformed by pollutants, or if his garden is
in  a known high-pollution  area. Other indirect losses more difficult to  assess
include,  among others,  the  deterioration  of esthetically-pleasant  landscapes,
erosion following denudation of the land, stream silting, permanent injury to the
soil by heavy metals, and deleterious changes in ecological systems.
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Assessment Methods
   To arrive at an accurate estimate of real economic loss, a number of variables
must be  considered in assessing crop damage. The time of the growing season
during  which injury occurs is particularly important. Plants injured early in the
season  may recover fully in a matter of days, provided the growing points have
not been injured. If the plant is growing actively it may produce a new set of
leaves and may recover in a few days, even after being completely defoliated by
an acute fumigation.  In  this  case, no real loss has been incurred, although the
situation may have appeared disastrous immediately following the fumigation.
However, if fumigation  of this nature occurs later in the growing season, or if
fumigations occur repeatedly, the plant may not be able to produce a new set of
leaves and recover.
   In evaluating air pollution effects on vegetation, it has been suggested that the
term damage be  reserved for cases where economic loss has occurred, and injury
for cases where foliar or other effects are also manifested but no economic loss
has resulted. Thus air pollution injury is defined as any identifiable and measur-
able response of a plant to air pollution. Damage is defined as any identifiable
and measurable  adverse effect upon the desired  or intended use or  desired
product of the plant that results from air pollution injury.
   Reduction in  yield, whether it is quantitative or qualitative, is  also of prime
importance.  Although estimation of yield loss may sound like a straightforward
variable to measure,  it  can be very  elusive. Foliar damage  to root  crops, for
example, may  bear no  relationship  to the amount  of "economic" damage
incurred. If  injury occurs near harvest time, there may not be  detectable yield
loss. Sometimes, there may be a complete absence of foliar symptoms but a total
loss of the  crop —  for example,  if hay becomes contaminated  with harmful
quantities of fluorides, the crop may be worthless. It may be salvaged by diluting
it with uncontaminated  hay, or by using it as bedding. The important point to
remember when  confronted with such situations is that knowledge is required
about both types of "damage" — the biological and the economic —  and  both
should  be reported.
   The end use of the crop is also important, and the same injuries occurring to
the same crop grown for different purposes may  produce different  economic
results  (and  damages). For example, leaf scorch on a sugar maple in  a forested
area may not be of much economic consequence, whereas the same type of
injury  on sugar  maples at a syrup-maker's  could  have a significant  economic
effect.
   Whatever the  economic factors involved, only three things need to be known
in  estimating crop losses: what crop is affected, to what degree, and  by which
pollutant. However, for  these three items of information to be accurate, a great
deal more information must usually be obtained and sifted. Sometimes repeated
visits to an area will have to be made if the problem is chronic.
   A model developed in California  in  1970 uses a "rule of  thumb" method.
When field inspection of crops for air pollution damage revealed  1 to 5% leaf
surface injury, then a 1% loss factor was applied for that crop  in that particular
county. When the injury ranged from 6 to 10%, a 2% loss factor was assessed. If
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the injury reached 11 to 15%, it became a 4% loss, and so on. The losses from air
pollution for individual counties were then calculated from the harvest value of
the crops by applying the appropriate percentage loss assigned to  that county.
   This procedure, and others like it, have been used by others.  Although there
is no theoretical basis for this  technique, it does provide a  systematic way  of
obtaining uniform data.  But, further research is needed to establish the relation-
ships among plant growth state, injury, and damage.

Field Inspection
   There is  no substitute for on-site field inspection to determine  the extent  of
plant damage. For the field inspector to collect useful data, he must be able  to
recognize air pollution injury, and learn to properly evaluate the true impact  of
air pollutants upon  plants. This book  is designed to help do these two things.
There  are many  difficulties that  are encountered in the field which this book
attempts  to anticipate and offers guidelines to help the observer.  In the dis-
cussion of so-called typical symptoms, for example, the term "typical" is used in
the sense of a type specimen or as a composite  about  which variations occur.
Therefore, typical should not be interpreted to mean "normal"  or "usual" but
used more as a point of reference in diagnosis.
   Another  important point to keep in mind is that there are many factors under
field conditions that can modify or alter plant response to air pollutants. These
can be categorized as follows:
      -  Biological character of plants
      -  Environment in which plants are growing
      —  Pollution concentration, and duration of exposure
The biological characteristics  of plants include  their genetic make-up and their
stage of development. The sensitivity to various pollutants is known for many
cultivated plants. Native vegetation and forest species may exhibit the gamut  of
response even among a given species, e.g., some pine trees will be injured while
others  growing a few yards  away will be  intact. This variation is simply  a
function of  genetic variability which governs plant morphological, physiological,
and biochemical characteristics.  The stage of development of plants is important
because  some  plants are  not sensitive  when  young  but become  sensitive  at
maturity, and vice versa. Romaine lettuce is  sensitive to PAN in  the early stages
of growth, becomes  tolerant as the plant develops, and becomes sensitive again
just before  reaching maturity. Individual leaves also have sensitive and tolerant
stages.
   There  are  many  environmental factors which  affect plant response. These
include  climatic factors,  light   quality  and  quantity,  temperature, relative
humidity, and soil nutrition. In  general, the  conditions which tend to favor the
growth of the plant  also tend  to increase their sensitivity to air pollutants. This
aspect  is covered in each chapter.
   The  concentration of the pollutant  and the time during which the plant is
exposed  is referred to as the "dose," and the  lowest dose that produces an effect
is called the  "threshold  dose."  However, because of the interrelationship  of
concentration and time,  there is no single threshold dose for an effect to occur.
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For  example,  plant  injury  may occur  very quickly  when exposed  to  a high
concentration, but,  at  a  low  concentration,  several  hours may elapse  before
symptoms appear.  This  is not surprising since  repair or detoxifying mechanisms
are present in plants. There are some qualifications which should be made with
respect to thresholds. Theoretically, exposure to  a pollutant  under controlled
conditions will not produce injury on any individual plant until the dose exceeds
a certain  value  — the threshold. Practically speaking,  a plant is not exposed to
increasing doses, but to  one  dose. Thus, for that individual, its threshold is
unknown but is greater than the dose used if  no injury occurs, or less than that
dose if injury does occur. If several plants are exposed to the  same dose under
the  same  conditions,  some may  be injured and others  may  not.  Thus the
threshold or tolerance vanes from individual  to individual. If the dose  is such
that 50% of the individuals develop injury, it is called  the median effective dose
or median toxic dose. Moreover, if another group  of plants is exposed to a dose
that is half the median effective dose, 30%, 15%, or 3% of the individuals may be
injured, depending upon  the variability of tolerances for that group of  plants.
The frequency of  symptoms on plants  must  be viewed  as reflecting not only
their average tolerance but also their heterogeneity.
                              Selected References

Barrett,  L. B. & Waddell, T. Cost of Air Pollution Damage: A  Status Report. Research
   Triangle  Park, North  Carolina: National  Ecological  Research Center, Environmental
   Protection Agency, Publication AP-85, 1973.
Feliciano, A. 1971 Survey and Assessment of Air Pollution Damage to Vegetation in New
   Jersey. New Brunswick, New Jersey: Cooperative Extension Service, Rutgers University,
   1972.
Lacasse,  N. L. & Weidensaul, T. C. Statewide Survey of Air Pollution Damage to Vegetation
   - Results.  State  College, Pennsylvania:  Center for Air Environment Studies, Pennsyl-
   vania State University,  1970.
Millican, A. A Survey and Assessment of Air Pollution Damage to California  Vegetation in
   1970. Sacramento: California Department of Agriculture, 1971.
Naegele, J. A., Feder,  W. A., & Brandt, C. J. Assessment of Air Pollution Damage to
   Vegetation in New  England.  Amherst,  Massachusetts: Suburban Experiment Station,
   University of Massachusetts, 1972.
Stanford Research Institute. Assessment of Economic Impact of Air Pollutants on Vegeta-
   tion in the U.S. Menlo Park, California: Author, 1973.
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                                Chapter 2

            STRUCTURE AND  FUNCTION  OF PLANTS
           IN  RELATION TO AIR  POLLUTION INJURY

                               Introduction
   Higher plants, unlike most  animals, are  stationary organisms which  utilize
their surrounding environment for the synthesis of food and other life support-
ing processes.  Because of  their responsiveness  to and dependence  on their
immediate environment, any shift in the usual environmental pattern tends to
induce stress on the plant.  For example, variations in temperature, water in the
soil or  air, minerals in  the soil,  toxic  soil  chemicals, diseases, insects, light
characteristics,  and  gaseous  air pollutants all have their influence. Response of a
plant  to stress depends upon  a variety of plant characteristics such as age,
metabolism, genetic makeup and structure.  The  purpose  of this chapter is to
consider certain aspects of plant structure, growth and physiology.
   Higher plants usually have four basic organs: roots, stems, leaves and flowers.
For the purposes  of this  chapter,  discussion of each  organ is  undertaken
separately and includes general morphology, function, internal structure, pattern
of growth and, where appropriate, potential interaction with air pollutants. The
common ultrastructure of cells of these organs is considered separately.

                          Plant Cell Ultrastructure
   Chemical reactions in  plants are  not  ubiquitous, but  rather are  localized,
usually  into some structural entity. The basic structural unit of plants is the cell.
However,  cells  themselves are subdivided into  many  complex units, each asso-
ciated with one or several functions. The following few paragraphs and associ-
ated figures discuss  some of the basic structures of plant cells and the presumed
function of these structures.
   The  outside boundary of each plant cell is the primary  cell wall (Plate 2-1).
This is  the first  formed wall of  the cell and  is deposited adjacent  to  pectic
substances which separate  cells  and  cement them together. This pectic layer is
called the middle lamella (Plate 2-1). The primary cell wall consists mainly of
carbohydrates and  forms as the cell is  initiated. Only in rare cases does the
primary  wall  achieve any  appreciable  thickness. Some  plant  cells form  a
secondary cell wall  (Plate 2-1) comprised of additional layers inside the primary
wall. In this formation more carbohydrate strands are laid  down. Lignin is then
deposited  between the strands of both the primary and secondary wall, forming
a very  hard layer.  Lignification typically occurs after the cell has completed
expansion and is responsible for the hardness of  many plant  parts.
   A plasmalemma  or plasma  membrane occurs just  inside the cell wall (Plate
2-2). This outer layer of the cell cytoplasm is chemically and structurally active,
regulating the flow of ions, water and other material into and out of the cell. The
plasmalemma and some other cytoplasmic  components interconnect  between
adjacent cells through openings in the cell wall. The plasmalemma is the first
living  component of the cell exposed to air pollutants.  Studies  attempting to
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find primary  sites of air pollution  effects must  consider the  effect on  the
plasmalemma. Perchorowicz and Ting (1974) have found that ozone (03) alters
the permeability of the membranes of bean leaf cells. The  watersoaked appear-
ance of  leaves following exposure to certain pollutants is due in part to  the
disruption of the plasmalemma and other critical cell membranes.
   The largest single  component of the mature living plant cell is usually  the
vacuole  (Plate  2-1), which occupies the center of the cell.  Its main  chemical
constituent is water. Salts, organic acids, crystals and other metabolic  products
may also be present. The outer boundary of the vacuole is the tonoplast or
vacuolar membrane (Plate 2-1).  It functions much as the plasmalemma does in
regulating the  flow  of  substances  passing between  the  cytoplasm  and  the
vacuole.
   The thin layer  between the tonoplast and  the plasmalemma  comprises  the
cytoplasm (Plate 2-1), which contains many organized structures and is the site
of most of the cell chemistry. The most prominent cytoplasmic structure is  the
nucleus (Plate 2-2) which houses most  of the  genetic system of the plant. The
denser structures seen in the  nucleus in Plate 2-2 are chromatin which  make up
the chromosomes.  The genes  which regulate specific traits of the plant are found
here. Surrounding  the nucleus and regulating movement of  chemicals in and out
is  the nuclear envelope (Plate  2-2).  Evidence that air  pollutants  or their
secondary products can  penetrate the nuclear  envelope and alter the  genes or
chromosomes, thus causing inheritable  genetic change, is  not  available at this
time.
   Several other organelles  occur within the cytoplasm.  Of these, one group
unique to plant systems is the plastid.  The most familiar plastid is the chloro-
plast (Plate 2-3). The  chloroplast is surrounded by a double  unit membrane. The
internal  membrane   invaginates,  forming  layers  of  lamella  (Plate  2-3)   or
thylakoids. At intervals, stacks  of thylakoids (10 to 100) form cylinder-like
structures called grana where most of the photosynthetic reactions take place. A
matrix, the stroma, surrounds these membranous structures.
   During the process of photosynthesis light energy is absorbed by chlorophyll
and other pigments, and  used to form sugars  from carbon dioxide (€02) and
water (H2O). This process is  the only biologically significant way of converting
COj to usable organic matter for living organisms. Generally speaking all of  the
oxygen (O2) occurring in the earth's atmosphere is released  from the breakdown
of H2 O during photosynthesis.
   All  of the major air pollutants have been shown at some dose level, to slow or
stop photosynthesis.  The  rate of photosynthesis is in  part  dependent  upon
adequate  gas  exchange between cells containing  chloroplasts  and the outside
atmosphere. Therefore, any plant response to air pollution which restricts  gas
exchange will inevitably slow the rate of photosynthesis. This problem will be
considered more fully during a discussion of gas exchange in leaves. The amount
of chlorophyll may also regulate the rate of photosynthesis. Chlorosis  in leaves
indicates that less  chlorophyll is present. Chlorophyll is unstable and normally is
continuously replaced within the chloroplast. Chlorosis may result from a direct
attack on the chlorophyll molecule,  as it seems to be with  sulfur dioxide (SO2)
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and  possibly fluorine  (F), or it may result  from inhibition  of the chemical
pathway which  produces chlorophyll, as it seems to be with F,  O3 and per-
oxyacetyl nitrate  (PAN).  Photosynthesis  is  also  slowed when the chemical
energy used for COj fixation is in some way tied up. Any form of pollutant
which can enter the  chloroplast  and serve as an electron acceptor is potentially
capable of this type  of reaction. Rapid resumption of the rate of photosynthesis
following an air  pollution exposure indicates interference by the pollutant with
the energy  exchange mechanism in  photosynthesis or with regulation of the
opening  of  stomata, thus  inhibiting  gas exchange. Longer recovery  times are
required when critical molecules  and structures must be resynthesized.
   During photosynthesis  light  energy  is converted into  chemical  bonds of
organic  molecules. Utilization of the  chemical energy in these bonds requires
oxidation.  Respiration is the term applied to these oxidation processes. The
initial respiratory steps occur in  the cytoplasm. Products of the  initial steps then
pass  into mitochondria  (Plate  2-2) where they  are  further oxidized forming
molecules of the important energy carrying compound adenosine  tnphosphate
(ATP), a variety of  organic acids and CO2. Oxygen serves as the final electron
acceptor and  H2O  is also formed  within the mitochondrion. As in photo-
synthesis, gas exchange both  within the cell and with the outside atmosphere is
necessary in respiration.  Air  pollutants which inhibit gas exchange may inhibit
respiration. Ozone at low levels may cause mitochondria to increase their rate of
O2 uptake after an  initial  inhibition  (MacDowall, 1965). Other pollutants also
affect the rate of respiration.
   The  plant  cell  utilizes  the products  of photosynthesis and respiration to
construct all  of its  components. Proteins,  most important as enzymes and
components of membranes, are  formed within the cytoplasm.  This synthesis is
subject  to interference  by  some air pollutants.  Lipids, most important as
components of membranes, are also synthesized in the cytoplasm. Air pollutants
are known  to  attack the  hpid portion of membranes, so lipid synthesis becomes
very  important  in repairing injury   to  membranes  caused by air pollution.
Complex carbohydrates  and  other cell chemicals  are also formed in the  cyto-
plasm, usually in association  with some specific cell organelle. Since, as yet, air
pollution has  not  been  shown  to interfere  directly in these processes, their
associated structures will not be considered.  However, cell  systems are very
interdependent.  Effects   on one component are  often  reflected  in   other
components.

                               Plant Organs
   The following discussion covers the structural organization of the four basic
plant organs and  considers potential interactions of these structures with air
pollutants.

                                  Roots
   Roots function  in the absorption of water and  nutrients  from the soil.  They
often store  foods, transport  water and nutrients  to the shoot, and anchor the
plant in the soil.
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   To accomplish these functions a variety of root forms exist. These forms are
usually categorized into four groups. One of the common root types is the tap
root. The tap root is typically a single large root extending directly down from
the plant axis.  It may penetrate deeply into the soil providing an  avenue for
absorption of water from depths of twenty feet or more, such as it  does in
alfalfa  or some desert plants, or it may be  more  fleshy in form  providing
extensive storage space such as in carrot.
   A second type of root system is the fibrous root system. In this system, roots
branch frequently and  tend to remain  quite small in diameter. Very dense mats
of roots  are often formed. Many grasses have fibrous root systems as do shrubs
such as rhododendron.
   Fascicled roots constitute  an intermediate form between the tap root and the
fibrous root system. Here a large, fleshy, but branching system is produced. An
example  is the sweet potato.
   Finally, the fourth root system type is one which is produced by stem or leaf
tissue. This type, the adventitious root system, is often fibrous, but may be quite
variable.  In corn the original  root system dies and adventitious roots are formed
from the lower nodes of the  stem. Such roots are sometimes called prop roots.
Many grasses produce  roots from  their underground  stems. Some ivys produce
adventitious roots which  aid  in  clinging to  other structures.  Orchids  have
adventitious roots which absorb water and nutrients from the air. The ability of
plants to produce adventitious roots is utilized in vegetatively reproducing plants
via cuttings or air layering.

Root Tissues
   Specific functions  within roots are generally relegated to specific tissues.
Absorption initially occurs in the outer layer of the root called the epidermis
(Plate 2-4) in young roots. Usually many of  these epidermal cells are extended,
forming  root hairs.  Such  a system increases the  surface area  of the root, thus
providing a larger absorptive area.
   Typically the tissue just inside the epidermis is the cortex (Plate 2-4). Cortical
tissues often store  food, water, or  both, provide wall surfaces for water and
nutrient  transport, and intercellular spaces  for gas exchange across the root and
into the shoot.
   Separating the stele from the cortex is the endodermis (Plate 2-5). This single
layer of cells forms a cylinder which serves to regulate the passage of materials
into and  out of the stele (all tissue inside the endodermis).
   Inside the endodermis  is  the pericycle  (Plate 2-5), the site of initiation of
lateral roots and in some  instances part of the vascular cambium. During lateral
root initiation a new root apical meristem forms and grows outward through the
cortex (Plate 2-7).
   The internal tissue of the root is most commonly xylem (Plate 2-5), although
some roots do  contain a pith. Xylem is the water and nutrient conducting tissue
of the plant where the  direction of  transport is typically upward. Phloem (Plate
2-5),  also  occurs in the  stele.  Phloem is the manufactured food  conducting
system  and the direction of flow  is usually  downward toward the roots. In
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general  one would expect water and minerals  to move out of the soil, through
the epidermis,  cortex, endodermis, pericycle and finally into  the xylem where
they would be  transported to the rest of the plant. Sugars and other manu-
factured products move  out  of  the leaves in  phloem cells and are transported
throughout  the  plant, including the roots, where they  move through the peri-
cycle and endodermis into the cortical cells for storage or use.

Root Growth
   Growth  in roots occurs in two major ways. Primary growth results from cell
production at  the tip of  each root and the subsequent elongation of these  cells.
This elongation occurs near the root tip and precedes the formation of root hairs
and lateral  roots. The region  which forms the  new cells is called the root apical
meristem (Plate 2-6). An additional tissue layer is produced by the root apical
meristem, the  root cap, which surrounds and protects the root apical  meristem
as the root  tip grows through  the soil.
   Some roots exhibit an additional pattern of growth called secondary growth.
In this  case a  cylinder  of dividing  cells, the vascular cambium (Plate  2-7),
develops between the xylem and phloem and  produces more  vascular  tissue
(xylem  and phloem). The vascular cambium may remain active for as long as the
plant lives, producing new layers of xylem and  phloem each year, which connect
with the new vascular tissue produced at the root and shoot tip.  The activity of
this  cambium, like  that  of the apical meristem, is dependent  upon  energy and
building materials from the shoot.  Any  restrictions  placed on the metabolism
(e.g. photosynthesis) of  the shoot, such as those which might result from air
pollution,  can  be expected  to reduce  the  activity of these two meristems
resulting in less root growth.
   Since the dermal and cortical tissues cannot  expand  significantly, plants
which produce extensive secondary tissue also produce a cork cambium (Plate
2-7)  outside the stelar tissues.  This  layer is  part of the bark and functions
primarily in protection.
   Certain plants called legumes may become infected with microorganisms such
as bacteria.  The infection occurs through a root hair in the case of bacteria, and
results  in the  formation  of a growth  on  the root called a nodule. The bacteria
within  the  nodule have the ability to change atmospheric nitrogen into a  form
usable  by  plants. This is an important source of necessary nitrogen for  crop
plants and  for  plants in  natural ecosystems. In studies  on the effect of O3  on
legumes it  was found that nodule numbers were decreased by exposure to this
pollutant, but  their ability to fix nitrogen was not curtailed. The net result,
however, was a decrease in total nitrogen  fixed. It was presumed that the effect
resulted from a deficiency of food coming from the shoot  due to inhibition of
photosynthesis  and  was  not due  to  any direct effect  of  O3 on the roots or
bacteria. Similar responses can be expected from plants which  associate  with
nitrogen fixing blue-green algae.
   Another  instance  in which a lack of adequate photosynthate may reduce root
growth  was presented by  Tingey, et al. (1971) where marked effects occurred on
root and hypocotyl growth without visual injury to the shoot.  Over the growing
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season the effect of a reduction in root mass was a reduction in shoot produc-
tivity, since presumably less  water  and nutrient came from  the soil into the
plant.

                                  Stems
   Stems are the supporters and producers of leaves and flowers. They provide a
transport system  for water, minerals and manufactured food products between
the roots and  other plant  organs.  To  a  certain extent stems may  be  storage
organs and in  many herbaceous plants  they  are  photosynthetic.  In  general
morphology, stems  are composed of nodes, sites where leaves  are attached, and
internodes, areas  of the  stem between  nodes. They usually possess a terminal
bud at the tip and axillary buds in the axils of each leaf. The axillary buds may
produce stems or flowers.

Stem  Tissues
   The form and tissue  organization  of stems is extremely variable. However,
there  are several  common types. One type is the herbaceous  dicot stem (Plate
2-8), such as is found in alfalfa or squash. These stems are small in circumference
and rather succulent. In cross section the xylem and  phloem are localized in
discrete vascular bundles (Plate 2-8) in a  concentric ring near the stem periphery.
As in  the  root, a cortex and  epidermis surround the  vascular tissue, but the
cortex is much less extensive. The epidermis often has stomata, tnchomes and a
waxy  cuticle. Much of the stem is occupied by a central pith area which serves in
storage. The main distinguishing features of the herbaceous stem are its small
size and small amount of vascular tissue as compared to ground tissue (pith and
cortex).
   A second stem type is the woody dicot (Plate 2-9). In its initial development
it too has  vascular bundles in  a concentric ring. However, secondary growth is
initiated  very  early in  the stem's ontogeny, producing  extensive  xylem and
phloem.  The  new  vascular tissue forms  a continuous cylinder which is the
characteristic growth ring  of woody  plants. The term  wood  applies to xylem
tissue which surrounds a small amount of pith. Bark includes the phloem, cortex
and epidermis.  The epidermis and cortex are similar to that found in herbaceous
dicots. As secondary growth proceeds a cork cambium is initiated and gives rise
to the corky cells characteristic of the  outer layers of bark. In certain areas of
the stem  bark, clusters  of loosely associated  cells form  a  structure  called a
lenticel (Plate 2-18). This structure  provides a means  of gas  exchange for the
inner  living stem tissues. Bands of living cells extend laterally within the wood
and bark. These bands,  the rays,  are responsible for moving material across the
wood and bark, and for storage.
   Gymnosperms such  as  pine (Plates  2-10, 2-11), a  third stem type,  have a
similar tissue arrangement as the woody dicot. The main distinctions are differ-
ences in cell types in the  vascular tissue and the presence of resin ducts.
   A  final stem type, the monocot (Plate 2-12), is exemplified by plants such as
corn,  wheat, oats and other grasses. These plants  are  usually herbaceous and
relatively small. The stems are  often telescoped, at least until the time of flower
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production. Often, lateral stems are produced.  If they  grow laterally  under-
ground  they are  called rhizomes,  while  those  stems growing above ground
laterally are called runners or stolons (these terms apply to all plants producing
this type of branching). The internal structure of monocot stems is composed of
vascular bundles  irregularly arranged in parenchymous ground tissue. An epi-
dermis with stomata occurs around the outside and often is accompanied by one
or several  layers of cells which may be lignified. Frequently the vascular bundles
turn laterally  and  intermix at the nodes, producing a very disorganized con-
figuration. Many monocot stems are green, with the chlorophyll-containing cells
in the ground tissue near the periphery of the stem.

Stem Growth
   Growth in  stems occurs as it does in roots at several sites. Primary growth
results in  an increase in stem length and occurs as cell division and elongation at
the stem  tip. This  growing region is called an apical meristem (Plate 2-13). It
differs from the root apical meristem in that it does not possess a root cap and it
produces  leaves and lateral buds which become  the apical meristems of vege-
tative or floral branches.  Many stems further increase  their length by retaining
meristematic tissue (intercalary meristems, Plate 2-13) just above each node. An
example  of such growth  is in smooth cord grass, in  which all the  leaves  are
present when the entire stem is a few centimeters (1 to 2 inches) long. After the
terminal  inflorescence is  produced  the intercalary  meristems become  active,
forming the long internodes characteristic of this grass plant.
   Secondary growth is an additional facet of plant expansion for many stems. A
vascular cambium (Plate 2-11) may form between the  xylem and  phloem. This
layer forms more  vascular tissue and thereby causes  lateral expansion  of  the
stem. Accompanying the production of more vascular tissue is the activation of a
cork cambium  (Plate 2-11), usually in the outer ground tissue. Divisions in this
tissue result in the maintenance  of  a protective  corky layer and  some storage
tissue outside  the  phloem of the bark. As previously  implied, these  structures
may remain active  for many years in woody  perennials, producing new tissues
which are continuous with the new primary growth. Many annuals also possess
cambia  which  increase the  vascular tissue as the  plant expands during  the
growing season. Most monocots do not have secondary growth.
   It is apparent that to increase the mass of shoot tissue in a characteristic way
the apical meristem must  function normally. This function requires a  critical
balance of food for energy, nutrients,  water  and growth regulators.  Air pollu-
tants may upset the critical balance between these components, thus producing a
plant abnormal in  size or  shape. Several air pollution studies have  attempted to
use  the yearly increment of  wood as an indicator  of stress caused  by  air
pollution. While such studies do indicate varying degrees of growth from year to
year, it must  be noted that variation  occurs naturally  due to differences in
moisture  and  other environmental parameters. Although the accuracy  of this
method has been  questioned, it is nevertheless often  possible to demonstrate
significant growth reduction effects associated with some air pollution sources,
when compared to proper  control areas or ore-pollution growth rates at the same
sites.
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                                   Leaves
   The primary function of leaves on most plants is photosynthesis.  Leaves are
uniquely  designed  to accomplish what  may be  the most important of all
biological processes. In addition, some leaves  store food,  water, or both. A few
leaves are involved in asexual reproduction, and some in protection.
   There  are a few  general terms for various leaf parts and leaf arrangements.
The leaves of many  broad-leaved plants are composed of a petiole, the stemlike
portion,  and a blade or lamina,  the flattened  portion. The leaves of plants such
as grasses also have a blade,  but that portion corresponding to  the petiole  is
flattened  and often encircles the stem.  This  flattened portion is  called a leaf
sheath. The arrangement of leaves on a stem may be alternate, one leaf per node,
opposite,  two leaves per node, or whorled,  with more than two leaves per node.
A leaf may be simple with a single blade  per  petiole, or compound with several
leaflets per petiole.  This  determination is not always  easy, but the distinctive
feature is the presence of a lateral or axillary  bud at the base of the petiole. The
individual leaflets of a compound leaf do not have an axillary bud. There is one
axillary bud for the entire compound leaf located at the base of the petiole, just
as it is in simple leaves. In many plants, such as soybean, the first foliar leaf is
simple with later  leaves  being  trifoliate  (compound). Leaves of the common
gymnosperms are frequently needle-like. They may be born singly or in groups
in a fascicle. The base of each fascicle has an enclosing sheath.

Leaf Function
   The function of  leaves has  no doubt accounted  for  the  many structural
variations which occur in  nature under different environmental conditions. The
primary function of most leaves is photosynthesis. As has already been stated,
this involves the incorporation  of atmospheric CO2  into carbohydrates within
the chloroplasts and the  concomitant release  of O2 back into the atmosphere.
The gas exchange occurs as the  result of diffusion through openings  in the leaf
called stomata  (Plate 2-17). When photosynthesis  is  occurring, CO2  enters the
water solution in the leaf  mesophyll cell walls  and diffuses, probably as carbonic
acid, into the chloroplasts. This uptake of CO2 from the intercellular spaces of
the leaf   lowers the  CO2 concentration and provides the diffusion gradient
necessary for a net flow of CO2 into  the leaf. At the same time O2 leaves the
chloroplasts  because of  the high concentration  there, enters  the intercellular
spaces  and finally diffuses into the outside atmosphere where the concentration
is  lower.  This pattern of gas exchange would typically occur during daylight
hours when  photosynthesis is occurring.  At night one would not expect a net
CO2 uptake nor O2 liberation  with most plants.
   One problem which arises from this  mechanism  of gas exchange involves
water.  Each cell wall of the leaf mesophyll is  saturated with water and  at least
partially  exposed to intercellular  spaces.  This means  that water will evaporate
from the  cell wall surfaces and produce a saturated atmosphere within the leaf.
The relative humidity (RH) of the intercellular spaces of  a leaf is usually higher
than that of the outside atmosphere if the temperatures are equal. Therefore, if
the stomata are open, water  vapor diffuses from the leaf at a more rapid rate
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than it  diffuses  in. This process is called transpiration. Temperature influences
the rate of  molecular  movement and  thus the rate of diffusion. True transpir-
ation rates are calculated on the basis of vapor pressure gradients, which account
for both  RH and temperature differences between the leaf and  the outside
atmosphere. Water vapor lost by the plant is replaced with  water from the soil.
As a water molecule evaporates from the cell wall of a leaf it pulls another water
molecule behind it, thus providing the energy to transport  water. Minerals and
other material entering the roots are also moved up the  plant in xylem cells in
this stream of water.
   Since water loss is such a general problem for plants, it is  not surprising that a
variety of mechanisms have evolved to conserve water. For  instance  most  plants
close  their  stomata  at night.  This reduces water loss  and also  prevents the
substantial uptake of most air pollutants. The act of wilting closes stomata as a
general rule. Plants in a wilted condition are not very susceptible to air pollution.
Some plants have stomata  sunken into  the  mesophyll tissue  which tends to
reduce the rate  of gas  exchange  and  therefore  pollutant uptake. Many  desert
plants have  very tightly packed mesophyll cells, reducing  the surface area for
evaporation.  These plants are generally  quite  tolerant of air pollution. The
deciduous nature of many plants can be considered  water conserving. Evergreens
such as pines,  though  adapted to conserve water,  may be more  susceptible
because their leaves may receive pollution the year round.
   Many air  pollutants enter plants through leaf stomata. The degree to  which
the stomata  are open  is dependent upon how much water  is in the guard cells
surrounding  the stomatal aperture.  As  the guard  cells   fill  with water, the
aperture gradually increases in size. The reasons for water  influx are currently
thought to be related to the production of organic acids from insoluble starch in
the guard cell and the concurrent movement of potassium ions (K ) into the
guard cells. The accumulation of these ions effectively lowers the water potential
of the  guard cells and causes water  to move  in. The  chemistry  of this phe-
nomenon is not absolutely  clear, but  certain facts are known. The  presence of
light stimulates organic acid  formation  and  K+  movement  into  guard cells
resulting in stomatal opening. Darkness reverses the process. The concentration
of CO2  outside the leaf and in the internal  tissues of the leaf can regulate cell pH
and thus organic acid formation and K+ flux. Therefore, low leaf CO2 content
promotes stomatal opening.  Low temperature (0°C)  can override  the light
mediated  stimulation  and  thus  cause stomata to remain closed. Very high
temperatures  (40°C)  also  inhibit  stomatal opening in  light.  Intermediate
temperatures may induce  a range of degrees in the size of the stomatal aperture.
The  closing  of stomata  during  midday  periods  may  be  the  result of this
temperature phenomenon. Lack of water in the leaf induces stomatal closing in
light. At times when transpiration  exceeds  water uptake, leaves wilt and stomata
close.
   The uptake of any air pollutant into a leaf is dependent not only  on stomatal
opening but on what happens to the pollutant once it reaches the cell surface. If
the pollutant moves into the cell quickly, the diffusion gradient will be favorable
for more pollutant uptake into the leaf. The converse is also true.  The rate of
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movement of a gas into and out of a leaf is dependent upon stomatal  opening,
temperature, and diffusion gradient and is independent of the rate of movement
of any other gas.

Leaf Structure
   The outer covering of the leaves of broad-leaved plants is usually a single cell
layered epidermis (Plate  2-14). These epidermal cells are  covered by a waxy
cuticle, which varies in thickness according to species and environment. Hairs or
trichomes are common, protruding from the leaf surface. Stomata also occur in
the adaxial (upper), abaxial (lower) or both epidermal layers.
   Beneath the adaxial epidermis is one or more cell layers in which the cells are
perpendicular  to the  epidermis.  These cells of the palisade  layer (Plate 2-14)
often appear tightly packed when viewed in cross section, but in reality have air
spaces surrounding each cell. Beneath the palisade layer, cells become irregular in
their  orientation. This mass of tissue  comprises the spongy layer (Plate 2-14).
Together  the palisade and spongy layers  make up the  leaf mesophyll,  which is
the tissue  of the leaf involved in photosynthesis.
   Embedded  in  the leaf mesophyll is the  vascular bundle  or vein system. The
branching arrangement of the  veins is variable, depending on the species  The
major  veins contain xylem  and phloem and a certain amount of tissue which
supports the leaf. As branching continues there is progressively less tissue until
only a few  xylem cells are left in the smallest veins.  In some  plants the vein
endings occur  at  the  margins  of the  leaf, while  in others they are scattered
throughout  the leaf,  a factor  which  can  influence the location of pollution
injury.
   When veins  end at the margins or  tips  of leaves  there  is often a cluster of
loosely associated  cells,  the epithum, just beyond the last xylem cell.  The
epidermis at this point has  a stomata-like structure in which the guard cells do
not function, leaving the  aperture open at  all times. This entire structure is called
a hydathode.  When stomata are  closed, the water taken  into  the plant can
exceed  that which is  released. This tends to build up internal  pressure in  the
xylem called root pressure. Under  these circumstances water droplets are exuded
from  the leaf hydathodes, in a process called guttation. Droplets seen on leaves
during the night and early morning are often guttation droplets rather than dew.
These  droplets  make excellent  collectors  of air pollutants.  At times toxic
solutions  can build up in these droplets and can  cause  severe lesions on the leaf
margin. Plants like blackberry and strawberry are good indicators of this type of
response in the field.
   A second leaf type characteristic of many grasses  is that of corn, sometimes
called  a narrow-leaved plant (Plate 2-15). This leaf  too  has a single epidermal
layer  with a covering cuticle. Stomata are present in both leaf surfaces  although
in many leaves of this type only the upper epidermis has a significant  number.
Trichomes are also common.
   The mesophyll (Plate 2-15) of corn and other grasses is not divided into a
palisade and  spongy layer,  but is a mass  of rather irregularly arranged cells. In
some  narrow-leaved  plants the  mesophyll  cells are oriented perpendicular to and
                                    2-10
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 in a ring around the veins.
    The vascular bundle in corn is surrounded by a bundle sheath which encloses
 the xylem and phloem.  As in the broad-leaved  plants there are major veins with
 extensive branching. However, the major veins of corn and  other  grasses run
 parallel to each other from the base to the tip of the leaf. Air pollution injury is
 common in such leaves at the tip or as lesions running parallel to the veins.
    The needle-like leaves of gymnosperms such as pine have a somewhat more
 complex structure (Plate 2-16). The epidermis is covered with  a thick cuticle. In
 some instances the outer walls of the epidermal  cells are lignified. Stomata  occur
 in  rows  along the length of the leaf and are sunken into the  mesophyll tissue.
 Usually hairs and wax occur in stomatal depressions.
    Beneath the epidermis occurs a layer of small lignified cells, the hypodermis,
 and subtending these are several layers of mesophyll cells. These mesophyll cells
 are rather compact with limited intercellular spaces. The mesophyll terminates at
 the endodermis which  is composed of a single layer of cells. Inside the  endo-
 derrms  are several  layers of larger, thin  walled storage cells comprising the
 transfusion  layer. Embedded in the center is a  vascular bundle with  one to two
 areas of  xylem and phloem. Large resin ducts are common in the mesophyll with
 smaller ones occurring inside the endodermis.
    Stewart, et al.  (1973) attempted  to  use tissue analysis in conifers to dis-
 tinguish  the cause of injury. They had some success in narrowing the cause  down
 to  two or three  possible agents if the stress was not  too severe.  More recently
 Evans and Miller (1975) report that they are able to determine  whether injury to
 ponderosa pine leaves is  caused by O3, SO2 or winter  injury by determining
 which cells of the leaf are injured and how the cell organelles respond.

 Leaf Growth
    Some of the  metabolic characteristics influencing variability in injury re-
 sponses  to air pollution in leaves are due  to age differences of individual cells.
 Many of the cell  divisions involved in leaf formation occur before the  leaf can be
 seen. The major  expansion of many leaves is due to cell enlargement, plus the
 formation of intercellular spaces.
   Broad-leaved leaves most commonly grow first with apical  growth. The flat
nature of the leaf develops when activity begins to occur in lines marking the
presumptive leaf  margins. The actual  shape  is  regulated  by marginal and sub-
marginal meristerns.  As growth continues and the shape is determined, many of
the young leaf cells divide  to  produce the final mass of the leaf. Interference
with these divisions or those of the marginal and submarginal meristems pro-
duces the savoying and cupping caused by some air pollutants.
   Leaves of corn or other grasses have early  apical growth, but subsequently
most of  the new  growth is basal via two  intercalary  meristems.  One  of  these
meristems is located  at the base of the blade while the other  is located at the
base of the sheath.
   Pine   needles  also  elongate  initially by  apical  growth,  with  intercalary
meristem activity at the leaf base producing most of the actual needle. Bands of
injury caused  by air  pollution are  more likely  to  develop  in  leaves  of pine or
                                    2-11

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narrow-leaved plants where gradients of tissue age occur along the length of the
leaf.

                          Flowers, Fruits and Seeds
   A discussion of floral structure is beyond  the scope of this text, but several
features  of this organ and its  function relate to air pollution injury. First the
longevity of  the flower itself is rather  short as compared  to other organs.  This
means  that the time available  for  direct acute pollution injury is less than for
other organs. This is not to say that effects are less likely, since the fruit and
seed are  directly dependent on the rest of the  plant  for  their growth and
development.
   In many plants the stimulation to produce a flower comes from the leaves.
The leaves may measure the  length of day through  the reaction of the pigment
phytochrome to light and darkness. Once a certain biochemical state is achieved
the shoot vegetative meristem is converted  to a  floral meristem  and flower
production begins. It is possible  for stress  such as air pollution to  upset  the
timing of this process.
   Once  flower development  is  complete pollination  can occur. The male sex cell
is carried in pollen grains by wind or insects in many plants. Pollen seems to be
very tolerant  of air  pollution. Germinating  pollen  grains may be injured when
exposed  to pollution in dishes  in a chamber.  Reduction of the yield of corn in
the field has  been attributed in one instance to the interference of air pollution
in the  successful growth of pollen grains. If changes occur in the  chromosomes
of sperms in  pollen grains, these changes may show up as different  traits in the
next generation.  A more likely  result would  be sterility  with  no embryo
formation.
   Fertilization  takes place deep within the  floral  tissue  and is probably  well
protected from direct air pollution injury. However, the growth of the embryo,
the seed and the fruit  may be subject to  effects indirectly produced by air
pollution. These structures are dependent upon the rest of the plant for the food
which builds  their mass. If, at the time when these tissues are building, leaf tissue
is severely injured, the metabolites which normally  go to the flower may not be
available. Heagle, et  al. (1974) have shown that reduction in soybean yield  can
occur if  O3 is administered at a time when the flower is developing the fruit and
seed. Exposures early in the life cycle allowed  time for  the plant to recover,
while later exposures had no effect on  yield.  Taylor, et al. (1958) have shown a
reduction in  avocado  fruit  yield  due  to  photochemical  oxidant in southern
California. In this case there  were no visible  symptoms, but merely a reduction
in photosynthate available to form fruit mass.
   The petals of flowers often have thin  cuticles  and  may be sensitive  to air
pollution. In the  cut flower industry pollutants like F are damaging to plants
such as  gladiolus. Ethylene  also  is  potentially  destructive to flowers such as
orchids.
                                   2-12
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                                 Selected References

Bobrov, R. A. The leaf structure of Poa annua with observations on its smog sensitivity in
   Los Angeles County. American Journal of Botany, 42:467-474,1955.
Esau, K. Plant Anatomy. New York: John  Wiley and Sons, Inc., 1965.
Evans, L. S. & Miller, P. R. Ozone damage to ponderosa pine:  a histological and histo-
   chemical appraisal. American Journal of Botany, 59(3):297-304, 1972.
Evans, L. S.  & Miller, P. R.  Histological  comparisons of single and additive O3 and SO2
   injuries  to  elongating  ponderosa  pine  needles.  American  Journal  of  Botany,
   62(4):416421, 1975.
Evans, L. S. & Ting, I. P. Ozone-induced membrane permeability changes. American Journal
   of Botany, 60(2):155-162, 1973.
Glater, R.  B., Solberg,  R. A. & Scott,  F.  M. A  developmental study of the leaves of
   Nicotiana glutinosa as related to their smog-sensitivity. American Journal of Botany,
   49(9): 954-970, 1962.
Heagle, A.  S., Trent, L. & Neely, G. E. Injury, growth and yield responses of soybeans to
   acute  doses of ozone in the field. Manuscript in preparation, 1974.
Hill, A. C. & Littlefield, N. Ozone effects on apparent photosynthesis, rate of transpiration
   and stomatal closure in plants. Environmental Science and Technology,  3:52-56, 1969.
Katz, M., Ledingham, G. A., & McCallum, A. W. Symptoms of injury on forest and crop
   plants. In: Effect of Sulfur Dioxide on  Vegetation.  Ottawa: Association on Trail Smelter
   Smoke of the National Research Council of Canada, 51-103, 1939.
Linzon, S. N. Histological studies of symptoms in semi-mature  needle tissue blight of eastern
   white pine. Canadian Journal of Botany, 45:2047-2061, 1967.
MacDowall,  F.  D. A.  Stages of ozone damage to respiration  of tobacco leaves. Canadian
   Journal of Botany,  43(4)-419-426, 1965.
Mudd, J. D.  Biochemical effects of some  air pollutants on plants.  In: Naegele, J., ed., Air
   Pollutant Damage to Plants. Washington, D.C.: American Chemical Society, 3147,1973.
Perchorowicz, J. T. & Ting, I. P. Ozone effects on plant cell permeability. American Journal
   of Botany, 61(7):787-793, 1974.
Salberg, A. & Adams,  D. F. Histological responses of some plant leaves to hydrogen fluoride
   and sulfur dioxide.  American Journal of Botany, 43:755-760, 1956.
Salisbury, F. B. & Rose, C. Plant Physiology.  Belmont,  CA.: Wadsworth Publishing Co., Inc.,
   1969.
Stewart,  D., Treshow,  M. & Harner, F. M. Pathological anatomy of conifer needle necrosis.
   Canadian Journal of Botany, 51:983-988, 1973.
Taylor, O. C., Cardiff, E. A., Mersereau, J. D. & Middleton, J.  T. Effect of airborne reaction
   products of ozone and  1-N-hexene  vapor  (synthetic  smog)  on  growth  of avocado
   seedlings. Journal of the American Society of Horticultural Science, 71:320-325, 1958.
Thomson, W. W.,  Dugger, W.  M., Jr., & Palmer, R. L. Effects of ozone on the fine structure
   of the  palisade  parenchyma cells of  bean  leaves. Canadian  Journal of Botany,
   44:1677-1682, 1966.
Ting, I. P. & Mukerji,  S. K. Leaf ontogeny as a factor in susceptibility to ozone: amino acid
   and carbohydrate changes  during expansion. American Journal of Botany, 58:497-504,
   1971.
Tingey, D.  T., Heck, W.  W.,  &  Reinert, R. A. Effect of low  concentrations of ozone and
   sulfur dioxide  on foliage, growth and yield of radish. Journal of the American Society of
   Horticultural Science, 96(3):369-371, 1971.
Treshow, M.  The effect of flouride on the anatomy  of Chinese  apricot leaves.  Abstract.
   Phytopathology, 46:649, 1957.
                                        2-13

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                                   INTERCELLULAR
                                   SPACE
                PLASMODESMATA, PIT


                         MIDDLE LAM EL
                           CYTOPLASM

                         TONOPLAST
Plate 2-1. Leaf Cells of Spartina alterniflora (Smooth Cord Grass)
       Showing Cell Organelles
                    2-14
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                                                   CELL
                                                   WALL
Plate 2-2. Portion of Hoot Meristem Cell of Chrysanthemum
        Showing Cell Organelles
                        2-15

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                      " ;*v
CHLOROPLAST


   STROMA
   Plate 2-3. Sect/on Through Chloroplasts of a Chrysanthemum Leaf
           Cell Showing Details of Grana and Lamella
                            2-16
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                                             EPIDERMIS

STELE
                                  PERICYCLE
    Plate 2-4. Cross Section of a Ranunculus sp. (Buttercup) Root
                         2-17

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Plate 2-5. Cross Sect/on Showing the Stele Area of a Ranunculus sp.
         (Buttercup) Root
                            2-18
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                                     EPIDERMIS


                                       CORTEX




                                       STELE
                                   ROOT
                                   APICAL
                                   MERISTEM
                                    ROOT CAP
Plate 2-6. Longitudinal Section Through the Apical Meristem of
        Strophostyles helvola (Beach Pea) Root Showing Area
        Where Primary Growth Occurs
                      2-19

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                      PERIDERM
     VASCULAR
     CAMBIUM
CORK
CAMBIUI
   LATERAL ROOT
   Plate 2-7. Cross Section of the Root of Nicotiana tobaccum (Tobacco)
          Showing Secondary growth and Lateral Root Formation
                           2-20
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                               CAMBIUM
                                                LEM
                                              LOEM
                                             RTEX
          STOMA
                         EPIDERMIS
Plate 2-8. Cross Section of the Herbaceous D/'cot Stem of
        Medicago Sativa (Alfalfa)
                     2-21

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                  BARK
PERIDERM

   PHLOEM
                                           VASCULAR
                                           CAMBIUM
                                                 RAY
Plate 2-9. Cross Section of the Woody Dicot Stem of Liriodendron
        tulipifera (Tulip Poplar)
                       2-22
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                                                   BARK
Plate 2-10. Cross Section of the Gymnosperm Stem of Pinus sp. (Pine)
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Plate 2-11. Cross Section of the outer area of the Gymnosperm Stem of
          Pinus sp. (Pine) Showing Sites of Secondary Growth
                             2-24
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                                                  EPIDERMIS
Plate 2-12. Cross Section of the Monocot Stem of Zea mays (Corn)
                         2-25

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                                    ' •'•,
                                    . >4
                              ;v'>/lt|??v v'rr,
                                        ..  «»».#. • -
                                   -'  ,.'»>-!&.  '»
                                       ,            (
                                       '...
                                       -'
Plate 2-13. Longitudinal Section of the Shoot Tip of Spartina
        a/ternif/ora (Smooth Cord Grass) Showing the Apical
        Meristem, Young Leaves and Intercalary Meristems
                        2-26
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          CUTICLE
ADAXIAL
EPIDERMIS
PALISADE
LAYER
MESOPHYLL
 SPONGY
 LAYER
ABAXIAL
EPIDERMIS
                                   £f.
                     STOMA
    Plate 2-14. Cross Section of the Broad-leaved Leaf of Clycine max (Soybean)
                           2-27

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PHLOEM
     VASCULAR
     BUNDLE
                                            ADAXIAL
                                            EPIDERMIS
  XYLEM
ABAXIAL
EPIDERMIS
                           BUNDLE
                             SHEATH
                               BULLIFORM
                                  CELLS
   Plate 2-15. Cross Section of the Narrow-leafed Ledf of Zea mays {Corn)
                        2-28
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           XYLEM
                                       PHLOEM
                                                   RESIN
                                                   DUCT
                                                       STOMA
               TRANSFUSION
EPIDERMIS      TISSUE
                       HYPODERMIS


MESOPHYLL     ENDODERMIS
Plate 2-16. Cross Section of the Needle-like Leaf of Pinus sp. (Pine)
                       2-29

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Plate 2-17. Surface View of a Stoma of Zebrina sp. Wandering Jew]
                           2-30
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Plate 2-18. Cross Section of the Outer Bark of Liriodendron
          tulipffera (Tulip Poplar) Showing a Lenticel
                         2-31

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                               Chapter 3


                THE PHOTOCHEMICAL OXIDANTS


                               Introduction
   In the early 1900's when a dearth of wood fuels forced Londoners to use coal
as a domestic fuel, coal smoke, combined  with fog, became a public nuisance
which was to last many years and cause much suffering and many  deaths. The
term  "smog" was coined then, a combination of the words  smoke and fog.
During the rapid industrial and  urban  expansion that followed World War II, air
pollution episodes began to appear with increasing frequency in the larger urban
areas of the world. It was only  natural that people referred to this nuisance also
as smog since there  was general belief, even among  the scientific community,
that the basic problem was  sulfur dioxide in coal smoke. However, during the
1950's the  chemical constituents of this  smog  were identified,  and it was
discovered that this smog arose  from a series of atmospheric reactions between
hydrocarbons and oxides of nitrogen from automobile exhaust in the presence
of sunlight. Among the products produced by the reactions are substances called
"oxidants."  Since  sunlight  was needed  to initiate  the  reactions, the terms
"photochemical  smog," or  more  specifically  "photochemical oxidants," are
presently being used to differentiate it from the  London-type smog.
   Because of the complexity  of  this subject matter, this chapter has  been
divided into three sections, based on the three most important constituents from
the standpoint of plant damage. The interrelationship of  the three  parts,  how-
ever,  and their relation to the  total air  pollution  problem, should be kept in
mind. The three  phytotoxic  constituents consist of ozone (03), the peroxyacyl
nitrates (Pans),  and oxides of nitrogen.  Four peroxyacylnitrates have  been
identified: peroxyacetyl nitrate  (PAN), peroxypropionyl nitrate (PPN), peroxy-
butyryl nitrate (PBN), and peroxyisobutyryl nitrate (P1SOBN). Although PPN is
more toxic to vegetation than PAN, and PBN and P;so BN are more toxic than
PPN,  only PAN has been studied extensively. PAN also appears to be the only
one  of this  homologous series  to be present  in srnog at concentrations high
enough to cause injury and, therefore, will be the only member of the series
discussed in this chapter.
                                   3-1

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                         SECTION 1.  OZONE


                                 Sources

   Ozone is formed naturally by the action of sunlight on oxygen in the upper
atmosphere (15,000 to 37,000 meters). Ozone can also be formed by electrical
discharge during thunderstorms.  These two  natural sources, however, do not
contribute significantly to the smog problem because: (1) the electrical energy
available from the atmosphere is not adequate to form significant ozone concen-
trations over large urban areas, and (2) although ozone in the upper atmosphere
can be  transferred  to  the ground in  the vicinity of jet streams and  weather
fronts, these  concentrations are  not believed  to  be high. The anthropogenic
source of ozone is the principal cause of plant injury from this pollutant. Many
pollutants arrive at the leaf surface in the same form in which they are emitted
from  smokestacks or automobile tailpipes. But photochemical oxidants are quite
different. These compounds are called  "secondary" pollutants, because  they are
formed  in the air by  the action of sunlight on primary air pollutants. Such
reactions are  chemical  in nature,  and are mediated  by sunlight. Thus they are
called "photochemical" reactions. Since some  of  the photochemical products
formed  are capable of "oxidizing" certain materials (such as nylon, rubber, plant
tissue, etc.), they are called  photochemical oxidants. The two  most important
photochemical oxidants from  the standpoint  of  plant injury are  ozone and
peroxyacetyl nitrate.
   The  primary pollutants involved in  the photochemical reactions producing
ozone and PAN are hydrocarbons and oxides  of nitrogen. Hydrocarbons  arise
during the incomplete  combustion of petroleum products such as natural gas,
gasoline, or  oil. Although many  industries emit hydrocarbons, transportation
sources account for more than half of the total emissions.
   The  photochemical  reactions  that  take place in  an atmosphere  containing
oxygen and oxides of nitrogen  without hydrocarbons can  be generalized as
shown in Figure 3-1. The oxides  of nitrogen  are broken down into nitric oxide
(NO) and atomic oxygen (O). The atomic oxygen then reacts with  the normal
oxygen (O3)  of the air to form ozone (O3).  The O3 may further react  with the
NO to form NO^ and Oj, in a balanced, cyclic reaction.
   However, if ozone (O3) always reacted with NO to form NOj, a steady-state
system would exist with no ozone build-up.  Of course, ozone does  build up in
polluted areas, because hydrocarbons enter into the  reaction (Figure 3-2). It is
postulated that the hydrocarbons disrupt the cyclic nature of the reaction by
combining first with Oj to form a peroxyacyl radical  and then with NO2  to
form  PAN. This removal of NO from the system allows for a build-up of ozone.
                                   3-2
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                     Figure 3-1.  Atmospheric NO2 Photolytic Cycle

Source: Air Quality Criteria for Photochemical Oxidants. Washington, D.C.: Public Health
        Service, Department of Health, Education, and Welfare, 2-4, 1970.
                    Figure 3-2. Photolytic Cycle with Hydrocarbons

Source: Adapted from: Air Quality Criteria for Photochemical Oxidants. Washington, D.C.
        Public Health Service, Department of Health, Education, and Welfare, 2-7, 1970.
                                        3-3

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                           Atmospheric Chemistry
   The  photochemical  reactions and subsequent high oxidant  levels are  most
severe during inversions  and stagnant weather. Normal  background levels of
ozone are  0.02  to 0.04 ppm* (39  to 78 /ig/m3),** but during inversions the
concentrations  of  primary  pollutants build up  in the stagnant air,  and the
photochemical reaction causes an increase in the  oxidant concentration. Levels
of total oxidants (90 percent or  more of which are ozone) exceeding 0.50 ppm
(880 ;Ug/m3) have been recorded during such weather in Los Angeles. Peaks of
0.15 to 0.25 ppm (294 to 490 jUg/m3 ; the levels are for oxidants) are common in
many urban areas during  inversions.  Such levels are capable of severely injuring
sensitive plants.
   Maximum oxidant levels often occur in mid to late summer (Figure 3-3). In
this figure, the  curve for  Denver is probably more representative for the entire
country than the curves for Los  Angeles and Phoenix. Oxidant levels at various
            FEB.
                  MAR,   APR.
                               MAY
                                      JUN    JUI_.


                                       MONTH
                                                        SEP.
                                                              OCT.  NOV.   DEC.
Figure 3-3. Monthly Variation of Mean Daily Maximum One-Hour Average Oxidant Con-
          centrations for Three Selected Cities
Source: Air Quality Criteria for Photochemical Oxidants. Washington, D.C.: Public Health
       Service, Department of Health, Education, and Welfare, 3-8, 1970.
  *ppm = parts per million, v/v
 **Mg/m3 = micrograms of pollutant per cubic meter of air
 NOTE: See Appendix A for explanation of conversions between ppm and Mg/
                                     3-4
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1
1
times of day also show consistent patterns (Figures 3-4, 3-5, 3-6). Typically,
• oxidant concentrations are low during the night, begin to rise in the morning,
peak in early afternoon, and then drop again as evening approaches.
• 0.50
I

0.40
I


IE 0.30
a
8
I i"
O 0.20
2
I

H 0.10
•
• °v

1 1 1 1 1 1 1

NO
""" 1 """
jj
i
i
i
i
i
n
1 j\ N02
/f JO °3

/i \l \ A. \
// /!>A\XV\

:_co_.y// V x\ \~;/-^
— ~rf'\J\ i i ^^*f=irr
100 0300 0600 0900 1200 1500 1800 2100 24
50


40



30
E
Q.
a
o"
O
20



10

0
00
^ TIME OF DAY
I
Figure 3-4. Average Daily One-Hour Concentrations of Selected Pollutants in Los Angeles,
. July 19, 1965
^1 Source: Air Quality Criteria for Nitrogen Oxides. Washington, D.C.: Environmental Protec-
^^ tion Agency, Air Pollution Control Office, 1971.
I
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1

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   0 30
   0.25
   0.20
H  0.15
Z
UJ
o
Z

8  0.10
LLJ
   0.05
                           I    T
                              i   ii
                                           10 12
                     HOUR OF DAY
    0.16




    0.14



    0.12




    0-10



    0.08




    0.06



    0.04



    0.02



       0
                                   ST. LOUIS
                              *   \ JUNE 1966
                         LOS ANGELES,
                    ' AUGUST 1964 AND 1965
                                                   Figure 3-5.
                                                   Diurnal Variations of Mean Hourly
                                                   Average Oxidant Concentrations in
                                                   Philadelphia, August 6-8, 1966
                                                   Figure 3-6.
                                                   Diurnal  Variation of Mean Hourly
                                                   Average Oxidant Concentrations in
                                                   Los Angeles and St. Louis
       12  2  4   6  8  10  12  2  4   6   8  10
        ^	a.m	^4	p.m	^

                      HOUR OF DAY
Source: Air Quality Criteria for Photochemical Oxidants. Washington, D.C.: Public Health
        Service, Department of Health, Education, and Welfare, 3-8, 1970.
                                        3-6
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                             Monitoring Data
   Long-term trends for oxidants are presented in Table 3-1 for four major U. S.
cities. Although the maximum hourly averages have increased over the sampling
period,  there  does  not appear to  be  a  uniform predictable pattern. There is
likewise no  pattern discernible if the available data are analyzed by number of
days with at least one hourly average equal to  or exceeding a given concentra-
tion. The  reason  for a lack of pattern may be  related to the fact that photo-
chemical pollutants are products of the weather in one sense. Since sunlight is
required for ozone  formation, the  amount of cloudiness would affect concen-
trations, and cloudiness is variable from year to year.
Data
Table 3-1
Showing Long-term Trends in
Oxidant Concentrations Recorded at CAMP Sites
from 1964


City
Chicago



Denver


Philadelphia



Washington, D.C.



Source:
Adapted from: Air Quality
to 1967 in Four Large Urban


Year
1964
1965
1966
1967
1965
1966
1967
1964
1965
1966
1967
1964
1965
1966
1967

Areas
Maximum
hourly average.
ppm
0.13
0.13
0.19
0.16
0.25
0.19
0.21
0.20
0.33
0.52
0.17
0.20
0.21
0.16
026

Criteria for Photochemical Oxidants. Washington, D.C.:
Public Health Service, Department of Health, Education, and
Welfare, 3-4, 1970.
   The  oxidants  formed over large urban  areas may cause plant injury many
miles away. For  example,  oxidants formed over the Los Angeles basin injure
pines in the San Bernardino Mountains, 60 to 70 miles from the city's center, as
the polluted air  mass moves eastward.  Recent studies by the  Environmental
Protection  Agency (EPA) have suggested that high ozone concentrations in rural
parts of Maryland and West Virginia may result from primary pollutants released
from  urban-industrial areas many miles away.  As these precursor pollutants
move eastward with  the prevailing  weather patterns, ozone is  formed in the
                                    3-7

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presence of sunlight, and the precursors are consumed, leaving fairly high ozone
levels which are capable of causing plant injury in  remote areas Thus, it is
important to consider ozone injury to vegetation in remote rural areas, as well as
metropolitan areas.

                              Symptomatology
   Ozone probably  causes  more plant damage  in the  U. S. than  any other
pollutant. Injury has been observed in the eastern, central, and western U. S., in
rural  as  well  as  urban areas,  and on  a wide  range  of  plants including leafy
vegetables, grains, and conifers.
   Ozone is taken into the leaf through the stomata during normal gas exchange.
Once inside the leaf, the ozone (or possibly a secondary product) attacks the
cells,  probably first disrupting the cell membrane. As these structures break
down, groups of cells collapse and symptoms appear on the leaf surface. If the
leaf contains  palisade mesophyll cells, as do most broad-leaved  plants,  ozone
preferentially  attacks these  cells and the symptoms may be initially restricted  to
the upper leaf surface.  On narrow-leaved plants, conifers,  and  broad-leaved
plants in which  the mesophyll is not  differentiated into palisade and spongy
mesophyll, cells usually near  stomata are  attacked, and symptoms may appear
on either leaf surface.
   In general, ozone injury develops initially at the tips of young leaves, and
becomes more widespread over the leaf surface  as the leaves mature. The oldest,
mature  leaves are usually tolerant to  ozone, while the next-to-oldest are often
sensitive, as  on tobacco, although there are exceptions to this. Occasionally,
older leaves may show severe ozone injury late in the  season, possibly because
they  were exposed for a longer period of time, including their period of peak
sensitivity. Many other factors such as  plant age, nutrition, climatic factors, time
of year, shading, etc. may affect symptom development to varying degrees.

Broad-leaved (Dicotyledonous) Plants
   Usually, although not always, the  first symptom of ozone injury on broad-
leaved plants is a watersoaked appearance of the upper leaf surface (Plate 3-1).
The leaf appears to be shiny, or oily, and if the tissue is injured, the watersoaked
areas  become  dry  and characteristic  symptoms  form. If  the tissues are  not
irreversibly  injured, the  watersoaked  look  may  disappear, and the  leaf  will
recover.  The most common ozone symptoms  on broad-leaved plants are small
flecks or stipples visible on the upper leaf surface.
   The  individual flecks, as seen with a hand  lens, are small lesions of dead
tissue, formed when groups of palisade cells die. The upper epidermal cells over
the injured palisade cells also collapse. The cells  in the affected area may die and
become bleached. The individual flecks may be  white, yellow, or tan (Plates 3-2
through  3-12). If the  flecks  are numerous,  the  entire  leaf  appears chlorotic
(yellowish or pale green), or bronzed (Plates 3-13, 3-14). Premature defoliation
often accompanies chlorosis or bronzing.
   Acute injury.  If a plant  is extremely sensitive, or if a high dose of ozone is
involved, the flecks may coalesce into  larger lesions, occasionally  visible on both
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leaf surfaces. Small veins may even be killed in this larger "bifacial" lesion (Plate
3-15). This severe symptom is observed in the field only on extremely sensitive
plants,  and is more commonly described  for plants  subjected to  artificial ex-
posures of ozone.
   Stipples are small,  dark, pigmented groups of palisade cells that appear as
small dark dots visible on the upper  leaf surface after exposure (Plates 3-16,
3-17, 3-18). The  upper epidermis often remains uninjured, and the symptom is
thus actually observed through the epidermal cells. Stipples may be red, reddish-
brown, reddish-purple,  or black. Veins  and veinlets  are uninjured, and  the
smaller veinlets actually form a boundary for the pigmented area, causing the
lesion to be angular in shape. Stipples are best viewed with a hand lens, and, on
dark green leaves, may be best observed when the leaf is held up to the light.
   Chronic injury. Chronic injury  is usually associated with vegetation exposed
to relatively low concentrations of ozone for fairly long time periods. Depending
upon the plant species, either the fleck or the stipple symptom type may be
present on broad-leaved  plants. Although  the stipple type of symptom is gener-
ally regarded as a less severe reaction than the fleck type, the symptom produced
is more often correlated with the plant species  than with the concentration or
duration of pollutant.
   Symptom expression is often not intense in the case of chronic injury. Few
symptoms may  appear  on the leaf surface. However,  if the chronic  injury is
prolonged, the symptoms may gradually coalesce on the leaf surface, giving the
injured  leaf a bronzed  or yellowed  appearance. Bronzing or yellowing may be
accompanied by  premature defoliation. Reduced  growth and/or reduced yield
may also result from long-term exposures of vegetation to low levels of ozone. It
has been  shown that ozone  can cause reduced crop yield in potatoes,  grapes,
citrus, and other plants.

Narrow-leaved (Monocotyledonous) Plants
   Most  narrow-leaved plants  such as grass or  grains,  including corn, have
photosynthetic cells and stomata on both surfaces of the leaves. Ozone injury on
these plants  thus appears on  either leaf surface. The most common symptoms
are small  chlorotic spots or white flecks between the veins. Injury on sensitive
plants appears as  long  white-to-yellow streaks between the  veins, often being
most  severe at the bend in the leaf blade. A complete bleaching of the leaf blade
(Plate 3-19) may also develop.

Coniferous Plants
   The two most common ozone symptoms observed on conifers are "chlorotic
mottle" and  "tipburn." Chlorotic mottle  develops as small patches of tissue in
the needle are injured and become  yellow. These islands of yellow tissue are
surrounded by healthy green  tissue, giving the needle a "mottled" appearance.
Tipburn  refers to  the  condition  when  the  entire needle  tip dies,  becomes
reddish-brown, and later gray as it weathers (Plate 3-20).
   Acute  injury.  Acute ozone  injury to  most  coniferous  species is  usually
observed as  tipburn  of the  current  season's  needles. Chlorotic mottle may
                                    3-9

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accompany  the tipburn in some  cases. Previous seasons' needles are often not
affected  by  acute  exposures, nor are the needles  of plants exposed in seasons
other than spring and early summer.
   Chronic injury. The chlorotic  mottle symptom is a common expression of
chronic ozone injury on individual needles of many coniferous species. However,
needles of certain species such as eastern white pine may also exhibit tipburn
after chronic exposure  to ozone.
   In general, chronic ozone injury  to  conifers is manifested as reduced growth.
Symptoms include a reduction  in both terminal and diameter growth, loss of all
but the current season's needles, reduction in amount and size  of the needles,
deterioration of the fibrous root system, and a gradual  decline  and sometimes
death of the tree (Plate 3-21).
   In addition, chronic injury  may result in a conifer's inability to withstand
extremes in  environmental factors such as drought, or secondary parasites such
as root-rot  fungi or bark beetles.  Cone production may also be  impaired by
chronic ozone injury.

Symptoms of Common Disorders
   Several specific  disorders commonly observed  in the field  are  caused by
ozone, A knowledge of these disorders, since they are  common, is valuable to
the diagnostician. A brief description of each follows:
   Grape Stipple. This disorder was the first major plant problem diagnosed as
being caused by ozone. Although first  observed in southern California, it is now
thought  to  be  widespread in the East. The syndrome includes leaf bronzing,
yellowing, premature  senescence and  leaf fall. Symptoms first appear on the
upper surface of young  leaves early in the season as  brown-to-black stipples
bounded by the smallest veinlets. The  small lesions often coalesce to give rise to
larger stipples (Plate 3-16).  As the season progresses, the  older leaves become
bronzed and fall prematurely. Grape yields may be  drastically reduced.
   Weather Fleck of Tobacco. This problem has been severe on sensitive varieties
of tobacco,  especially  cigar  wrapper varieties from  southern Canada to south-
eastern U. S. The primary symptom is the presence  of white, light gray, or tan
flecks on the  upper  leaf surface  of  fully expanded leaves  (Plate  3-2). The
symptoms are often confined by  the smallest veins, thus  forming lesions angular
in shape. On sensitive varieties such as Bel W-3 the lesion may go completely
through  the leaf  and be visible on the lower leaf surface  (i.e.,  it  becomes
bifacial). Premature  senescence, including yellowing, may  occur in all tobacco
species.
   Onion Tipburn or Blight.  This problem  has occurred sporadically over the
years in many widespread areas of the country. The symptom consists of typical
ozone flecking  and tissue breakdown, followed by  death and browning of the
onion leaf tip (Plate 3-22).
   Emergence  Tipburn of Eastern  White Pine. Emergence  tipburn, historically
known as "white  pine  blight," has been observed on scattered trees throughout
the natural range  of white pine since the early 1900's (Plate 3-23). The problem
is  characterized by a dying  of the  tips of young elongating needles in June or
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 July. The injured  tissue is reddish-brown at first, later  turning brown (Plates
 3-20, 3-21).  As the dead  tissue weathers, it turns gray and  the needle tip may
 break off.
   Ozone Needle Mottle of Ponderosa Pine. This disorder is widespread in many
 areas of California, but principally in the San Bernardino Mountains of southern
 California, where  it is  caused by ozone formed over  Los Angeles drifting
 eastward. The earliest symptoms on sensitive trees are small, chlorotic flecks on
 the older needles. The chlorosis and yellowing become more severe, the needles
 become yellow, then brown and finally drop prematurely. Eventually, all but the
 current year's needles are lost, contrasted with the normal three-to-five years of
 needles present  on resistant trees. Thus, the  branches have a tufted appearance,
 being bare except for the current year's needles. In severe  cases, even the current
 needles begin to die, then the branches die back and gradually the entire tree
 succumbs (Plate 3-21).

                      Factors Affecting Plant Response
 Genetics
   Genetically,  plants vary considerably in  their response  to ozone. Certain
 species  are quite sensitive, while others are very tolerant.  Even within the same
 species, different  cultivars  may vary  greatly in  sensitivity. For example, the
 Bel W-3 cultivar of tobacco is extremely sensitive  to ozone, whereas the Bel B is
 fairly tolerant.  Species  or cultivars of green beans, azaleas, radish, tomato,
 safflower, poplars, soybeans, petunia,  and others have  all  demonstrated this
 variation in response within the same species.

 Environmental Factors
   Many  environmental  factors influence the sensitivity  of plants  to ozone,
 including  climatic  parameters such  as  light, temperature, and  humidity.  In
 addition, various soil features such as moisture, texture, and nutrition also affect
 plant response.  Some of these variables  influence sensitivity simply by altering
 stomatal  opening,  thereby influencing  gas exchange and,  at the same time,
 pollutant  uptake.  The influence  of other variables is  more subtle,  possibly
 affecting internal physiological mechanisms which regulate sensitive membranes,
 repair mechanisms, and other internal functions of the plant.
   Temperature. In general, plants grown at warm temperatures (i.e., 27 to 32°C)
 prior  to ozone exposure are more sensitive to ozone than are those maintained at
 cooler temperatures (i.e., 10 to 16°C) before  a fumigation. However, during an
 ozone fumigation, an inverse  relationship between the amount of tissue injury
 and exposure temperature is observed. More injury occurs at lower temperatures
 than at  higher temperatures. This indicates that maximum sensitivity to ozone,
in terms of temperature,  occurs when plants are growing under warm conditions,
 and then exposed to ozone in relatively cool air.
   Humidity. Atmospheric humidity is usually directly related to ozone sensi-
tivity. Plants  grown and/or exposed at fairly  high  relative humidities (i.e., 80 to
90%)  are more sensitive than those grown and/or exposed at low humidities (i.e.,
 50 to 60%). Plants growing in parts of the country having low humidities, such
                                    3-11

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as the  arid  Southwest, are probably more tolerant to ozone  and other  air
pollutants than are plants grown in the more humid Northeast.
   Light.  Light also influences the sensitivity  of vegetation to ozone. Plants
grown at  low light intensities  (i.e.,  1000 to 2000 footcandles) prior to ozone
exposure are more sensitive than are plants grown at higher intensities (i.e., 2000
to 3000 footcandles).  However, during an  exposure, plants exposed at higher
intensities show more injury.
   The  amount of light during a day (photoperiod) also affects sensitivity. For
example, tobacco and pinto bean plants are more sensitive when grown under an
eight-hour  photoperiod than under one of  16 hours. Also, plants are generally
more sensitive at  mid-day than in early  morning or late afternoon, and  least
sensitive at night (during which time many species  have closed stomata). The
influence  of light on  ozone  sensitivity  is  of  special practical significance  in
commercial greenhouses, where light  intensity and duration are often varied to
induce growth, flowering, or fruiting.
   Soil. Edaphic (soil)  factors affecting the underground portion of a plant may
have a profound effect on  the ozone sensitivity of  the above-ground portion.
Moisture-stressed plants are  usually more tolerant  to ozone  than are  those
growing under ample soil-moisture conditions. Presumably, the moisture stress
induces closure of the  stomata, preventing pollutant uptake. The soil texture
(relative amounts of sand, silt, and clay) may also affect sensitivity. Plants grown
in light, well-aerated soils are  more sensitive than those in heavy clay soils. Soil
moisture and aeration interrelationships are probably involved. The  exact influ-
ence of soil nutrition  on sensitivity is not clear, but in general, plants growing
with optimal  nutrients for growth are more sensitive to ozone than are those
growing at nutrient deficiencies or excesses.

                           Injury Threshold Doses
   Pollutant concentration and the length  of the exposure period are  collectively
referred to as  "dose," and the lowest dose  that produces an effect  is termed a
"threshold dose."  Because of  the interrelationship of  concentration and time,
there is no single threshold dose for an effect to occur. For example, leaf injury
on a  given plant or set of plants exposed to .10 ppm (196 |Ug/m3) O3 might
occur  after only one hour, but when exposed  to .05  ppm (98 /zg/m3)  Oa  it
might require an exposure of up to 10 hours to produce leaf injury.
   The  threshold dose of ozone  that causes injury varies tremendously among
species, and even among  cultivars within the same species. However, the most
sensitive species of various types of plants are all injured  by approximately the
same  threshold concentration  of ozone. For example, certain  varieties of sweet
corn and oats (monocots) are injured by  exposure to 0.10 to 0.12 ppm (196 to
235  ,ug/m3) ozone for two hours. Bel W-3 tobacco  (a dicot), one of the most
ozone-sensitive plants,  shows leaf injury after exposure to 0.05 ppm  (98 //g/m3)
for four hours. Selected,  sensitive strains of eastern white pine (conifer) have
been injured by 0.07 ppm (137 jig/m3) for four hours.
   Each of the above  species or strains is extremely sensitive to ozone  under
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laboratory conditions. Therefore, 0.05 to 0.10 ppm (98 to 196 Hg/m3) ozone
for two  to  four hours probably  represents the absolute threshold dose  for
sensitive species  under conditions  approximating laboratory  conditions. Other
varieties or  strains  of the same species  are  much more tolerant  Table  3-2
illustrates  projected  ozone  concentrations  that  will  produce, for  short term
exposures, threshold injury to vegetation grown under sensitive conditions
        Time
       (hours)
        0.5
        1.0
        2.0
        4.0
        8.0
                   Table 3-2

Threshold Doses of Ozone Needed to Cause Injury
  to Plants Grown Under Sensitive Conditions

              Ozone concentration needed to cause injury
         Sensitive           Intermediate         Tolerant
        .15-.30ppm*
        .10-.25
        .07-.20
        .05-.15
        .03-. 10
.25-.60 ppm
.20-.40
.15-.30
.10-.25
.08-.20
< .50 ppm
«.35
<.25
< .20
         *1 ppm = 1,960 M9/m3 at 25°C.
    Source:
    Heggestad, H. E. & Heck, W. W. Nature, Extent, and Variations of Plant Response
    to Air Pollutants. Advances in Agronomy, 23:111-145, 1971.
                           Air Quality Standards

   The current air quality standard is 0.08 ppm (157 //g/m3) ozone for one hour
not to be exceeded more than once a year. This concentration is  frequently
exceeded  in urban areas. Recent reports have shown this level is often exceeded
in rural areas as well.
   Only extremely sensitive plants growing under the most ideal conditions are
injured after exposure to 0.05 to 0.10  ppm (98 to 196 /zg/m3) ozone for three
to four hours. Such ideal growing conditions rarely occur  in the field. It would
be unlikely, therefore, that injury from ozone would occur if the standard is not
exceeded. However,  in nature, plants are often exposed to low levels of ozone
many times throughout a  growing season. Also,  other air pollutants are often
present in the ambient atmosphere. The chronic exposure of highly sensitive
plants  to low levels  of  ozone  or to  multiple  pollutants simultaneously or
sequentially, may result in slight vegetation injury when the ozone level is at or
near the secondary air quality standard.
                                   3-13

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                      Relative Sensitivity of Plants to Ozone


        Table 3-3 shows the relative sensitivity of various plants to ozone.

Relative

Sensitive
Alfalfa
Barley
Bean
Buckwheat
Citrus
Clover, Red
Corn, Sweet
Grape
Grass, Bent
Grass, Brome
Grass, Crab
Grass, Orchard
Muskmelon
Oat
Onion
Potato
Radish
Rye
Safflower
Smartweed
Soybean
Spinach
Tobacco
Tomato
Wheat

Sensitive
Ash, Green
Ash, White
Aspen, Quaking
Azalea, Campfire
Azalea, Hmo
Azalea, Korean
Azalea, Snow
Bridalwreath
Browallia
Table 3-3
Sensitivity of Various Plants
Crops and Weeds
Intermediate
Cabbage
Carrot
Corn, Field
Cowpea
Cucumber
Endive
Hypencum
Parsley
Parsnip
Pea
Peanut
Pepper
Sorghum
Stevia
Timothy
Turnip









Ornamentals and Trees
Intermediate
Alder
Apple, Crab
Apricot, Chinese
Begonia
Boxelder
Carnation
Catalpa
Cedar, Incense
Cherry, Lambert

to Ozone*

Tolerant
Beet
Cotton
Descuramia
Jerusalem cherry
Lamb's-quarters
Lettuce
Mint
Piggy-back plant
Rice
Strawberry
Sweet Potato















Tolerant
Apricot
Arborvitae
Azalea, Chinese
Avocado
Beech, European
Birch, European White
Box, Japanese
Dogwood, Gray
Dogwood, White
*Absence of any species from this or other sensitivity lists does not indicate that it is toler-
 ant — only that it has probably not been studied. It should also be kept in mind that differ-
 ences in tolerance exist among cultivars of these species.
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           Table 3-3 (Continued)
Relative Sensitivity of Various Plants to Ozone
Ornamentals and Trees (Continued)
Sensitive
Cherry, Bing
Coleus
Cotoneaster, Rock
Cotoneaster,
Spreading
Grape, Concord
Lilac, Chinese
Lilac, Common
Locust, Honey
Mountain Ash,
European
Oak, Gambel
Oak, White
Petunia
Pine, Austrian
Pine, Coulter
Pine, Eastern White
Pine, Jack
Pine, Jeffery
Pine, Monterey
Pme, Ponderosa
Pine, Virginia
Poplar, Hybrid
Poplar, Tulip
Privet, Londense
Snowberry
Sumac
Sycamore, American
Tree of Heaven
Walnut, English

















Intermediate
Chrysanthemum
Elm, Chinese
Fir, White
Fir, Big-Cone
Douglas
Forsythia, Lynwood
Gold
Grape, Thompson
Seedless
Gum, Sweet
Honeysuckle, Blue-leaf
Larch, European
Larch, Japanese
Mock Orange, Sweet
Oak, Black
Oak, Pin
Oak, Scarlet
Pine, Knobcone
Pine, Lodgepole
Pine, Pitch
Pine, Scotch
Pine, Sugar
Pine, Torrey
Pomsettia
Privet, Common
Redbud, Eastern
Rhododendron,
Catawbiense Album
Rhododendron,
Nova Zembia
Rhododendron,
Roseum Elegans
Silverberry
Viburnum, Linden
Viburnum, Tea
Walnut, English
Willow, Weeping










Toleran t
Euonymus, Dwarf
Winged
Fir, Balsam
Fir, Douglas
Fir, White
Firethorne, Laland's
Fuchsia
Geranium
Gladiolus
Gloxinia
Gum, Black
Hemlock, Eastern
Holly, American
(Male)
Holly, American
(Female)
Holly, Hetz's Japanese
Impatiens
Ivy, English
Juniper, Western
Lemon
Laurel, Mountain
Linden, American
Linden, Little-leaf
Locust, Black
Maple, Norway
Maple, Sugar
Maple, Red
Mangold
Mimosa
Oak, Bur
Oak, English
Oak, Northern Red
Oak, Shingle
Pachysandra
Pagoda, Japanese
Peach
Pear, Bartlett
Periwinkle
Pieris, Japanese
Pine, Digger
Pine, Singleleaf Pinyon
Pine, Red
Privet, Amur North
Redwood
Rhododendron,
Carolina
                    3-15

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                           Table 3-3 (Continued)
                Relative Sensitivity of Various Plants to Ozone
          Sensitive
Ornamentals and Trees (Continued)

     Intermediate
                                                           Tolerant
                                                    Sequoia, Giant
                                                    Snapdragon
                                                    Spirea
                                                    Spruce, Black Hills
                                                    Spruce, Colorado Blue
                                                    Spruce, Norway
                                                    Spruce, White
                                                    Viburnum,
                                                     Koreanspice
                                                    Viburnum
                                                    Virginia-Creeper
                                                    Walnut, Black
                                                    Yew, Dense
                                                    Yew, Half ield's
                                                     Pyramidal
                                                    Zinnia
                             Leaf Tissue Analysis


   Ozone is  a  very strong oxidant. It breaks down immediately upon contact
with any oxidizable substance, including, of  course, plant tissues. It leaves no
residues which could be analyzed by chemical means to confirm diagnosis.
                                     3-16
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                           SECTION 2.  PAN
                               Introduction
   PAN (peroxyacetyl nitrate) injury to plants  is not as widely distributed as
ozone injury; it has been a major problem primarily on vegetables grown in the
Los  Angeles basin and has  occurred  to  a lesser degree in other large western
cities. PAN concentration reported in urban areas of California ranged from 0.01
to 0.02 ppm (49 to 99 /ig/m3) on average days, with a maximum concentration
reaching to  0.05 ppm (247 yUg/m3) for  one hour. In  the East, suspected PAN
injury has been described  on  vegetables  and  tomatoes  in  New Jersey  and
southern Canada. However,  the actual occurrence of PAN and subsequent plant
injury in the East has not been proven, and mimicking symptoms must carefully
be considered when diagnosing PAN injury.
   Since the Sources,  Atmospheric Chemistry, and Monitoring Data for PAN are
the same as for ozone, the reader is advised to see pages  3-2 to 3-8 for this
information.

                             Symptomatology
   PAN, like other gaseous pollutants, is taken into the leaf through the stomata
during normal gas exchange. Once inside the leaf, PAN  attacks preferentially the
spongy  mesophyll cells but may  also attack other tissues depending  on the
species. Thus,  on many  broad-leaved plants, the symptoms  are visible pre-
dominantly  on the lower leaf surface. On monocots, such as corn,  the symptoms
are present  on both leaf surfaces. Injury from ambient levels of PAN has not
been described on trees.
   Young, rapidly growing plants are  generally more sensitive to  PAN than are
older plants of the same species. For example, young tomato or petunia plants
with only three or four leaves are more sensitive than comparable plants with six
or eight leaves. On an individual plant, young, rapidly expanding leaves are most
sensitive. PAN injury appears on the apex of younger leaves, as a diffuse band on
intermediate-aged leaves, and at the base  of  older (but sensitive) leaves.  Mature
leaves are tolerant to PAN. Plate 3-24 shows a comparison of ozone and PAN
injury on alfalfa.

Broad-leaved (Dicotyledonous) Plants
   Herbaceous broad-leaved  plants  such as table beet, sugar beet,  lettuce, bean,
and spinach are among the plants most sensitive  to PAN. The earliest symptom
of PAN injury  on these plants is a watersoaking or shininess of the  lower leaf
surface. As the injury progresses, the spongy mesophyll cells, especially those
near the stomata, collapse and air pockets take their place. The air pockets give
the undersurface of the leaf  a  glazed or  silvery  appearance — the "classic"
symptom of PAN injury (Plates 3-25, 3-26). After two or three days, the glazed
surface may  become bronzed (Plates 3-27, 3-28).
   Some plants such as petunia do not develop the classic "silvering" symptom.
                                   3-17

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Instead, the  dominant  symptom  is a bifacial necrosis, very similar to injury
caused by some other pollutants (Plate 3-29).
   Banding. Banding is an important symptom associated with PAN injury. For
example, when leaflets  of compound leaves such as tomato  or potato are ex-
posed to PAN, symptoms appear at the tip of the youngest susceptible leaf. The
next-oldest leaf is usually injured near the base of the terminal leaflet and at the
apex of the first two terminal lateral leaflets. The third-oldest susceptible leaf is
subsequently injured at  the base of the  first  two lateral leaflets and at the  apex
of the second pair of lateral leaflets, while the more mature terminal leaflet
remains uninjured. As the leaf tissue grows and matures, the injured areas appear
as bands.  A  second exposure to PAN will  produce a second  set of bands,
separated  from  the first  set  by healthy leaf tissue. With  several successive
exposures to PAN, injury will develop over the entire leaf. On certain plants such
as petunia, the injured tissue  in the  band area  will form an  indented  or
"pinched"  area at the edge of the leaf because part of the expanding leaf has
been killed.

Narrow-leaved (Monocotyledonous) Plants
   Many monocots such as grasses and grains are injured by PAN. The symptom
appears as  distinct  bands across  the leaf blade (each band is 2 or 3 to 7 or 8
millimeters in width). The tissue  in the band may be chlorotic (yellow) if the
injury is slight, or totally collapsed and bleached out if the injury is severe (Plate
3-30). Glazing and bronzing seldom appear.
   A single exposure to PAN will produce  a band  near the tip of  a  young leaf,
near the middle of the next-oldest leaf, and at the  base of the next-oldest leaf.
As the tissue in the band collapses, the  entire leaf blade folds  downward at that
point.  The tip of  the blade retains  its  normal green color for several days or
longer. Further exposure over various time intervals will produce more bands
along the leaf, with green tissue separating the bands.

Coniferous Plants
   PAN injury has not been described on conifers.

PAN-Mimicking Symptoms
   Frost  and  Sunscald.  Perhaps  the  most  common agent  capable of causing
PAN-like symptoms is frost, which causes  an undersurface glazing or bronzing,
especially  on  broad-leaved  plants. However, frost  does  not attack the   same
specific leaf  tissue  by  age,  as PAN does.  Frost  injury is  also  usually   most
apparent on the upper  leaf surface  of  many plants. Banding is not associated
with frost  injury,  although cold  injury may cause such banding on monocots.
Sunscald on leaves turned over by the wind  may also resemble PAN injury.
   Insects.  Certain insect infestations such as mites,  leaf hoppers, and thrips may
occasionally cause a lower-surface whitening or glazing. However, banding is not
usually  associated  with such infestations, and the  presence of  the insect is
usually evident.
   Other Pollutants. Under certain  conditions, hydrogen chloride may  cause
                                    3-18
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under-surface  glazing and silvering.  Hydrogen  chloride does not usually cause
banding, and it injures more  mature tissue than does PAN. Further, hydrogen
chloride injury  is usually  a local problem adjacent to a recognizable source.
Other pollutants, including ozone, sulfur dioxide,  and a combination of these
two, can cause under-surface glazing as well.

                      Factors Affecting Plant Response
   As with ozone, both inherent  and environmental factors affect plant sensi-
tivity to PAN. Some plants, such as petunia, romaine lettuce, and pinto bean, are
inherently sensitive to PAN, while others such as pines, maples, and many other
tree species are  very tolerant. However, as with other pollutants, differences in
PAN sensitivity exist among varieties of the same species.
   Many environmental factors influence the sensitivity of vegetation to PAN.
Light is a particularly important factor in regulating PAN sensitivity. High light
intensity significantly increases sensitivity of plant tissue to PAN, and light must
be  present before, during, and after exposure for visible symptoms to develop.
Therefore, in the field, plants exposed to PAN at mid-day on bright, sunny days
would probably  show the maximum amount of injury.
   Any  factor that influences stomatal opening during exposure to  PAN influ-
ences sensitivity. More tissue is usually injured on plants exposed to PAN at high
humidity  than  at low humidity. Likewise, soil  moisture levels also affect sensi-
tivity. Plants growing at optimum  soil moisture levels exhibit more PAN injury
when exposed than do those growing at  soil moisture deficits, probably because
of resulting stomatal closure.
   Unlike ozone, the percent of leaf tissue injured by PAN is directly related to
exposure temperature. That is, plants exposed to  PAN at higher temperatures
(27 to  32°C) are more severely  injured than  those  plants exposed at lower
temperatures (10 to 16°C).

                          Injury Threshold Doses
   Plants  are  injured  with much  lower dosages  of  PAN  than  with  ozone.
Sensitive plants  exhibit leaf injury after exposure to 0.01 to 0.02 ppm (49 to 99
      )  for four hours. For comparison purposes, concentrations of 0.02 to 0.03
ppm (99 to  148 jug/m3) PAN occur frequently at Riverside, California, and a
maximum peak  of nearly 0.06 ppm  (297  jug/m3 ) was measured there for one
two-hour period. Peaks as high as 0.05 ppm (247 ^g/m3) were reported at Salt
Lake City, and a maximum concentration of 0.21 ppm (1,039 ^g/m3) was once
measured  in  downtown Los Angeles. These concentrations are all substantially
above the injury threshold  dose of 0.01 to 0.02 ppm (49 to 99 /Jg/m3). Such
levels of PAN, if of sufficient duration,  can  cause widespread plant injury,
especially on sensitive leafy vegetables.

                           Air Quality Standards
   Air quality standards have not been formulated specifically for PAN.

                    Relative Sensitivity of Plants to PAN
   Table 3-4 shows the relative sensitivity of various plants to PAN.
                                   3-19

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Relative

Sensitive
Bean
Celery
Chard, Swiss
Chickweed
Clover
Endive
Grass, Annual Blue
Ground-cherry
Jimson-weed
Lettuce
Mustard
Nettle, Littleleaf
Oat
Pepper
Pigweed
Tomato
Wild-oat

Sensitive
Aster
Dahlia
Fuchsia
Mimutus
Mint
Petunia
Primrose
Ranunculus
Sweet-Basil


















*None reported to be
Table 3-4
Sensitivity of Various Plants
Crops and Weeds
Intermediate
Alfalfa
Barley
Beet, Sugar
Beet, Table
Carrot
Cheeseweed
Dock, Sour
Lamb's-quarters
Soybean
Spinach
Tobacco
Wheat





Ornamentals and Trees*
Tolerant
Apple
Arborvitae
Ash, Green
Ash, White
Azalea
Basswood
Begonia
Birch, European White
Bromihads
Cactus
Calendula
Camellia
Carnation
Chrysanthemum
Coleus
Cyclamen
Dogwood
Fir, Balsam
Fir, Douglas
Fir, White
Gum, Sweet
Hemlock, Eastern
Ivy
Larch, European
Larch, Japanese
Lilac, Common

intermediate in sensitivity

to PAN

Toleran t
Bean, Lima
Broccoli
Cabbage
Cauliflower
Corn
Cotton
Cucumber
Onion
Radish
Rhubarb
Sorghum
Squash
Strawberry






Lily
Locust, Honey
Maple, Norway
Maple, Silver
Maple, Sugar
Mountain-Ash,
American
Narcissus
Oak, English
Oak, Northern Red
Oak, Pin
Oak, White
Orchids
Periwinkle
Pine, Austrian
Pine, Eastern White
Pine, Pitch
Pine, Red
Pine, Scotch
Pine, Virginia
Poplar, Hybrid
Poplar, Tulip
Snapdragon
Spruce, Black Hills
Spruce, Blue
Spruce, Norway
Spruce, White

3-20
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                                       Leaf Tissue Analysis
               Like  ozone, PAN breaks down when it comes in contact with plant tissues.
            No chemical test of injured plant tissue has been described to confirm diagnosis.
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3-21

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               SECTION  3.  OXIDES  OF NITROGEN
                               Introduction
   Oxides of nitrogen include nitric oxide (NO), nitrogen dioxide (NO2), nitrous
oxide (N2O),  nitrogen  sesquioxide  (N2O3), nitrogen tetraoxide  (N2O4), and
nitrogen  pentoxide (N2O5).  Of these, two are important as air pollutants' NO
and  NO2.  Although  all oxides-of-nitrogen-mduced plant injury  is believed  to
result from NO2 rather  than  NO, the latter will also be discussed in this section,
because of its  close association with NO2  in atmospheric reactions.  The two
oxides of nitrogen, NO and NO2, will be referred to collectively as NOX.
   Since the early  1950's, it has been known that nitrogen oxides are associated
with photochemical smog, but their effects have not been studied as thoroughly
as those  of  other  smog components. Nevertheless, it has been established that
NO2 in the  atmosphere  can  adversely affect plants, either directly or indirectly.
Direct effects  result mainly from  NO2 exposures and occur in localized  areas.
Indirect effects result from the key role of oxides of nitrogen in forming highly
phytotoxic  photochemical oxidants,  such as ozone and  PAN. At the present
time, this indirect effect has a greater influence on vegetation than direct assaults
of NO2.
   On an equivalent-concentration basis, oxides  of nitrogen are less phytotoxic
than most  of the  other major air pollutants discussed in this manual (ozone,
PAN, sulfur dioxide, and fluoride). Consequently, the  direct effects of NOX on
plants usually occur in localized areas, and are not too common. However, this
situation will  change if the  existing trend toward  increasing NOX  emissions
continues.

                                 Sources
   The sources  of  NOX  in the atmosphere are both natural and man-made. On a
worldwide basis, bacteria produce  about ten times more NO than the combined
total  of  NO and   NO2 emissions related  to man's  activities.  According  to
Environmental  Protection Agency estimates for 1972, industrial  processes ac-
counted for only 3%  of man-related  NOX emissions, and more than 90% of this
came from  the combustion  of  fuels. Nearly 22  million tons  of NOX were
emitted, of which  about 56% was  from stationary sources that burned coal, oil,
natural gas, or  other  fuels. Nearly 40% of the total NOX emissions were from
combustion of  motor-vehicle fuels, or related to other forms of transportation.
   Although industrial processes comprise only  a small proportion of  the total
NOX  released  to the atmosphere, these  sources provide a disproportionately
greater direct threat to  agriculture. Localized episodes of vegetation injury due
to accidental NOX  releases or spills  usually occur in areas where nitric acid is
manufactured   or  used,  or  near electroplating, engraving,  welding, or metal-
cleaning operations. The manufacture of munitions, detonation of explosives, or
release of rocket propellents may also result in NOX emissions.

                          Atmospheric Chemistry
   The most important  features of oxides-of-nitrogen atmospheric reactions are
                                   3-22
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those related to the generation of O3  and other photochemical oxidants. The
initial  step  in  this process is  the  photodissociation of NO2: ultraviolet light
energy disrupts chemical bonds in NO2 to form NO and atomic oxygen (O).
Atomic oxygen reacts  with atmospheric oxygen (O2) to form O3. (Some atomic
oxygen may react with hydrocarbons in the air and produce other oxidant-type
pollutants.) The NO produced  by the photodissociation of NO2 reacts with O3
to form NO2 and  O2.  The process  is essentially cyclic; it is rapid, and, with the
exception of minor secondary or intermediate reactions, it occurs as shown in
Figure 3-1.
   As shown in Figure 3-4, significant concentrations of O3 cannot accumulate
until the NO concentration has all but disappeared from the atmosphere through
reactions  of NO  with  hydrocarbon  compounds,  resulting in the sequential
occurrence of peak concentrations of NO, NO2, and  O3. (Injury to plants where
accidental releases  or spills of NO occur are probably due to NO2 rather than
NO, because NO is rapidly oxidized to NO2 in the atmosphere.)

                              Monitoring Data
   The amount of nitrogen oxides in the atmosphere varies greatly with location
and time. The potential for high NOX concentrations is much greater in urban or
industrial areas than in suburban  or  rural  environments. At any location,  the
combined effects of man's activities and climatic and meteorological conditions
result in diurnal, weekly, and annual influences on ambient NOX concentrations.
   Diurnal patterns of NOX  levels in urban areas are similar to those shown in
Figure 3-4.  Pre-dawn concentrations  of  NO and  NO2 are relatively stable. As
human activity, especially automobile traffic, increases after sunrise, the concen-
tration of NO  increases  rapidly.  Later, as  NO is converted to  NO2, the NO2
concentration increases and NO decreases. When the NO concentration is lowest,
03  and other  photochemical oxidants begin to accumulate.  In the late after-
noon, solar  radiation decreases, and the  NO resulting from evening automobile
traffic is not  accumulated  or  converted to other oxidants,  rather, it  rapidly
reacts with O3  to form NO2. This reaction  continues into the night until the O^
supply is consumed.
   The weekly  pattern  of  ambient NOX concentrations is a composite of  the
diurnal  patterns  described  above.  The  difference  between daily and  weekly
patterns is undoubtedly due to variations in automobile traffic, because there is
little day-to-day variability except  on weekends and  holidays.  The difference in
the average NO concentrations  in Chicago over a  two-year period for weekdays
and weekends, shown in Figure  3-7, clearly illustrates this phenomenon.
   The seasonal patterns for ambient NO and NO2 concentrations are dissimilar.
The average ambient concentrations of NO are highest in the winter months,
when  solar radiation for photochemical  reactions is limited and NO emissions
from power generation and space heating  are increased.  The  average monthly
ambient NO2 concentrations, on the other hand, are relatively constant through-
out the year (Figure 3-8). The  proportion of NO2 to the  total NOX  concentra-
tion is greatest  during the summer months, when the rate of the conversion of
NO to NO2 is greatest.
                                   3-23

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                  0.20
                     2400     0600      1200       1800

                               LOCAL STANDARD TIME
2400
               Figure 3-7. Weekday and Weekend One-Hour Average NO
                         Levels in Chicago, 1962 through 1964

Source:  The Automobile and Air Pollution, A Program for Progress. Part II. Washington,
        D.C.: Department of Commerce, December 1967.
             Figure 3-8. Average and Standard Deviation of Daily Maximum
                       Oxides of Nitrogen and Nitrogen Dioxide Concentra-
                       tions for Seven Locations in Los Angeles Basin, 1962

Source: Schuck, E. A., Pitts, Jr., J. N. & Wan, J. K. S. Relationships between certain mete-
       orological factors and photochemical smog. Air and  Water Pollution, 10:689-711,
       1966.
                                      3-24
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   Increased  combustion  of fuels has  resulted in increased NOX  in the at-
mosphere. The nationwide scope of these increases is illustrated by the rates at
which the annual average NOX  concentrations increased in the five major U.S.
cities included in CAMP (Continuous Air Monitoring Program). Measurements
covered  1962-1971, and the results are shown in Figure 3-9. Although most NOX
exposures sufficient  to  induce symptoms  on vegetation occur as  the result of
localized accidental releases, metabolic effects that may affect plant growth and
yield can be induced by extended exposures to much lower concentrations. The
general increase in ambient  NOX concentrations, if continued, may pose serious
problems for agriculture in the future.
           0 INDICATES INVALID AVERAGE (AVERAGE BASED ON INCOMPLETE DATA)

                   NOTE CHANGE IN ORDINATE SCALE FOR THESE DATA
   400



   200



     0

   200



   100



     0

   200



   100



     0

   200
cc
01
2
O
z

O
z
O   100
2
     0

   200
    100
                                  O
                                              O
                                        O
                                                                CINCINNATI
                                                                  CAMP
                                                               O
                                                              PHILADELPHIA
                                                               ,   CAMP
                       O
                            TT
                                              D
                                                                ST. LOUIS
                                                                  CAMP
          1962  1963   1964  1965  1966  1967   1968  1969  1970 1971

                                      YEAR



          Figure 3-9. Trend Lines for NOX Annual Averages in Five CAMP Cities

 Source: Air Quality and Emissions Trends Annual Report: Volume I. Research Triangle
        Park, North Carolina: National Air Monitoring Program, Environmental Protection
        Agency, 4-28, 1973.
                                     3-25

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                             Symptomatology
   There is no reliable "typical" symptom to aid the observer in diagnosing NC>2
injury. The extent  and type of leaf  injury or other effects can be affected by
many  factors.  Short-term exposures  to  high NO2  concentrations  (acute  ex-
posures) do not -necessarily result in the same symptoms as long-term exposures
to lower concentrations (chronic exposures). The relative sensitivity of plants to
NC>2 varies from species to species, and even from cultivar to cultivar  within a
species.  Climate  and  other  external  factors can influence the expression of
injury.
   The one primary symptom of chronic NC>2 exposure is chlorosis, but since
chlorosis per se is non-specific and  can be a symptom of injury caused by other
pollutants, it is therefore a very poor diagnostic tool for NC>2. Fortunately for
field-assessment purposes,  both  chlorosis and necrosis often occur on the same
plant when it is  attacked  by NO2'. older leaves tend to become chlorotic and
younger  leaves may show necrosis. Leaf chlorosis resulting from extended or
recurrent exposures to relatively low NO2 concentrations may be a transitory
symptom and not  a permanent one.  After chronic NC>2  exposure is stopped,
young leaves often  recover and become green again, but chronic NO2 exposure
initiates  irreversible aging in older leaves and the leaves often become dry and
drop.
   For many  chronic  exposures, chlorosis  precedes the appearance  of necrotic
lesions. Cereal grams and corn leaves often develop longitudinal chlorotic bands
before necrosis develops. In narrow-leaved monocots, chlorotic zones may occur
as transition  zones between  healthy tissues and  the  necrotic tips. On some
broad-leaved plants, chlorosis from chronic NO2 exposures  begins  with many
small yellow-green  areas over the leaf surface which may merge as the exposure
continues. In  some species, chlorosis may be concentrated near the leaf margins.
   There are no common plants that can serve as "bioindicators" for diagnosing
NOj injury m the field.
   Summarized  below are general symptoms resulting from acute NO2  ex-
posures, and symptoms that  may  be induced by chronic  NO2 exposures. But
even by  using these descriptions as guides,  NO2 will still rarely be confirmed as
being responsible for  symptoms observed in the field. At best, it may  only be
possible  to exclude  NO2 as the causal agent.

Broad-leaved (Dicotyledonous) Plants
   Injury to leaves  of  broad-leaved plants that results from acute NO2 exposure
is usually characterized by the rapid appearance of irregularly-shaped intercostal
lesions.  The  earliest  indications  of  injury are gray-green watersoaked areas
located  on the upper leaf surface (Plate  3-1). Tissues in these areas  collapse,
become  dry and bleached, turn white-to-tan, and extend through to the lower
leaf  surface (Plates 3-31, 3-32,  3-33). The  resulting necrotic  lesions are  usually
indistinguishable  from lesions produced by sulfur dioxide.
   Lesions  on most  broad-leaved  plants  are  distributed between the veins
throughout the leaf blade. NC>2-induced necrotic lesions may  fall from the leaf,
leaving irregular  holes with darkened margins. Occasionally,  the lesions  may
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increase in size, coalesce, and form necrotic strips between the veins.
   In some  plants the injury tends to be more marginal. For example, necrosis
on maple and oak leaves often begins at the margins or the tips of the lobes and
extends  into  the mid-portions of  leaves.  For  species  with finely dissected
compound leaves, such as carrot and parsley,  NO2 injury is usually  confined to
the tips  and margins. Very high NO2  exposures of  citrus trees may result in
defoliation of young leaves without the development of necrosis

Narrow-leaved (Monocotyledonous) Plants
   Acute  NO2  exposures of narrow-leaved  plants  most often result in yellow-
to-ivory-to-white necrosis that begins at  or just  below  the tips  of  leaf blades.
Necrotic margins and striped necrotic  lesions between  the veins also occur. In
most grams  and grasses, injury from  acute exposure affects the entire width of
the leaf blade. The length of the affected portion varies with the NO2 exposure.
Grains also  show longitudinal necrotic strips  between the veins, and these can
coalesce  to  form large necrotic areas on  the leaf surface. The awns (beards) of
rye and  barley  spikes  are  also susceptible to  NO2   injury.  Bleached  necrosis
begins at the tips and progresses downward.

Coniferous Plants
   Injury to leaves of conifers from acute NO2 exposures usually begins at the
tips  of  the  needles and progresses towards  the base  The boundary between
healthy  and  injured  tissues is sharply delineated  by a  brown or red-brown band.
In the initial stages of injury, the tips of needles  take on a dull, gray-green color
which, in time,  becomes light brown,  then dark brown or  red  brown  Young
emerging  needles  show NO2  injury  at  the  tips, whereas older needles may
occasionally develop necrosis in the central or basal portions of needles
   Injured needles  may drop prematurely; spruce needles  drop shortly after
injury develops;  larch  and  fir needles may  not fall for several months, and
injured pine needles  can remain on the tree for  more than a year.  However, if
injury is severe, with necrosis covering more than half of the needle surface,
defoliation usually occurs within a month.

                      Factors Affecting Plant Response
   The  extent,  severity,  and  type of foliar lesions  caused by  a  given NO2
exposure can be affected by both external and internal factors. Climatic and soil
conditions are the  external factors, and  the  internal factors are plant  genetic
make-up, stage of development, age, etc.

External Factors
   The effects of external factors such as light, temperature,  relative humidity,
and soil moisture on  the sensitivity of plants  to NO2  are not well known. Night
fumigations  usually  result  in  more severe injury than  comparable daytime
exposures; however, the progression  of symptoms from incipient injury to dry
necrotic lesions is most rapid on warm sunny days. Reduced soil moisture or low
relative humidity make some plants  more tolerant to NO2.
                                   3-27

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   The presence of other pollutants in the atmosphere with NO2 adds another
variable.  When  NO2  and  SO2  occur together in the atmosphere, each  at  a
concentration that is  not harmful to plants, their combined effect can result in
plant injury. A similar interaction has  been reported for NO2 and O3. NO2  may
possibly interact in this manner with other air pollutants as well.

Internal Factors
   Genetic effects are obvious when one  compares the differences in sensitivity
among species, cultivars, or  clones of the  same species.  The age of leaves can
affect their sensitivity to NO2, as in  tobacco, in  which the oldest leaves  turn
yellow,  the middle-aged  leaves become yellow with necrotic lesions, and injury
to the younger leaves is limited to necrosis. Middle-aged leaves are most sensitive
in dandelion, cheeseweed, lamb's-quarters, pigweed, and  Kentucky  bluegrass,
whereas  the sensitivity  of  middle-aged and old leaves  is about  the same  in
sunflower, annual bluegrass, and  nettle-leaf goosefoot. Emerging or elongating
needles of conifers are more sensitive than mature needles.

                           Injury Threshold Doses
   The  effects of NO2  on  plants are not only dependent on the pollutant
concentration, but are also influenced by the duration of exposure.
   Threshold doses are described as functions of the pollutant concentration and
exposure time, as shown  in Figure  3-10.
                                                        LEAF SYMPTOMS
                                                        NO EFFECT
                                DURATION OF EXPOSURE (HOURS)
        Figure 3-10. Approximate Thresholds for Death, Leaf Injury, and No Ef-
                  fect, as Related to /VO2  Concentration and Duration of
                  Exposure.
                                    3-28
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   For  every effect  of NO2, a threshold curve  can be computed if enough
information  is known about that effect over a relatively wide range of concen-
trations and  exposure periods. In Figure 3-10, three threshold curves are shown.
These are approximate, rather than absolute, and are based on information from
experimental exposures of many plant species. The threshold for NO2 doses that
result in the death of plants is based on a limited amount of information, the
threshold for leaf symptoms (chlorosis or necrosis) is based on many observa-
tions. In the area between the threshold curves for leaf symptoms and no effect
are NO2 doses that do not injure leaves, but result in reduced growth, or effects
on photosynthesis, or effects on other plant processes.

                            Air Quality Standards
   The current Federal Air Quality Standards for NO2 are 0.05 ppm (94 /ug/m3)
for an  annual average, and 0.13 ppm (244 ^g/m3)  for a 24-hour average  In
addition to providing protection for most vegetation  against the  direct effects of
NO2, these  standards  may also  limit  the  amount  of NO2  available for the
production  of  photochemical oxidants,  thereby providing some protection
against the production of these pollutants as well.

                     Relative Sensitivity of Plants to N02
   The relative sensitivities of some plant species to NO2 are shown in Table 3-5.
The  three  classes, sensitive, intermediate,  and  tolerant, should be considered
approximate because  they are  based on subjective  criteria from  several sources.
Most  of the classifications are derived from experimental fumigations carried out
at various  locations  at different times of the  year, using  different NOj ex-
posures. Methods for assessing injury (e.g., percentage of leaves injured; amount
of leaf surface affected; defoliation, etc.) were also variable. For  these reasons, a
plant  species considered tolerant by one investigator may be considered sensitive
by another.
                                 Table 3-5
                 Relative Sensitivity of Various Plants to NO2
       Sens; five
       European larch
       Japanese larch
       Sensitive
       European white birch
        Conifers
      Intermediate
      Spruce
      Fir

Deciduous Trees and Shrubs
      Intermediate
      Norway maple
      Japanese maple
      Linden
     Tolerant
Yew
Pine
     Toleran t
Black locust
European hornbeam
Elder
Gmgko
Elm
Purple beech
Oak
                                    3-29

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           Table 3-5 (Continued)
Relative Sensitivity of Various Plants to NO2

Sensitive
Apple
Pear

Sensitive
Oats
Barley
Red clover
Spring clover
Spring vetch
Alfalfa
Tobacco

Sensitive
Lettuce
Peas
Carrot
Parsley
Leek
Rhubarb
Pinto bean

Sensitive
Snapdragon
Tuberous begonia
Rose
Sweet pea
Oleander
Bougamvillea
Azalea
Hibiscus
Pyracantha


Sensitive
Mustard
Sunflower

Fruit Trees
Intermediate
Orange

Field Crops and Grasses
Intermediate
Rye
Annual blue grass
Corn
Wheat
Potato
Field beans

Garden Crops
Intermediate
Bush bean
Celery
Tomato




Ornamental Shrubs and Flowers
Intermediate
Brittlewood
Pittosporum
Ligustmm
Ixora
Cape jasmine
Gardenia
Petunia
Fuchsia
Catawba
rhododendron
Weeds
Intermediate
Dandelion
Chickweed
Cheeseweed

Tolerant



Tolerant
Kentucky blue grass







Tolerant
Kohlrabi
Cabbage
Onion
Asparagus




Tolerant
Dahlia
Carissa
Croton
Shore jumper
Daisy
Lily of the
Valley
Gladiolus
Plantain lily
Heath

Tolerant
Nettle-leaf
goosefoot
Lamb's-quarters
                                    Pigweed
                  3-30
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                               Leaf Tissue Analysis
    Chemical analyses of leaves, used to confirm suspected symptoms for some
 air pollutants, are of little value for NO2 injury, due to  the  high and variable
 levels of nitrogen compounds that are normally found in plant tissues.
                                Selected References

Air Quality Criteria for Nitrogen Oxides. Washington, D.C.: Air Pollution Control Office,
   Environmental Protection Agency. January 1971.
Benedict, H. M., & Breen, W. H. Los Angeles: Proceedings of the 3rd National Air Pollution
   Symposium, 111, 1955.
Berry, C. R. & Ripperton, L. A. Ozone, a possible  cause of white pine emergence tipburn.
   Phytopathology, 53:552-557, 1963.
Czech, M. & Nothdurft, W. Landwirtschaftlichs. Forschung, 4:1-36, 1952.
Davis, D. D., &  Wood, F.  A. The relative susceptibility of eighteen coniferous species to
   ozone. Phytopathology, 62:14-19, 1972.
Engle, R. L., Gableman, W. H., & Romanowski, R. R. Tipburn, an ozone incited response in
   onion (Allium cepa L.). Proceedings of the American Society of Horticultural Science,
   86:468-474, 1965.
Heck, W. W. Factors influencing expression of oxidant damage to plants. Annual Review of
   Phytopathology, 6:165-188,1968.
Heggestad,  H. E.  Ozone as a  tobacco toxicant.  Journal  of the Air Pollution  Control
   Association, 16:691-694, 1966.
Hill, A. C., Pack, M. R., Treshow, M., Downs, R. J., & Transtrum, L. G. Plant injury induced
   by ozone.Phytopathology, 51:356-363, 1961.
lacobson,  J. S.,  & Hill, A. C., eds. Recognition of Air Pollution Injury to Vegetation. A
   Pictorial Atlas. Pittsburgh: Air Pollution Control  Association, 1970.
Ledbetter, M.  C., Zimmerman, P. W., & Hitchcock, A. E. The histopathological effects of
   ozone on plant foliage. Contributions to Boyce Thompson Institute, 20: 275-282, 1959.
Linzon,  S. N.  Damage  to eastern white pine by sulfur dioxide, semi-mature tissue needle
   blight, and  ozone. Journal of the Air Pollution Control Association, 16:140-144, 1966
MacClean, D. C., McCune, D. C., Weinstein, L. H.,  Mandl, R. H. & Woodruff, G. N. Effects
   of acute hydrogen  fluoride and nitrogen dioxide exposures on citrus and  ornamental
   plants of central Florida. Environmental Science and Technology, 2:444-449, 1968.
Miller, P. R., Parmeter, Jr., J. R., Taylor, O. C. & Cardiff, E. A. Ozone injury to the foliage
   of pmus ponderosa. Phytopathology, 53:1072-1076, 1963
Noble, W. A. Smog damage to plants. Lasca Leaves,  15:1-24,  1965.
Noble, W.  M. The pattern of damage produced on vegetation by smog. Journal of Agricul-
   tural and Food Chemistry, 330-332, 1955.
Rich, S. Ozone damage to plants Annual Review of Phytopathology, 2:253-261, 1964.
Richards, B. L., Middleton, J. T., & Hewitt, W. B. Air pollution with relation to agronomic
   crops: v. oxidant stipple of grapes. Agronomy Journal, 50:559-561, 1958.
Sechler, D., &  Davis,  D.  R.  Ozone  toxicity  in  small  grains.  Plant Disease Reporter,
   48:919-922, 1964.
                                       3-31

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Stephens,  E. R. Chemistry  of atmospheric oxidants. Journal of the Air Pollution Control
   Association, 19:181-185,1969.

Taylor,  0. C.  Importance  of peroxyacetyl nitrate (PAN) as a phytotoxic air pollutant.
   Journal of the Air Pollution Control Association, 19:347-351, 1969.

Taylor,  O. C. & MacLean, D.  C.  Nitrogen  oxides and  the  peroxyacetyl nitrates. In:
   Jacobson, J. S. & Hill, A. C., eds., Recognition of Air Pollution Injury to Vegetation: A
   Pictorial Atlas. Pittsburgh: Air Pollution Control Association, E1-E14, 1970.

Treshow, M. Environment and Plant Response. New York: McGraw-Hill, 1970.

Treshow, M. Ozone damage  to plants. Environmental Pollution, 1:155-162, 1970.

van Haul, H.  & Stratmann, H.  Schriftenreihe der Landesanstalt  f(ir  Immissions - und
   Bodennutzungsschutz des Landes Nordrehein-Westfalen. Essen, 7:50-70, 1967

Weaver, G. M., Jackson, H. O. Relationship between bronzing in white beans and phytotoxic
   levels of atmospheric ozone in ontarios. Canadian Journal of Plant Science, 48:561-568
   1968.

Wood, F.  A. & Coppolino, J. B. The influence of ozone on deciduous forest  tree species.
   Vienna: Proceedings of the International Symposium of Forest Fume Damage Experts,
   Report of the Forestry Council Research Institute, 1972.
                                       3-32
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Plate 3-1. Example of Initial Water-Soaked Appearance on Broccoli Immediately after
         Exposure.  This Plant was Fumigated with 10 pphm O3 and 0.5ppm SO^
 Plate 3-2. Bel W-3 Tobacco Injured by Ambient Oxidant in St. Louis, Mo. Showing
          Both Fleck and Bifacial Necrosis
                                   3-33

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Plate 3-3. Ozone Injury (Flecking) to White Ash
   Plate 3-4. Ozone Injury to Swiss Chard
                  3-34
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Plate 3-5. Ozone Injury to Tobacco
 Plate 3-6. Ozone Injury to Radish
              3-35

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Plate 3-7. Ozone Injury to Radish and Subsequent Reduced Yield on Right
  Plate 3-8. Cucumber Injured by Ambient Oxidant Near Cincinnati, Ohio
                               3-36
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                Plate 3-9. Oxidant Injury to Squash
Plate 3-10.  Tomato Leaflet Showing Oxidant Injury (Probably Ozone)
                             3-37

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      Plate 3-11. Safflower Leaf Showing Oxidant Injury (Probably Ozone)
Plate 3-12. Soybean Leaves Showing Various Stages of Oxidant Injury (Normal
          Leaf in Center; Leaflet on Right is Secondary Response to Oxidants)
                                 3-38
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     Plate 3-13. Tempo Bean Leaves Showing Oxidant Injury (Probably Ozone)
  *:,:"-^ -..
.rAV--**-. -
             #$K;
>-t| *  . ' '. v V :" -
                   '•'•
        ^
   Plate 3-14.  Bronzing of White Bean Leaves Caused by Oxidant /Probably Ozone)
                                  3-39

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Plate 3-15. Severe Ozone Injury and Bifacial Necrosis of Browallia Leaves
           Plate 3-16. Severe Crape Stipple Caused by Ozone
                                3-40
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Plate 3-17. Pinto Bean Injured by Ambient Oxidant Near Cincinnati, Ohio, Showing
          Stipp/e Symptom
         Plate 3-18. Ozone Stipple of White Ash as Observed in the Field
                                   3-41

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Plate 3-19.  Bluegrass Injured by Ambient Oxidant in the Los Angeles Basin
                               3-42
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Plate 3-20. Severe Oxidam Injury to Ponderosa Pine
                     3-43

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Plate 3-21.  Chronic Ozone Injury of Ponderosa Pine. Note Dif-
           ference  in  Tolerance Between Trees and  Tufted
           Appearance of Foliage
                         3-44
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            Plate 3-22. Tipburn of Onion Caused by Ozone
Plate 3-23.  Eastern White Pine Displaying Oxidant Injury (Probably Ozone)
                               3-45

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Plate 3-24. Comparison of Ozone and PAN Injury on Alfalfa. Upper row: Ozone
          Injury; Lower row: PAN Injury
Plate 3-25. PAN Injury to a Bean Leaflet. Left, Upper Leaf Surface; Right, Lower
          Leaf Surf ace Showing Silvering or Glazing Due to PAN
                                  3-46
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Plate 3-26. Young Primary Leaf ofPinto Bean Injured by PAN After Exposure to
          Irradiated Auto Exhaust
      Plate 3-27.  Escarole Showing Oxidant Injury (Probably Due to PAN)
                                  3-47

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Plate 3-28. PAN (Ambient) Injury to Swiss Chard
 Plate 3-29. Petunia with PAN or Ozone Injury
                    3-48
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                      Plate 3-30. PAN Injury to Oats
Plate 3-31. Injury on Broccoli One Week After Exposure to NO^. Leaves Show
          Some Recovery from Initial Water-Soaking and Also Some Marginal and
          Interveinal Necrosis
                                   3-49

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Plate 3-32- Marginal and Interveinal Injury on Periwinkle Fumigated with 19.3 ppm of
         NO 2 for 0.5 Hours
  Plate 3-33. Marginal and Interveinal Injury on Cherry Belle Radish Fumigated with
           7.7 ppm /VO2 for Four Hours
                                    3-50
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                                Chapter 4
                           SULFUR DIOXIDE
                               Introduction

   Sulfur dioxide (SO2)  was one  of the  first  man-made pollutants  to  cause
economic damage to vegetation. Coming as it does from combustion of fossil
fuels, plant materials, and refuse, green plants must have recorded its  presence
since early in the industrial revolution. Since that time, as industries and cities
have  expanded,  concentrations of   combustion  products  have  continually
increased.

                                  Sources
   In addition  to combustion, sulfur dioxide is released when ores containing
sulfur  are  roasted in  the  smelting process,  when  oils are  refined, and  when
sulfuric acid is manufactured.  In all  these processes, the sulfur present in the
materials is released  by heat, whereupon it reacts with oxygen in the air to form
SO2.
   The  size  (volume) of  the  emitters and their height  and numbers are of
considerable  importance in influencing  ground-level SO2 concentrations. The
trend in industrial operations has been away from low-level sources and toward
releasing large  volumes of pollutants from tall stacks (some reaching 600 to
1,200 feet high). Such high-elevation emission points disperse the pollutants over
a wide area, with dilution normally adequate to avoid any effect on vegetation at
ground level.
   With the development of tall stacks in this century, a significant change has
occurred in the "ground pattern" of SO2 plant injury. During the early part of
the century, plant  damage  frequently  occurred  in  rather  well-defined  areas
around  a  particular  industrial  operation, with  the damage  being most  severe
nearby the source. In those days, SO2 acquired the name "smelter smoke," and
plant damage became known as "smoke injury." However, with the use of tall
stacks and  controls on large SO2 emitters, the occurrence of severe plant damage
to many species in restricted areas has  all but disappeared.
   During  the  1950's and 1960's,  widespread damage from SO2 occurred to
highly  sensitive plant species in the New York megalopolis, and in other  cities
where coal or oil was burned. Injury on tulip, violet, and crabapple was readily
observed in such areas. The development of injury on so few plant species over a
rather large area, with no  apparent centers of increased injury, suggested that
relatively  smaller quantities  of the  phytotoxicant were coming from  many
widespread, rather small emitters, perhaps space heaters.
                                    4-1

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                          Atmospheric Chemistry
   Laboratory and  field studies show that SO2  may be oxidized to SO3  under
conditions occurring in ambient air. This trioxide rapidly combines with water
to form sulfuric acid mist.  The  mist  consists of small airborne droplets  of
sulfuric acid (H2SO4), which vary in size with the relative humidity. Humidity,
sunlight, and catalytic particulate matter (such as manganic and manganous salts,
aluminum oxide, active carbon, and even coal soot) all affect the production of
acid particles.
   In addition, when photochemical-smog reactions involving unsaturated hydro-
carbons and nitrogen oxides occur in the presence of SO2, oxidation of the SO2
to H2SO4 occurs at a significant rate. This happens even with concentrations of
hydrocarbons and nitrogen oxides that are typical of the levels occurring in only
moderately-polluted atmospheres (about 0.1 ppm). A similar oxidation occurs in
the presence of ozone-olefin reactions, which may take place in the dark.
   The rate of SO2  oxidation to H2SC>4 reportedly ranges from 0.1% to 10% per
hour.  Reactions  between  SO2 and ammonia  in the atmosphere also  occur
rapidly, to form  ammonium sulfate. Droplets of sulfuric acid and particles  of
ammonium sulfate  tend  to settle in time  but reduce visibility while suspended.
In addition, SO2 is readily dissolved in rain or  snow, and settles to the  earth's
surface in those forms. This solubility in water suggests that the oceans may be a
major sink for  atmospheric SO2.  In addition, plant foliage and moist soil also
serve effectively to remove this  phytotoxic gas  from the atmosphere.

                              Monitoring Data
   To  understand the problem of  SO2  pollution, it is  helpful  to  know the
quantities and  sources  of  this phytotoxic  pollutant, and  the  trends in  total
quantities and ground-level concentrations. Table 4-1  shows the  estimated total
SO2  emissions  in the U.S.,  1940-1970.  Table  4-2 shows the sources of SO2
emissions for 1970.
                                 Table 4-1

                 Estimated Total Nationwide SO2  Emissions
                             Levels, 1940-1970

            Year                        S02  emitted (TO6 tons/year)
            1940                                  22.8
            1950                                  24.9
            1960                                  23.2
            1968                                  31.1
            1970                                  33.4

    Source:
    Air Quality and Emissions Trends Annual Report: Volume I. Research Triangle
    Park, North Carolina: National Air Monitoring Program, Environmental Protection
    Agency, August 1973. p. 1-13.
                                    4-2
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                                  Table 4-2

                    Nationwide Estimates of SO2 Emissions
                      from Various Sources During 1970
            Source                               SO2 in 106 tons/year

            Transportation                                1.0

            Fuel combustion in
            stationary sources                             26.4

            Industrial processes*                           6.4

            Solid waste disposal                            0.1

            Miscellaneous                                 0.2
                       Total                            34.1
    *Includes  refinery  operations,  ore  smelting,  coke  processing, and  sulfuric
     acid manufacture.

    Source:
    Air Quality and Emissions Trends Annual Report:  Volume I. Research Triangle
    Park, North Carolina: National Air Monitoring Program, Environmental Protection
    Agency, August 1973. p. 1-7.
   Air-sampling data secured  by the National Aerometric Surveillance Network
show that in all  four air quality  Control Regions (Northeast, North Central,
South, and West), the composite annual averages for  both the arithmetic mean
and  the average maximum daily SO2  concentrations exhibit a downward trend
for the eight-year period 1964-1971 as summarized in Table 4-3.
Table 4-3
Sulfur Dioxide Annual
of Four Air Quality
Average Concentration
Control Regions for


1964 and 1971, in /Jg/m3

Region
Northeast
North Central
South
West
YEAR
1964
88
49
34
25

7977
41
24
14
14
   Only one sampling site out of 32 showed a significant upward trend. During
the last four years of the period only three out of 95 sampling sites revealed an
upward trend. Thus, the SO2  analysis work shows a pronounced downward
trend,  with  the composite average dropping over 50 percent. However, a review
of the data for  the  same period  recorded in Table  4-1 shows  a substantial
increase in  SO2  emissions. How can this  apparent inconsistency be accounted
for?  The  following  considerations offered by the  National Air Monitoring
Program help explain:

     First,  emissions are determined  for the nation as a whole, whereas
     air-quality data  are  generally  collected from specific sites in center-
     city  locations.  Second,  SO2 emission rates in most urban areas are
                                     4-3

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      declining. The use  of coal in  residential  and small  commercial
      sources is practically non-existent. Cleaner fuels such as natural gas
      and  distillate  fuel oils have replaced coal  to  a large extent. The
      impact on total nationwide emissions as a result of this fuel replace-
      ment is relatively small, but the  effect  on  local air quality  is pro-
      nounced. Third, large point sources such as power plants are not able
      to locate near or in center-city areas. Increased fuel transportation
      costs favor the generation of electricity near the fuel source.*

                              Symptomatology
   It is universally accepted that SO2 enters the leaves of plants through open
stomata. Inside the  leaf, large surface  areas of moist cells that are oxygen-rich
during daylight hours are  exposed to this gas.  In  such an environment, SO2 is
oxidized to highly toxic sulfite (SO3) and then to less-toxic sulfate (SO4). When
sublethal concentrations of SO2 are absorbed by the cells, they oxidize to highly
toxic SO3, which is slowly  oxidized to less-toxic SO4 and  neutralized in the
plant cells. This reduces the toxicity of the sulfur by a factor of about 30.
   If SO2 is not absorbed  too rapidly,  a concentration of SO4 may accumulate
in the  cells that is several times greater than that occurring m unexposed plants
of the same species. Thus, plants exposed to sublethal concentrations of SO2
may in time develop chronic sulfate (804) injury.  However, since the highly
toxic SO3  is slowly  oxidized in the plant cells to the less-toxic sulfate form, it is
apparent that, if SO2 is absorbed more rapidly than SO4  is formed, the highly
phytotoxic SO3 will accumulate in toxic proportions, causing acute injury.
   Since the earliest investigations, alfalfa has been considered one  of the most
SO2-sensitive plants. The acute injury symptoms to this plant usually consist of
a bleaching appearance, and  can occur both between  the veins and marginally.
The most  typical symptoms are marginal, with the bleached areas extending
progressively toward the midrib with increasing severity of  fumigation.
   Bracken fern (Plate 4-1) in woodlands is an extremely useful indicator plant.
The injury is typically orange-red and marginal on  the fronds. Wild and culti-
vated mustard and swiss chard are also excellent indicator plants. Their injuries
are typically ivory-white and occur between the veins. The younger, expanding,
and the older leaves remain free of injury. Injury to sow thistle is marginal and
intercostal, and varies in color from gray to dark. In wooded areas, fox and bank
grapes (Plate 4-2) are quite sensitive, and exhibit typical SO2  intercostal and
interveinal markings that are light brown.
   White birch (Plate 4-3) and trembling aspen (Plate 44) are the most SO2-
sensitive deciduous  trees.  The markings  on trembling aspen leaves are usually
intercostal but often also occur on the margins. The necrotic  areas are reddish-
brown at  first, but darken with age. A  dark-colored line often develops between
the injured and green tissue.
 *From: Air Quality and Emissions Trends Annual Report: Volume I. Research Triangle
       Park, North Carolina: National Air Monitoring Program, Environmental Protection
       Agency, August 1973.
                                     4-4
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   In the South, the Brazilian  pepper bush is an excellent S02  indicator. The
spotting occurs interveinally  on all but the youngest leaves. The  color of the
injury is a grayish-tan.
   White pine  and jack pine  are the most sensitive conifers. Since needles that
are nearly mature or have recently reached full elongation are the most sensitive,
conifers are especially sensitive during late spring and early summer. Needles
showing acute  injury develop an orange-red color. (An entirely green needle is
rarely found in a sulfur dioxide-affected fascicle.)
   Some SO2 symptoms are highly similar to symptoms of other plant problems.
Needle  blight  resulting from  fungus  infections  often  has green and  blighted
needles  together in a fascicle.  Diseased needles  may  show small,  dark, spore-
bearing fungus structures in an area at the base of the injured tissue. This is not
visible to the naked eye but is clearly visible using a hand lens. The diseased area
is usually a  slightly darker brown than the necrotic terminal. On conifers, needle
blight resulting from  acute  SO2 toxicity might also  be confused  with injury
caused by other atmospheric pollutants, such as chlorine, fluoride, and even cold
temperatures.

Broad-leaved (Dicotyledonous) Plants
   Acute Injury. Acute injury  due  to  rapid absorption of a toxic dose of SO2
causes marginal and intercostal necrotic areas  which at first have  a dull,  dark-
green, watersoaked  appearance. On drying and bleaching, these areas become
ivory-to-white in most plant  species, such as garden pea (Plate  4-5), corn (Plate
4-6),  and alfalfa (Plates 4-7, 4-8). But  in some species various  shades of brown
predominate. Examples include chrysanthemum,  lettuce, blackberry (Plate 4-9),
fox grape (Plate 4-2), hickory (Plate 4-10), and eggplant  (Plate 4-11). In a few
species, red  predominates (e.g., quince, Plate 4-12).
   The  necrotic areas extend through the leaf and are visible on both surfaces.
The  areas   immediately bordering the veins  are  seldom injured.  These  areas
generally have  few stomata and very limited intercellular spaces. The leaves  most
sensitive to  SO2 are younger, fully-expanded leaves, and those  that are near full
enlargement (Plate 4-13).  Older leaves are less sensitive. The smaller,  enlarging
leaves are the last to show acute injury.
   Histological  examination  of a lesion that is  beginning to develop  reveals
collapse  of  mesophyll cells near the stomata. Mesophyll cells collapse  not  only
from  SO2   toxicity, but  from  other causes as well. The absence  of collapsed
mesophyll adjacent to necrotic  areas can definitely eliminate SO2 as a  cause of
necrosis, but the collapse of such tissue, because  of its ubiquitous  nature,  does
not definitely establish SO2 toxicity as the cause.
   There may be considerable variability in sensitivity to a phytotoxic pollutant
among individual plants of a given species.
   Chronic or Sulfate Injury.  Plants exposed to sublethal concentrations of SO2
may in  time develop chlorotic symptoms (Plate 4-14), especially if the exposure
is  continued. (The  symptoms may also be  white  or reddish-brown.)  Such
yellowing affects  the margins  and interveinal areas,  with the  affected  areas
remaining turgid. The loss of green color results from the plasmolysis of the
                                    4-5

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chloroplasts in affected  mesophyll  cells, with  the destruction of chlorophyll
causing a bleached appearance. The veins on such leaves usually remain green.
   In cotton, a yellowing first appears on the undersurface of the leaf which
gradually  extends through to the upper surface. This has been called  "sulfate
toxicity,"  and  it frequently appears  as white  or brownish-red  turgid areas
between the veins. Such  leaves usually drop prematurely. Silvering of the lower
leaf  surface may  occasionally  occur in cotton  when  gas  concentrations  and
humidity  are low. This response results from a collapse of the cells immediately
internal to the epidermal  cells.
   A similar type of marking may occur following an acute SO2 fumigation.  The
mild chlorosis results  from accumulation of SO3  at concentrations sufficient to
bleach chlorophyll, but not sufficient to kill the cells. Evidence of chronic injury
may occur on leaves that  are also exhibiting acute symptoms described above.

Narrow-leaved (Monocotyledonous) Plants
   Acute Injury. Monocot leaves vary in their response to SO2 from injured  tips
at low concentrations, to almost completely necrotic leaves at high concentra-
tions. Injury usually develops first at the leaf tips, then extends downward with
increasing concentrations and exposure time. The markings that appear  on grain
crops, lilies, and  gladioli usually  appear as necrotic streaks between the  veins,
and usually appear first at the bend of the leaf when present (Plate 4-15).

Coniferous Plants
   Acute  Injury.   In  the case of conifers  exposed  to large dosages, needles
develop a watersoaked appearance that soon changes to reddish-brown as shown
in Plates  4-16 and 4-17.  As  lesions develop in white pine needles, they  fill with
resin. Fully-expanded needles,  and those  that  are  nearly so, exhibit the most
necrosis. Very young needles are seldom injured, perhaps because of inactivity of
the stomata in needles of that age. Conifer  needles  absorb more SO2  and are
much more sensitive  to  the gas during spring and  summer months than during
the autumn and winter period.
   Chronic or Sulfate Injury. This is expressed by chlorosis, especially in  the
older needles. Such needles are underproductive and are dropped prematurely.
                      Factors Affecting Plant Response
Light
   Researchers generally agree that stomata are the sole or principal avenue of
ingress of  gases into the leaf.  The view  has been expressed  that  SO2 is not
dependent upon stomata for entrance into the leaf, but common experience
contradicts this: plants  that close their stomata at night become highly tolerant
during this period, while plants whose stomata remain open at night (such as the
potato) retain  SO2 sensitivity during the  dark  hours. In fact,  potato foliage is
more sensitive to SO2 during dark hours than during the daylight. Sensitivity is
also considerably greater in the morning than in the late afternoon.
                                    4-6
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Soil Moisture
   The degree of turgidity of leaves at the time of fumigation is one of the most
significant factors in SO2 sensitivity. This has been shown by fumigation studies
of turgid and wilted  foliage from four species of plants. In these experiments,
SO2 concentrations ranged from 0.82 ppm (2,148 Hg/m3) to 4.0 ppm (10,480
Mg/m3). Injury on turgid plants ranged from moderate to very severe (involving
all  leaves), while  the  wilted foliage exhibited little or no injury, even at the
highest concentrations used. The pronounced difference is believed to be due, at
least  in part, to the condition  of  the  stomata, which  close during times of
moisture stress.
   Many investigations  have reported  great increases in tolerance  of plants to
SO2 as soil moisture approaches the wilting point. On the other hand, when soil
moisture is adequate  for  growth, wide variations in moisture do not influence
sensitivity in  barley and  alfalfa plants.  Thus, it is  believed that soil moisture
influences sensitivity  mainly through its  effect  on  the stomata. When the soil
moisture is low the stomata tend to close, thus limiting the ingress of SO2.

Humidity
   Humidity  also  exerts a marked  influence on stomatal openings  and  plant
response to SO2. Plants  at 30% relative humidity are  about three times as
tolerant to SO2 than plants at 100%  relative humidity. However, variations in
the range between 50% and 75% relative humidity do not significantly affect
plant  sensitivity. The  sensitivity of alfalfa to SO2, for example, is not influenced
to a great extent by changes in relative humidity between 40% and 70%.

Temperature
   The toxic effect of  SO2 is  at a minimum during exposures at low tempera-
tures. For example, conifers during winter months are more tolerant  to  SO2.
Toxic effects increase  with rising temperatures, within certain limits.  There
appears to be  a critical  temperature of 7°C, above which plant injury may occur
in nature. In addition, several investigators consider that plant response to SO2 is
not markedly affected between 18°C and  40°C, providing other influencing
factors are uniform.

Nutrition
   From field experience it has been repeatedly observed that trees, vegetables,
and  flower  crop  plants  that  are  growing well are more responsive  to SO2
exposures than are plants  of the same species that are not growing well. This
observation was confirmed by researchers when  they fumigated plants deficient
in nitrogen or sulfur.  The  plants exhibited reduced  susceptibility and increased
stomatal resistance to  SO2, as compared with plants that  were making better
growth at higher nutritional levels.
   Also, tobacco and tomato plants grown at various sulfate levels in nutrient
solution and  exposed to SO2  fumigations showed increased sensitivity to SO2
with increased sulfate nutrition. The increased injury paralleled elevated foliar-
total sulfur absorption  from both  the nutrient  solution and atmospheric  SO2.
                                    4-7

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However, it has also been shown that absorption of S  O2 from SO2  fumigations
was least by  plants growing in nutrient  solutions high in  sulfur content.  Still
other researchers have  found that varying  the  sulfur content of the nutrient
supply of alfalfa and buckwheat had no significant effect  on the sensitivity of
these plants to SO2.
   Sulfur dioxide absorbed from the atmosphere  has been found to be present in
greater concentrations in the inorganic fraction of test plants, rather than in the
organic. However, when sulfur-deficient tomatoes were exposed to S35O2, about
one-half of the absorbed sulfur had been converted into organic forms within six
hours, thus demonstrating the nutrient value  of SO2.
   Sulfur absorbed from the atmosphere has also been found in reduced concen-
trations  in the roots.  Sulfate  formed in  the  leaves of alfalfa is held quite
tenaciously; however, a considerable amount of sulfate formed  in  leaves of
tomatoes is translocated. It is of interest also that a considerable concentration
of sulfate  has been  found  in  the soil  around  the  roots  of treated plants,
suggesting a passage outward of the sulfate from the roots. It  has been suggested
that atmospheric SO2, absorbed  by the leaves, moves inside the plant and can be
eliminated through the roots.

Plant and Tissue Age
   Full-grown and nearly full-grown leaves are among  the most sensitive to SO2.
Young and  old leaves  usually exhibit less  sensitivity to  this pollutant (Plate
4-13). For example, uptake of gaseous SO2  by leaves of Bel W-3 tobacco plants
is high in the intermediate age and low in young and  old leaves. It  is suggested
that these differences in SO2 uptake could account for the visible injury patterns
observed on  plants  that have been exposed to  a phytotoxic concentration of
SO2. In  addition, because plants that are growing well are more sensitive  than
those that are nutrient-deficient, it may be possible that physiological activity of
the leaf contributes  to its own sensitivity.

                          Injury Threshold Doses
   O'Gara,  in an attempt to classify plants on  the  basis of  their sensitivity,
fumigated about 300 species and cultivars of plants. He used alfalfa  to represent
the most sensitive of plants, giving it a rating of 1. He found that injury could be
induced on this plant when it was exposed to a concentration of 1.2 ppm (3,144
/ig/m3) SO2  for one hour. The rating he gave  to a  plant was determined by
taking  the concentration  of  SO2 required to induce  injury  during a one-hour
exposure and dividing it by 1.2.
   Canadian  studies in  an area containing smelters near  Sudbury, Ontario,
classified a plant's  sensitivity to SO2  as  100 when it responded to an average
concentration  of SO2  of 0.95  ppm  (2,489 Mg/m3)  for 1 hour, or 0.55  ppm
(1,441 jUg/m3) for two  hours, or 0.35 ppm  (917 /ig/m3) for four hours, or  0.25
ppm (655 f;g/m3) for eight hours. These studies extended over a ten-year period
and involved over 300,000 hours of air sampling. During this sampling period, a
correlation was made among ground-level average SO2 concentrations occurring
during daylight hours,  duration of the  fumigation,  and the species of plants
4-8
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growing near  the  recorders that responded  to  the  fumigation. All significant
fumigations that occurred  were given an intensity rating, and the plant species
that developed acute markings from each  fumigation were noted. The intensity
ratings were arrived at by multiplying the average ppm SO2 for one hour by 105,
or two hours by 182, or four hours by 286, or eight hours by 400.
   From such  work as O'Gara's and the Canadian studies, sensitivity tables have
been constructed (Table 4-4). These are quite useful when observing suspected
SO2 injury in the field.
Table 4-4
Relative Sensitivity of Plants
Crops
Sensitive
Alfalfa Sweet Potatoes
Buckwheat Lettuce
Barley Beans
Cotton Broccoli
Red Clover Squash
Oats Wheat
Peas Carrot
Spinach Tomato
Flowers
Sensitive
Sweet Pea Sweet William
Four O'clock Gladiola
Cosmos Tulip
Bachelor Button Violet
Aster Zinnia
Sensitive Trees
Trembling Aspen Alder
Jack Pine Red Pine
White Pine Austrian Pine
White Birch Hazel
Larch Apple
Large-Toothed Aspen Douglas Fir
Willow Ponderosa Pine
Sensitive Garden Plants
Peas Cucumber
Rhubarb Lettuce
Spinach Radish
Swiss Chard Squash
Beans Tomato
Beets Cultivated Mustard
Turnips Kohlrabi
Carrot

to SO2

Tolerant
Celery
Corn
Onion
Potato
Cabbage




Tolerant





Tolerant
Cedar
Citrus
Maple
Linden



Tolerant
Muskmelon
Corn
Onion
Potato
Cabbage
Broccoli
Turnips

                                   4-9

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                           Table 44 (Continued)
                     Relative Sensitivity of Plants to SO2
„ . . Miscellaneous
Sensitive
Prickly Lettuce
Ragweed
Dock
Bracken Fern
Wild Mustard
Careless Weed
Sow Thistle
Yellow Clover
Night Shade
Chickweed
Annual Bluegrass
Brazilian Pepper Bush
Tolerant
Privet
Lilac




                           Air Quality Standards
   To  protect man  and his possessions  against injury  from SO2 fumigations,
primary and secondary standards have been set by the Federal Government. The
primary standards, effective April 30, 1971, require that the annual SC>2 average
in the atmosphere not  exceed 0.03 ppm (80 /xg/m3).  In addition,  an average
concentration of 0.14 ppm (365 /ug/m3) of SO2  for a 24-hour period is not to be
exceeded  more  than once a  year.  A secondary  standard  has also  been set,
requiring that a three-hour average of 0.5 ppm (1,300 fxg/m3) not be exceeded
more than once a year.
                    Relative Sensitivity of Plants to SO2
   Plants vary widely in their sensitivity to SO2.  Alfalfa and barley are usually
considered to be among  the most  sensitive. However, some of the common
weeds, such as the velvet-weed, dock, mallow, and prickly lettuce are nearly  as
sensitive. In addition, these plants are so sensitive that they must appear in the
same  grouping:  zucchini  and yellow summer squash  (Plate 4-18), trembling
aspen (Plate 4-4), white birch (Plate 4-3), bracken fern (Plate 4-1), tulip (Plate
4-19), wild geranium, buckwheat, red clover, jack pine, white pine, sow thistle,
and Brazilian pepper bush.
   It would appear that in the Sudbury area some injury  to the most  sensitive
plant species could occur without the secondary standard being exceeded. In this
area, large quantities of SO2  are emitted daily into the atmosphere from smelter
stacks that are not considered  to be really tall, compared with recent installa-
tions. Thus, average and short  duration ground levels of SO2 might be high  in
this area. It should  be remembered that plants on high-sulfur nutrition are more
sensitive to SO2 fumigations  than are comparable  plants on a normal sulfur diet.
Therefore, plants in a high SO2  environment might be more responsive to SO2
than plants in less contaminated areas.
                                   4-10
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                              Leaf Tissue Analysis
   Sulfur is  an essential plant nutrient and  as such accumulates in plant tissues
whether taken in from  the soil  or air. Therefore, analyzing the amount of sulfur
m leaves provides a rough approximation of the amount of sulfur to which those
leaves have been exposed. Because of this accumulation, some investigators have
tried to use the sulfur content  of leaves as a measure of sulfur-dioxide con-
tamination.  Unfortunately,  as  a  normal and important constituent  of plant
proteins,  sulfur is already  present in fairly high concentrations (roughly about
0.1 to 0.2 percent of the dry weight), so that further increases originating from
SO2 tend to be obscured. The only real value from sulfur analysis comes when
background  levels in the foliage are already known. Even then, analysis provides
only a general idea  of the degree  of exposure. It does not reveal the duration of
exposure  or the concentrations of SOa to which the plant was exposed. Most
importantly, it does not disclose  the extent of toxicity or injury from the SO2.
                               Selected References


Abeles, F. B., Cracker, L. E., Forrence, L. E. & Leather, G. R. Fate of air pollutants.
   removal   of  ethylene,  sulfur  dioxide  and  nitrogen   dioxide  by  soil.  Science,
   173(4000):914-916, 1971.

Air Quality and Emission Trends Annual Report: Volume I. Research Triangle Park, North
   Carolina:  National Air Monitoring Program, Environmental Protection Agency, August
   1973.

Atkins, D. H. F., Cox, R. A. & Eggleton, A. E. J. Photochemical ozone and sulfuric acid
   aerosol  formation  in  the  atmosphere   over   Southern  England. Nature,
   23S(5338):372-376, 1972.

Dreisinger, B. R. The impact of sulfur dioxide pollution of crops and forests. Background
   Papers  Prepared for the National  Conference on Pollution  and  Our Environment:
   Volume 1, Oct. 3-Nov. 4, 1966.

Furrer, O. J.  The  amount  of SO2 absorbed by plants  from the  atmosphere. Vienna:
   Proceedings of the Symposium on Isotopes in Plant Nutrition and Physiology, Inter-
   national Atomic Energy Agency, 403-407, 1967.

Le Blanc,  F.  & DeSlover, J. Relation between industrialization and the distribution and
   growth of  epiphytic  lichens  and  mosses in Montreal. Canadian Journal of Botany,
   48:1485-1496, 1970.

Terragho,  F.  P. &  Manganelli, R.  M.  The  influence of moisture on the absorption of
   atmospheric SO2 by soil. Air and Water Pollution,  10:783-791, 1966.

Thomas, M. D. & Hill, G. R. Relation of sulfur dioxide in the atmosphere to photosynthesis
   and respiration of alfalfa. Plant Physiology, 12:309-383,  1937.

Thomas, M. D. Gas damage to plants. Annual Review of Plant Physiology, 2:293-322, 1951.

Thomas, M.  D. Effects of Air Pollution On Plants.  Geneva:  World  Health Organization,
   Monograph No. 46, 233-278, 1961.
                                     4-11

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   Plate 4-1. Acute Sulfur Dioxide Injury to Bracken Fern. Typically Orange-Reef,
            Occurs on Margins of Fronds
Plate 4-2. Typical Sulfur Dioxide Injury to Fox Grapes. Light Brown, Occurs Between
         Veins,- Top Leaves Show Undarsurface, Bottom Leaves Show Upper Surface
                                   4-12

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Plate 4-3. Acute Sulfur Dioxide Injury to White Birch Foliage
                          4-13
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Plate 4-4. Acute Sulfur Dioxide Injury to Trembling
         Aspen Leaves. Injured Areas are Reddish-
         Brown and Darken with Age
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       Plate 4-5. Typical Acute Sulfur Dioxide Injury to the Garden Pea
Plate 4-6. Corn Foliage Exhibiting Acute Sulfur Dioxide Injury (Injured Areas are
         Composed of White-to-lvory Colored Collapsed Cells!
                                   4-15
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           Plate 4-7. Light Acute Sulfur Dioxide Injury to Alfalfa
Plate 4-8. Severe Acute Sulfur Dioxide Injury to Alfalfa Leaves. Injury Ivory
          Colored, Marginal with Intercostal Spotting
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Plate 4-9. Acute Sulfur Dioxide Injury on Blackberry Growing Within Five Miles
         of the Source
  Plate 4-10. Typical Acute Sulfur Dioxide Injury to Hickory. Reddish-Brown;
            Frequently Extends from Near Midrib to Near Edge of Leaf
                                   4-17
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  Plate 4-11. Acute Sulfur Dioxide Injury to Eggplant Leaves (Ivory-to-Light Tan)
Plate 4-12. Acute Sulfur Dioxide Injury to Quince Foliage (Colorful Brownish-Red)
                                    4-18

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Plate 4-13. Acute Sulfur Dioxide Injury to Careless Weed (Ivory-Colored; Note
          Little or No Injury on Young Expanding Leaves)
Plate 4-14. Chronic Sulfur Dioxide Damage to Cotton Foliage in Palm of Hand.
          Note Injured Areas are Chlorotic But Not Collapsed; Veins Usually
          Remain Green


                                  4-19
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Plate 4-15.  Acute Sulfur Dioxide Injury to Sonora Wheat (Ivory-Colored)
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Plate 4-16. Suspected Sulfur Dioxide  Injury on Virginia Pine
           Crowing 1.5 Miles from a Source
                            4-21
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  Plate 4-17  Typically Acute Sulfur Dioxide Injury to Loblolly Pine Needles
Plate 4-18. Acute Sulfur Dioxide Injury to Yellow Summer Squash. Acute Injury
          to all Squash and Pumpkin Plants is White or Ivory-Colored

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Plate 4-19. Acute Sulfur Dioxide Injury to Tulip. Note Ivory-Colored Injury Occurs
          at Leaf Tips and Margins
                                   4-23
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                                Chapter 5
                              FLUORIDES
                                Introduction

   Fluorine is a relatively common and abundant element of the earth's crust. It
is present in soils as fluoride, and in minerals, such as fluorspar, biotite, apatite,
hornblende,  and muscovite.  In  one ton of soil, on the average, there is about
four-tenths  of  a pound of fluoride or  190 parts per million (ppm). It has been
estimated that  about 30 million tons of soil enter the atmosphere of the United
States each year and this is equivalent to about 6,000 tons of fluoride per year as
the rate of emission for one natural source. By comparison, it was estimated that
industrial emissions in  the United  States totaled  119,000  tons of fluoride for
1968.
   Atmospheric fluoride had adverse effects on agriculture as a natural pollutant
long before it  became  a man-made one. Air-borne fluoride sometimes affected
agriculture adversely without directly  affecting plants.  Livestock  in  parts of
North Africa  developed  an  illness called  "darmous" when prevailing  winds
carried a relatively fluoride-rich fluoroapatite dust onto vegetation. This  illness
was due  to fluorosis that  occurred when the vegetation  was consumed by the
animals.  Volcanoes  and fumaroles are another natural source  of gaseous and
particulate atmospheric fluoride. Roholm has written, "In the  Icelandic litera-
ture  from round about the year 1000 up to recent  times we find accounts of
how the  domestic  animals  turned sick and  died  when there were  volcanic
eruptions . . . the disease attacked animals which ate the grass contaminated with
the fallen  ash,  which means sheep especially,  as cattle and  horses were kept
stabled as much as possible and so escaped [illness] . . ."
   It  is not  known exactly  when  man's activities first generated atmospheric
fluoride to the  extent that it adversely  and  directly affected plants. Reports of
fluoride-induced injury  to vegetation began to appear in  the  late  19th century
with the  advent of certain industrial processes  and became more frequent as new
processes  developed and  others expanded.  In general, man's activities can  be
viewed as gradually augmenting  and changing the natural rates at which fluoride
is transferred among earth, air, water, and organisms; a  composite picture of
environmental fluoride is given in Figure 5-1.

                                  Sources
   Atmospheric fluoride reaches the plant in  the form of  a  gas, particulate
matter, or gaseous fluoride adsorbed to particles. The most phytotoxic and best
studied form of atmospheric fluoride  is gaseous hydrogen fluoride (HF). Al-
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                                                              Deposition of
                                                              sediments
              Figure 5-1. Composite Picture of Environmental Fluoride

Source: Fluorides. Washington, B.C.: Committee on Biological Effects of Atmospheric Pol-
       lutants, National  Academy of Sciences, Publication ISBN  O-309-01922-2,  1971.

though silicon tetrafluoride (SiF4) may be evolved, atmospheric reactions proba-
bly convert it to HF  before  it reaches  the  plant. The particulate  forms of
fluoride have not been  so extensively studied as the gaseous forms with respect
to their effects on plants. In general, they exist as salts and their toxicity may be
determined by the characteristics of the particles and the environmental condi-
tions  that  affect their  collection and retention  by foliage  and  the subsequent
penetration of fluoride into the foliar tissue. However, when forage crops or
vegetation  that is eaten by wildlife is of concern, the presence of particulate
material on the foliage must also be considered.
   Any process  that  utilizes  fluorine-containing material  can  be  a  potential
source of   atmospheric fluoride.  Fluorides  may be  emitted  when  fluorine-
containing material is ground,  crushed, or pulverized; treated with strong acids;
heated; or  used in some process in a gaseous or volatile form. The magnitude of
the source  depends upon the kind of process, kind of material, volume of
material processed, and degree  of emission control. An estimate of the quantities
of fluorides emitted by  different industries is given in Table 5-1.
   The emission  of  fluorides  can  result  from the  manufacture of phosphate
fertilizers  and feeds, phosphoric acid, or elemental phosphorus. The phosphate
rock used  as a raw material in these industries contains 3 to 4% fluorine.  Dust
can be produced in the  grinding and drying of the rock, and gaseous fluoride can
be produced (as HF or SiF4) when  the  rock is treated with sulfuric acid to
produce  phosphates or is heated  in  electric furnaces for   the production of
elemental phosphorus. The ponds that contain waste process water may also be
significant sources of atmospheric fluoride.
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                                   Table 5-1

                 Estimated Total Fluoride Emissions from Major
                 Industrial Sources in the United States in 1968
       Source
       Manufacture of brick and tile products
       Manufacture of steel (open-hearth furnace)
       Manufacture of aluminum
       Combustion of coal
       Manufacture of steel (electric furnace)
       Manufacture of normal superphosphate
        fertilizer
       Manufacture of steel (basic-oxygen furnace)
       Manufacture of elemental phosphorus
       Nonferrous-metal foundries
       Manufacture of wet-process phosphoric acid
       Manufacture of glass and frit
       Welding operations
       Manufacture of triple superphosphate
        fertilizer
       Manufacture of diammonium phosphate
        fertilizer
       Manufacture of phosphate animal feed
         TOTAL
A tmospheric Emissions,
      tons/year
        18,500
        16,800
        16,000
        16,000
        14,900

         9,700
         8,400
         5,500
         4,000
         3,000
         2,700
         2,700

          300

          100
          100
                                                         118,700
    Source:
    Fluorides. Washington,  D.C.: Committee on Biological Effects  of Atmospheric
    Pollutants, National Academy of Sciences, Publication ISBN O-309-01922-2, 1971.
   In the manufacture of aluminum, alumina is dissolved in molten cryolite and
reduced electrolytically.  Both cryolite and fluorite, which is also present in the
process, contain fluoride, and in the electrolyte cell fluorine is evolved in gases
such  as hydrogen fluoride,  or  as  particulate  matter such as  fluoride salts. In
steel-making, fluorspar is used as a flux from which hydrogen fluoride may be
generated.  The  combustion of  coal can  be  another  source of  atmospheric
fluoride because coal  contains an average of 0.008% fluoride. The clays used for
the manufacture  of bricks, pottery,  and  cement  contains fluorine, and gaseous
fluorides may be emitted from the kilns. In the manufacture of glass and enamel,
fluoride-containing  materials  that  are heated evolve gaseous and particulate
fluorides.  Other  sources of fluorides are  industries that  produce hydrogen
fluoride and those that  use it  for  petroleum refining  or the production of
fluoro-carbons.

                           Atmospheric Chemistry
   There is no general set of concentrations that can be expected for all fluoride
sources. The extent and  magnitude of atmospheric concentrations over the area
affected will depend  upon the rate  of emissions. Most  major  sources are  char-
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acterized  by a relatively  constant rate of emission. Therefore, pattern of dis-
persion, in time and space, will  be  determined by the combination of source,
topography, and meteorology. Diurnal and seasonal fluctuations can be expected
to follow the changes in those climatic and meteorological factors that  deter-
mine dispersion. Occasional high concentrations (relative to the mean or median)
may occur due to failure of controls, accidental spills, or unusual meteorological
conditions.

                              Monitoring Data
   In contrast to  the  better  studied  urban and industrial air  pollutants —
photochemical oxidants and sulfur dioxide — there is no  extensive compilation
of ambient levels of atmospheric fluoride. The lower limit of detection may
range from 0.01  to 0.05 Aig/m3  (about .012 to .06 ppb)* in a 24-hour sample
depending upon the methods used. The lower limits for shorter sampling periods
are higher.
   The analysis of more than 7,700  air samples  for total  water-soluble fluoride
by the National Air Pollution Control Administration over the years 1966 and
1967 showed that 97% of the samples from non-urban  areas had no detectable
fluoride.  The highest concentration was 0.16 /Jg/m3  (.195 ppb). In urban  areas
the corresponding values were 87% and 1.89 HS/m3  (2.306 ppb). In the heavily
industrialized  Ruhr  area of Germany, samples in the city of Duisburg during
1965 and  1966 showed a mean of 1.3/zg/m3 (1.586 ppb).


                              Symptomatology                                       H|
   The HF-induced  symptoms  that appear on the foliage of plants result from  a
series of complex events: the interaction  of fluoride and  metabolic processes in
the  leaf and the action of environmental factors upon it. Some general aspects of
symptom development will be considered here so that the symptoms and their
variations  can  be  more easily described and understood.  Specific  guidelines for
diagnosing fluoride-induced symptoms are presented in Chapter 10.
   Of  what  do symptoms  consist? First, there is a change in the  color of  a
portion of the leaf due  to a loss of chlorophyll in the affected area.  When the
amount  of this pigment is reduced, the  yellow pigments that remain are  un-
masked and a condition of chlorosis, which may range from a slight paling of the
green to an appearance of a yellow color in the affected area, appears. Second,  a
color change  may  be due to death of the tissue and  the formation of brown
pigments as  the affected area  dies. To a  certain extent, the coloration of this
necrotic area depends upon the  species and  how rapidly the necrosis develops.
Third, symptoms may consist of deformation  as well as discoloration of  the
foliage. These  deformations  occur usually on broad-leaved plants as a result of
*ppb = parts per billion, in which "billion" means "thousand-million" or 109 and not 1012
 as in British and German usage. American and French usage agree however. See Appendix
 A for methods of conversion between ppm and jug/m3. One ppb is 10"3 ppm. Atmospheric
 concentrations for HF use ppb to avoid awkward numbers. The unit ppb refers only to
 atmospheric concentration and is v/v.
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necrosis which occurs as the leaf is expanding.  The tip of the leaf may become
necrotic and the rest of the leaf may become cupped as it expands, or the tissue
between the veins may expand  more rapidly than the veins, giving the leaf a
savoyed appearance. Sometimes the edges of the leaf take on a ragged appear-
ance owing to the loss of necrotic marginal tissue.
   Where do symptoms occur? The distribution of the affected areas, or lesions,
on the  leaf is usually determined by two factors: (1) the species of plant, which
determines the morphology of the leaf; (2) the severity of the exposure, which
determines the  response of the leaf. Of these two factors, species as related to
leaf morphology is probably the more important. Generally, the lesions induced
by fluoride appear first or  are more intense in  the apical and marginal areas of
the leaf. Young expanding  leaves are most likely to be injured by an exposure.
Exceptions to these generalizations occur and will be discussed later.
   How does fluoride  produce these symptoms? The mode of action of fluoride
is imperfectly understood, but fluoride is known to act as an inhibitor of plant
metabolism. As fluoride accumulates in the leaf, it causes an increased inhibition
of metabolism,  and chlorosis appears as the first visible sign of this metabolic
disruption. With further increases in the concentration of fluoride in the tissue,
the cells die and necrosis is observed. When the leaf is exposed to relatively high
concentrations of HF  for short  periods of time, local concentrations of fluoride
in the  leaf may rapidly  exceed the toxic threshold, and irregular  patches of
necrosis may occur in the intercostal areas. But more often,  the leaf is exposed
over  a  longer period  of  time, constantly  or periodically, to relatively  low
concentrations.  Under these  conditions, the fluoride  absorbed by  the leaf is
translocated to and accumulates in the apical or marginal tissues where  the more
characteristic symptoms of fluoride toxicity appear.
   The  short-term, high-level  and the long-term, low-level exposures are com-
monly referred  to  as acute and  chronic, respectively. Whereas acute exposures
usually  produce necrotic lesions, chronic exposures may produce either necrosis
or chlorosis depending  upon the species and tolerance of the plant. Therefore, it
matters not so much  whether a symptom be classified as acute  or chronic  but
what  the severity of the symptom, its distribution on the plant, and its occur-
rence  on different species tell about the kind of exposure that  has occurred.

Broad-leaved Plants
   Within  this  group  of plants, symptoms  consist of chlorosis of  varying in-
tensity, or necrosis, or both. The affected areas are initially located  at the tips or
margins of leaves and,  with increasing  severity, extend  toward the base of the
leaf from the tip or toward the middle of the leaf from the margins.
   Citrus.  In naval orange,  irregular chlorotic patches appear in  the  intercostal
areas of the leaf near the margin and tip. With prolonged exposure, these patches
extend  further towards the midrib and base and increase in  intensity until  the
midrib and venation appear  as a green-arborescent figure on a pale chlorotic field
(sometimes called the  "Christmas  tree" pattern of chlorosis). Necrosis  occurs
principally at the  tips of nearly mature leaves with a  chlorosis and  mottling
which affect the  remaining  portion but decrease in intensity toward  the base of
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the leaf. In lemon, chlorosis develops also along the margins and tips of leaves
and with increasing severity involves the intercostal areas to give the "Christmas
tree" pattern of chlorosis. In grapefruit, symptoms may first appear as irregular,
ill-defined chlorotic blotches in the intercostal areas or as a thin marginal area of
chlorosis. With increasing severity the  marginal and  interveinal chlorosis intensi-
fies and the  affected areas merge (Plate 5-1). This pattern is most common on
older leaves.
   Some of  the  chlorotic and necrotic symptoms of  citrus foliage  resemble
injury from excessive  boron,  but a gumming of the undersurface of the leaf is
found when  boron  toxicity is responsible. The "Christmas  tree"  pattern  of
chlorosis also resembles that induced by manganese deficiency.
   Other fruit crops.  On grape  (European)  necrosis  may  appear  along  the
margins of the leaf and extend irregularly  into the intercostal areas, with some
zonation or banding of the necrotic areas.
   On blueberry  (Plate 5-2) necrosis of the apical and marginal portions of the
leaf can develop under chronic exposure. With low  bush blueberry, a reddening
of the tip and apical margins of the leaf can precede  the development of necrosis
in chronic exposures. However, this  reddening can also be  induced by  other
conditions.
   Apple leaves show a very dark-reddish brown coloration at the tip and margin
of the leaf with very little necrotic flecking of the interveinal areas. Grape leaves
(Plate 5-3) show  necrosis of both the marginal and intercostal tissues after more
acute exposure. Injured areas  are initially dull or pale green, then change to buff
or light tan with death and desiccation. Frequently, these dry, brittle portions
fall away from the uninjured  portion of the leaf,  leaving an irregular margin.
Prune foliage shows about the same pattern of injury as apricot, but the necrotic
areas  may  be  colored  a  much darker brown.  If recurrent injuries occur, the
necrotic areas show zonation or bands of darker necrotic tissue within the paler
necrotic areas.  On peach and sour cherry foliage, necrosis in trace amounts will
appear at the tip of the leaf. The damaged area may fall from the leaf leaving a
notched leaf tip. If this  kind of injury occurs before  the leaf has completed
expansion, a  cupping of the leaf may occur. On the foliage of apple, sour cherry,
and peach, chlorosis may appear on the tips and margins of the leaf after chronic
exposures. Intensification of this symptom results in more pronounced chlorosis
and an expansion of the chlorosis into the intercostal areas.
   As with citrus, certain nutrient deficiencies, such as zinc or manganese, can
also induce the "Christmas tree" pattern typical of chlorosis. Low temperature
and  drought  injury,  oil  sprays,  and  virus diseases  can  induce  fluoride-like
symptoms.
   Other Deciduous Trees and  Shrubs. The range of symptoms seen  on decidu-
ous trees follows the same patterns seen on other broad-leaved plants (Plate 5-4).
Acute exposures  may  cause necrosis of the tips and margins and sometimes of
intercostal areas of leaves with irregular but distinct demarcation between dead
and live tissue. Chronic exposure will  tend to cause  chlorosis, first of the tips or
serrations, then of the apical  and marginal areas, and finally of the intercostal
areas.  The venation  of damaged  intercostal  tissue  is a  darker green than  the
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laminar tissue. Sometimes chronic injury  may appear only as a necrosis of the
tips of lanceolate leaves or tips of lobes  of palmate leaves, such as maple. On
some  species, such  as  poplar,  intercostal chlorosis  may accompany marginal
necrosis.
   To the same extent as with other groups of plants, the kind of exposure, kind
of  leaf, and  tolerance of the  plant  will determine  the kinds  of symptoms.
Moreover, natural or other kinds of stresses  can induce symptoms that mimic
those induced by atmospheric fluoride (Plate 5-5).
   Herbaceous Weeds.  St.  John's wort  is one  of  the more ubiquitous and
sensitive species of herbaceous weed. Fluoride-induced injury appears on it as a
red-brown necrosis of the apical portion of the leaf. Chronic exposure produces
a light-green flecking and  then chlorosis on the  younger, expanding leaves  of
lamb's-quarters (Plate 5-6). More intense symptoms appear as an increase in the
intensity  of chlorosis,  chlorosis of the intercostal areas, and a cupping and
puckering of the leaves.
   In  chronic  exposures,  chlorosis develops  at  the  tips and  margins  of the
expanding leaves  of  night-shade, knotweed,  mares tail, and crab grass. When
necrosis  of leaf  tips  occurs,  relatively little chlorosis precedes it. Pigweed,
smartweed,  ragweed, golden rod, and oxalis also show these kinds  of symptoms.
In acute exposures, apical markings are more common on chickweed, nettle-leaf
goosefoot, and blue  grass; marginal markings are more common on mustard,
sunflower, dandelion, and  cheeseweed; and both kinds of markings appear on
pigweed.

Narrow-leaved Plants
   There  is probably  no  single  type of symptom that would apply to all
monocots, but there  are certain kinds of symptoms that are typical for many
species.
   Grains and Cane. Sweet corn is  a  reasonably  ubiquitous and  sensitive indi-
cator of atmospheric fluoride,  although sensitivity depends upon the  cultivar
(Plate  5-7).  Fluoride-induced symptoms usually can be distinguished from those
caused by disease, insect  injury, mineral deficiencies,  or other  pollutants by
appearance, pattern, and development. At the lowest  exposures  that produce
symptoms, there  are scattered chlorotic flecks or stipples near the  tip of  the leaf
and along the apical margins of the  leaf. With an  increase in exposure, the area
affected by  stippling extends down toward  the base of the leaf along the margins
and inward on the leaf toward the midrib. The intensity of the stipple diminishes
toward the  basal  or medial areas of the leaf. Also, with an increase  in severity,
the stippling  along  the apical  margins will  increase  and coalesce to  give  a
chlorotic band of tissue at the tip and along the margins. As with the stipple, this
band of chlorosis decreases in width toward the base of the leaf. With a  further
increase in  severity, necrosis  appears at  the  tip and then  spreads along the
margins of the leaf toward the base and inward toward the midrib.
   The symptoms produced by  fluoride in milo maize (sorghum)  are similar to
those of corn. The effect starts  at the  tip and  the immediately  adjacent margins
of the  leaf.  As the effect increases, the affected area enlarges  by an extension of
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the marginal areas down the leaf and toward the midrib. Lesions in the affected
area start as chlorotic stipples, coalesce into chlorotic bands, and  may finally
become necrotic with increasing severity of exposure. In milo maize, irregular
red areas  may border the first observed necrotic areas. The patterns and severity
of symptoms tend to be more intense on  the  older leaves if exposure occurs
around the time of heading.
   In grasses and  small  grains, fluoride symptoms may sometimes appear as
chlorotic stipples or chlorosis on the tips and margins of leaves. But most often
they appear as a necrosis of tissue at the apical portion of the leaf. In barley, the
apical portions of the awns may become necrotic if exposure occurs during the
later phases of head development or maturation.
   Injury  to  sugar cane by HF shows about the same pattern and sequence of
chlorosis and necrosis as injury to sorghum and corn leaves.
   Several climatic  and  environmental conditions  can  produce  symptoms in
grains and other grasses that mimic fluoride-induced  injury. Hot winds can cause
terminal  bleach of  cereals. Subfreezing temperatures  may  cause  a marginal
necrosis and red discoloration  on milo maize  that is  similar to HF-induced
necrosis, except  that a silvering of the upper surface at the arch of the leaf may
frequently be present. Some mineral nutrient deficiencies in corn, such as zinc or
potassium, can produce a  pattern of chlorotic and necrotic banding on the
leaves; however, the  distribution of the symptom over the plant is different from
that  induced by HF. Similarly, mite injury or genetically-induced mottling may
have a different appearance or distribution over the leaves of the corn plant than
fluoride-induced injury.
   Gladiolus  and  Similar  Plants. The most popular  biological indicator  of
fluoride effects is gladiolus; more data exist, and more observations are made in
the field, for this species than for any other. The typical symptom of fluoride-
induced injury on gladiolus is necrosis of some apical portion of the leaf.  With
most kinds  of exposure in the field, necrosis starts  at the apex of the  leaf and
proceeds downwards toward the base (Plate 5-8).  The color of the necrotic area
depends  upon the  variety  of gladiolus and ranges  from ivory or light tan to
various shades  of  brown.  Generally, light-flowered varieties show the lighter
shades. The  necrotic area is sharply delineated from live tissue, usually by a dark
brown band  of necrotic tissue at the base of the necrotic area and sometimes by
a very narrow band of chlorotic tissue below the necrosis. An evenness of the
band or front of necrosis across the leaf indicates a relatively constant chronic
exposure. The length of tipburn is often used as a quasi-quantitative measure of
the dosage received by the plant. Variations in this type of symptom can occur.
With acute dosages,  the line separating necrotic and live tissue, although sharp,
tends to become uneven and may extend  further  along one  margin than the
Other.  With  high concentrations of HF, isolated necrotic areas may appear along
the  margins  or  between  the veins  (Plate 5-9).  When several exposures  have
occurred,  dark  brown bands may be seen in the necrotic  portion  of  the leaf.
Each band marks the increments of  necrosis produced by successive exposures.
   The flowers of gladiolus are more tolerant to  fluoride than the foliage, but
bracts  are relatively sensitive  and injury  appears  as a necrosis that  extends
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toward  the  base  of the  bract from the tip. When injury occurs on flowers it
appears first as a watersoaked tissue at the margins of the sepals and petals. This
tissue then dries and becomes necrotic.
   Tulips  (Plate 5-8), iris, lilies, and similar monocots show HF-induced symp-
toms that appear as a necrosis that starts at the leaf tip  and extends along the
margins and toward the base of the leaf.
   Several agents can produce fluoride-like symptoms  on gladiolus and similar
plants. Water stress produces tip and marginal necrosis of the flower bracts that
can  be  indistinguishable  from fluoride-induced injury. When foliar necrosis is
induced by  moisture stress, zonations in the necrotic area may be lacking, and
there may not be a sharp demarcation between dead  and live tissue.  Botrytis
lesions  on gladiolus may  be  distinguished by  their dull color and indefinite
margins; severe leaf tip necrosis is accompanied by many lesions, 1/16 to 1/4 of
an inch in diameter, which are not confined to the marginal and apical  portions
of the leaf.  Finally, gladiolus may show a fluoride-induced  necrosis that results
from fluoride  in the soil, not the air. The occurrence and severity of this injury
depends upon the fluoride content of the fertilizer, its rate  of application, and
the kind of soil.

Coniferous Plants
   The  typical fluoride-induced symptom on the foliage of conifers is a necro-
sis  of the apical portion  of the needle.  It is  often  called "needle scorch" or
"tipburn" (Plate  5-10). The boundary between dead  and live tissue is even and
well defined, and the band of necrotic tissue next  to the live portion may be a
darker shade of brown than the adjacent necrotic tissue. The percentage of the
total length  of the needle that is necrotic usually increases  with the severity of
the exposure and may involve only a few millimeters at the tip, to the tip-half,
or  almost  the entire  needle.  On many  conifers, the  necrotic  portion is a
reddish-brown  color, and, if  on the  current year's needles, fairly  constant in
color (Plate 5-11). If the needle is  observed immediately after  an  injurious
exposure has taken place, the apical tissue may have a  pale gray-green appear-
ance. After  another time period, this  tissue will have become necrotic and the
boundary  between  necrotic and healthy tissue  may  have this same gray-green
appearance  as  additional  necrotic involvement  occurs.  The  appearance of a
slightly  darker brown  band delimiting the necrotic and  healthy tissues may be
the final stage  of symptom development.  Another portion of the needle, im-
mediately below  the necrotic  area, may turn necrotic if a subsequent exposure
occurs. Thus, when several episodes have occurred, one may see more than one
band in the necrotic tissue, each  corresponding to the  appearance of another
increment of necrosis.
   In general, there are three kinds of exposures that  can result in an easily
discernible amount of necrosis on the needle: a single acute exposure; several not
so acute exposures; and continuous or intermittent exposures over an extended
period of time with  necrosis appearing  with  the  onset  of some period  of
environmental stress. Although one can distinguish between  several occurrences
of necrosis and a single one upon examination, the distinction between necrosis
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due to a single acute exposure and that due to prolonged, chronic exposure is
made  mainly by  repetitive examination of the vegetation  through a growing
season.
   Chlorosis, if it appears, may only involve the one to two millimeters of the
needle's tip. Color may vary  with the species. For example, necrotic areas of
blue spruce appear to be purple.

Fruit
   Suture red spot (or "soft  suture") is a fluoride-induced syndrome of peach
fruit, which was first noted when fluoride-containing sprays were tested for the
control of insects. It  has since been produced by experimental fumigations of
peach trees with HF. This syndrome is characterized by the premature ripening
of the flesh along both sides of the suture towards the stylar (terminal) end of
the  fruit (Plate 5-12). Externally,  the  skin over the affected tissue shows a
reddening; internally (in yellow-fleshed varieties), a wedge of red tissue extends
from the skin towards the pit in clear contrast to the paler unaffected tissue. By
the time the rest of the fruit ripens, the affected  tissue becomes soft or rotten.
Sometimes  the flesh may separate along  the  suture  or  the pit  may split.
Although enlargement or swelling along the suture may accompany discoloration
of tissue, hypertrophy of the affected tissues is not  common. The concentrations
of gaseous fluoride that can induce suture red spot on fruit are less  than those
that induce foliar symptoms.
   A premature ripening of the suture of  peach  fruit can have other causes.
Growth regulants, such as the phenoxyacetic acids  (e.g., 2,4-D), which may
come  from neighboring agricultural operations, induce a  premature ripening of
the suture, but the effect is most severe towards the stem end of the fruit and
hypertrophy of the affected tissues occurs. This hypertrophy may  affect one
side of the  suture more than the other. Premature ripening of the suture has also
been attributed to  virus infection, aberrant fruit development,  and unknown
agents.
   Symptoms similar to suture red spot have been described on apricot, cherry,
and pear fruits and attributed  to atmospheric fluoride. They may consist of a
necrosis of  tissue or premature ripening and shrivelling of  tissue at the stylar end
of the  fruit. Similar symptoms on  these fruits also  have been associated with
moisture stress.


                      Factors Affecting Plant Response
General Characteristics
   The  factors  that  affect  the  plant's response to atmospheric fluoride can be
considered in several different ways. First,  these factors can be categorized by
their nature and origin as follows:
      1. Biological characteristics of the plant, including its genetic complement,
        and stage of development;
      2. Environmental conditions, such as  climate, light  quality and intensity,
        temperature,  relative   humidity,  precipitation,  soil  conditions  and
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         presence of pathogens or insects;
      3.  Pollutant  characteristics, including  physical  and  chemical forms of
         fluoride, concentration and  duration of exposure, and  frequency of
         exposure periods.
   Second, their mode of action on the plant can be postulated as an effect on:
      1.  Absorption or penetration of fluoride into the foliar tissue;
      2.  Accumulation of fluoride in  an active form at a sensitive site or tissue;
      3.  Metabolic and physiological  state of a tissue  that determines its sensi-
         tivity to the toxic action of fluoride.
   Third, the operation of these factors can be separated into three phases:
      1.  Before exposure occurs
      2.  At the  time of exposure
      3.  After exposure has occurred
   Because the primary objective is to diagnose and assess the plant response to
fluoride  in  the  field, certain aspects of  these  factors and  their actions are
emphasized while others receive lesser  attention.

Genetic and Specific Differences  in Tolerance
   Variations  in plants' genetic tolerance to fluoride-induced injury are greatest
among different species; however, differences  in tolerance  among varieties are
better indicators of the role  that  the genetic  complement  of a plant  plays in
determining its  tolerance to HF. Various cultivars of corn (Plate 5-7), sorghum,
gladiolus, and  tomato,  and  the variability  of  individuals in  populations of
conifers  (Plate 5-13) display  marked  differences  in their tolerance to HF. It is
not known how many  genetic factors are involved  in tolerance.

Stage of  Development
   As has been  mentioned before, the young elongating or expanding foliage of
plants is the tissue most sensitive to  HF.  In an  indeterminate  plant, in which
shoot growth  and leaf initiation  occur throughout the growing season, sensitive
tissues are present throughout the  season. In  plants,  such  as pine or oak, the
sensitivity of  the plant will parallel the development  and maturation of foliage
each  year. In other plants, such as citrus, in which periodic flushes of foliage
occur during a year, the sensitivity of the plant will show periodic changes.
   The age of the needle in relation to the occurrence  and kind of exposure can
influence the  distribution  of  injury (needle  tip necrosis) on conifers. In pines,
spruce, and  fir,  for example, needle elongation is relatively synchronous over the
entire tree.  Therefore, relatively greater homogeneity  in the response could be
expected when  needles on  a  single shoot  (and in the  pine's needles within the
same  fasicle) are compared. On larch,  in which needles appear first on the spurs
and then on the new shoots, a difference in occurrence or severity of injury may
be used  as an indication of the time at which the exposure occurred.  Discon-
tinuities  or heterogeneity  in  injury  to the  foliage  of western red cedar or
hemlock may  also be  used as an indication of the interaction between stage of
development and time  of exposure.
   Different species of plants have different  tolerances for fluoride, and symp-
                                    5-11

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toms should be  expected to be  most frequent and  most severe on the least
tolerant species. But this would be true only if the foliage of all the species were
sensitive at the time that the exposure occurred. Differences in the age of foliage
at the time of exposure can produce apparent anomalies, as  illustrated by two
examples. Consider two species  of plants, a coniferous (sensitive) and a decidu-
ous  (tolerant) plant; symptoms are  present  and more severe on the deciduous
species because it broke dormancy first, and the exposure occurred before the
new shoots had emerged from the conifer. Suppose also that the same condition
is observed when the observations are made  in late summer. The  more tolerant
species  may  have symptoms because of its indeterminate growth:  its  newer
foliage, which  is present at the time of exposure late in the season, is  more
sensitive than the more mature foliage of the  conifer. Although it is important to
know the sensitivity of the  species, it  is also important to know their growth
characteristics and the way in which exposures to gaseous fluoride may or could
have  occurred. It cannot be emphasized  too strongly that an  evaluation of
symptoms  must consider not only the  severity and kind of symptom, but also
the distribution of the symptom  in relation to the pattern of growth for that
species.

Environmental Factors
   The edaphic factors that have been found to affect the tolerance of plants to
HF  are mineral nutrient  status, soil temperature,  and soil moisture. Nitrogen
deficiency increases sensitivity of beans and tomato. Calcium, magnesium, potas-
sium, and  phosphorus  deficiencies increase  the sensitivity of tomato. On the
other hand, excess levels of nitrogen, phosphorus, or calcium in  the root zone
also increase the  sensitivity of tomato.  In gladiolus, deficiencies of iron or
manganese have  no effect; while deficiencies of phosphorus and potassium
increase, and  deficiencies of nitrogen  and  calcium  decrease the severity of
tipburn. Field reports  indicate that apricots and other fruit trees show greater
necrosis in those  parts of an orchard where soil moisture is less available. On the
other hand, reduced soil moisture availability increases tolerance in the experi-
mental fumigations of beans. The accumulation of fluoride by  the aerial portions
of some crops decreases as soil temperature increases.
   The major climatic  factors that affect the tolerance of plants to HF are light,
temperature, relative humidity,  and wind  speed. In general,  plants exposed to
HF in the dark are more tolerant  than those exposed  in the light; however, the
exact nature of  the modifying effect  of light depends  upon the  species. In
sensitive species the effect of darkness appears to be an effect on foliar accumu-
lation: less  fluoride accumulates  in  the  dark, but injury in light  and  dark  is
associated with about the  same  foliar concentrations of fluoride. In tolerant
species less fluoride accumulates in the  dark but injury is associated with lower
foliar fluoride  concentrations than  in  the light. Moreover, in one species the
effect  of fluoride is latent:  no injury is present after  a fumigation in the dark,
but injury rapidly appears in the light after the fumigation is stopped. A greater
amount of foliar injury  on  gladiolus occurs when  the temperature is increased
during exposures. Also,  when gladioli are exposed to HF at different relative
                                    5-12
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humidities, a greater amount of injury occurs at 85% than at 50% or 65% relative
humidity. Plants exposed to air pollutants tend to be more sensitive or show
more injury when the velocity of air past the foliage is greater.
   Although several environmental factors are known to affect the tolerance of
plants to HF, the  effects of others are still to be determined. Environmental
factors enter into  the diagnosis of injury in three major ways. First, they may
produce symptoms that mimic those produced by atmospheric fluoride. Second,
in combination  with genetic factors they can affect the tolerance of the plant.
Third, to the extent that environment alters or  determines the growth cycle of
the  plant,  it thereby indirectly affects the plant's sensitivity  to  HF and the
expression of symptoms.
   The mimicry  of  fluoride  by environmental conditions can be detected if the
conditions  and their symptoms are known.  Genetically-  and environmentally-
produced variability can be accounted for in different  ways. For example, the
occurrence and  severity of symptoms should  be expected to  be  much more
uniform  in a field of hybrid corn (since it is more genetically uniform) than in a
planting  of Scotch  pine. One kind of interactive  effect of environment and plant
development in  symptom expression has already been illustrated,  but another
kind  occurs  as  a latency in the  expression of an effect. If  conifers receive
low-level and long-term  exposures, fluoride may  be taken up  by  the needles
without any symptoms appearing. Later in the growing season, when a hot, dry
period occurs that may induce moisture stress, symptoms may suddenly appear
on the fully elongated needles. On the other hand, symptoms may  not develop
so quickly  on some  plants when  a  period of cool, moist weather follows
exposure to atmospheric fluoride.

                           Injury Threshold Doses
   Symptoms induced by atmospheric  fluoride  on plants  become  more severe
and  frequent as  the concentration, the  length of  the exposure period, or the
frequency of exposures become  greater.  It is difficult to say what the thresholds
for injury  may   be,  but  the  lowest  concentrations of HF and  the shortest
duration of exposure, for which  investigators have reported injury to be present,
can  be  indicated. These kinds of data are illustrated in  Figure 5-2, in which
individual species are not represented, but general and approximate categories of
tolerance — sensitive, intermediate, and tolerant — are indicated. The positions
certain species occupy with  respect to these categories may be seen in Table 5-2.
                                    5-13

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                         CONCENTRATION OF ATMOSPHERIC FLUORIDE ppb (VM

                                        jug F x M
Figure 5-2. The Relationship of Concentration of Atmospheric Fluoride (Vertical Axis) and
           Duration of Exposure (Horizontal Axis) to the Threshold for Foliar Symptoms
           for Sensitive, Intermediate, and Tolerant Species of Plants
                                        5-14
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                             Table 5-2
             Relative Sensitivity of Various Plants to F
                Flowering Shrubs and Ornamental Plants
Sensitive
Gladiolus
Jerusalem cherry
Tulip
Iris
Sensitive
St. John's Wort
Crabgrass
Smart weed
Chickweed
Lamb's quarters
Pigweed
Johnson grass
Sensitive
Pine, Ponderosa,
 Scotch (young
 needles)
Western larch
Douglas fir
Blue spruce
Sensitive
Oregon grape
Boxelder
Serviceberry
Intermediate
Azalea
Rose
Narcissus
Dahlia
Lilac
Rhododendron
Aster
Violet
Geranium
Peony
Sweet William
Flowering cherry
Flowering plum
Jerusalem cherry

           Weeds
Intermediate
Johnson grass
Nettle-leaf goosefoot
Goldenrod
Sunflower
          Conifers
Intermediate
Grand fir
White spruce
 (young needles)
Spreading Japanese
 yew
Tolerant
Mock-orange
Bndalwreath
Firethorn
Chrysanthemum
Camellia
Petunia
Privet
Toleran t
Burdock
Nightshade
Dock
Plantain
Purslane
Tolerant
Pine, Lodgepole,
 Mugo (mature needles)
Arborvitae
Juniper
                    Broad-leaved Trees and Shrubs
Intermediate
Serviceberry
Quaking aspen
Red mulberry
Black walnut
English walnut
European mountain
 ash
Silver maple
Common chokecherry
                               5-15
Tolerant
Sycamore
American linden
Currant
London planetree
Sweetgum
Birch, white
Birch, cutleaf
Mountain laurel
Dogwood

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         Table 5-2 (Continued)
Relative Sensitivity of Various Plants to F
Broad
Sensitive












Sensitive
Italian prune
Apricot, Chinese
Apricot, Royal
Bradshaw plum
Peach (fruit)
Blueberry
European grape




Sensitive
Milo maize
Barley (young)
Oats (young)
Rye (young)
Wheat (young)






Sensitive
Sweet corn
Sweet potato







-leaved Trees and Shrubs
Intermediate
Poplar, Carolina
Poplar, Lombardy
Maple, Norway
Maple, hedge
Little-leaf linden
Sumac, staghorn
Sumac, smooth
Green ash



Fruit Trees
Intermediate
Apricot, Moorpark
Apricot, Tilton
Peach (foliage)
Sweet cherry
Apple
Lemon
Tangerine
Grapefruit
Orange
Concord grape
Field Crops
Intermediate
Field corn
Barley (mature)
Oats (young & mature]
Rye (young & mature)
(Continued)
Tolerant
Modesto ash
Virginia creeper
Elderberry
Black locust
Oak
Balsam poplar
Elm, American
Elm, Chinese
Russian olive
Tree-of-heaven
Willow

Toleran t
Pear
Red raspberry









Tolerant
Cotton
Tobacco


Wheat (young & mature)
Crimson clover
Sweet clover
Soybean
Alfalfa
Sugar cane
Garden Crops
Intermediate
Tomato
Strawberry
Bell pepper
Pea
Carrot
Snap bean
Potato
Eggplant
Spinach






Toleran t
Eggplant
Asparagus
Spinach
Celery
Cabbage
Cauliflower
Summer squash
Cucumber

                  5-16
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                           Air Quality Standards
   No air quality standards have been established for fluorides.

                     Relative Sensitivity of Plants to HF
   Many investigators have compiled lists in which various species are assigned to
certain  categories on  the basis of  their sensitivity  or  tolerance to  air-borne
fluorides. Different  lists  sometimes assign the same species  to  different  cate-
gories. There are several reasons for this. Most of the rankings are based upon the
appearance  of symptoms  or  lesions on  leaves.  This is  quite relevant  to the
problems of surveying vegetation  for the assessment  of effects but ignores two
other aspects. An effect on productivity or the accumulation of fluoride may be
more important than foliar symptoms and is  only loosely related to them in a
species  which is usually classified  as tolerant,  such as alfalfa.  Also, great differ-
ences in tolerance exist not only among species but among cultivars of the  same
species  and  among individuals in a natural population. Therefore, the category a
certain  species occupies depends upon what portion of the species was observed.
Many  rankings  are  based on field  observations whereas others come  from
experimental fumigations. In  some fumigations,  a species is rated according to
the concentration or the  length of exposure that was required to first produce
symptoms. In other fumigations, species may be rated according to the degree or
severity of  injury produced by a single fumigation. There is also the possibility
that conditions of experimentation and the  kind of response  observed  may
determine the ranking of species.

                            Leaf Tissue Analysis
   As  has  been  mentioned  before,  the chemical analysis  of  vegetation for
fluoride is  an important  aspect  of  field surveys and comprises the following
interrelated  activities: sampling vegetation in the field; preparing the material for
fluoride analysis; and evaluating the analytical results.
   Three kinds of problems illustrate how sampling of vegetation is influenced
and  directed  by the  particular  objective and  ways in which  environmental
conditions, biological factors,  and  the characteristics of exposure affect accumu-
lation, distribution, and retention of fluoride by foliage.

Aiding or Confirming a Diagnosis
   The  sampling of  foliage to determine if  tipburn  on a pine is  caused by
fluoride should be done with an awareness that the fluoride, which may indeed
be present, can be both internal and  superficial. Dust particles  from roads or the
soil residing on the foliage may contain fluoride but may not be relevant to that
in the  tissue  or  to  an injury. If the distinction between  these two  kinds  of
fluoride  in  the  sample is  wanted, the needles may  be partitioned into  two
sub-samples  and one can  be  washed to  remove superficial  fluoride  before the
tissue is dried for analysis.  Needles from higher limbs tend to have  greater
concentrations of fluoride, therefore samples should be taken from at least two
elevations on  the tree.  Since  fluoride  continues  to accumulate in old needles,
samples should be taken from current year's needles.  Fluoride, after it has  been
                                   5-17

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absorbed by the needle, moves to the tip and accumulates. Thus, there should be
a difference between tip and basal portions of the needle. However, the trans-
location of fluoride takes a certain  amount of time and  if needles are sampled
immediately after exposure, the process may not be complete and the difference
between tip and base will not be so great. Control samples should be obtained
from trees of the same species in an area that is known to be free or remote from
a source of atmospheric fluoride. These  samples should be treated and analyzed
in the same way as those from affected trees so that the results from the affected
trees can be compared with a baseline value.
                                Selected References

Benedict,  H.  M. Field sampling for  the presence of fluorides in  forage crops. Toronto:
   Proceedings of a Symposium on the Impact of Air Pollution on Vegetation, 30, April
   7-9, 1970.
Biological Effects of Atmospheric Pollutants.  Washington: Committee  on the  Biological
   Effects of Atmospheric Pollutants, National Academy of Sciences.
Brandt, C. S. & Heck, W. W. Effects of air pollutants on vegetation. In: A. C. Stern, ed., Air
   Pollution,  Volume I. New York: Academic Press, 2nd ed., 401443, 1963.
Fluorides and Human Health.  Geneva:  World Health Organization, Monograph Series No.
   59,364, 1960.
Lillie, R. J. Air Pollutants Affecting  the Performance of Domestic Animals. U.S. Depart-
   ment of Agriculture, Agricultural Handbook No. 380, 109, 1972.
Phillips, P. H., Greenwood, D. A., Hobbs, G. S., Huffman, C. F. & Spencer, G. R. The
   fluorosis problem in livestock production. In: A Report of the Committee on Animal
   Nutrition.  Washington,  D.C.: Committee on Animal Nutrition, National Academy of
   Sciences, Publication 824, 29, 1960.
Thomas, M. D. Effects of air pollution on plants.  In: Air Pollution. Geneva: World Health
   Organization, Monograph Series No. 46, 233-278, 1961.
Thomas, M. D. & Alther, E. W. The effects of fluoride on plants. In: Eicher, O., Farah, A.,
   Herken, H., Welch, A.  D.  & Smith, F. A., eds., Handbook of Experimental Pharma-
   cology. Volume 20, Part 7. New York: Springer VerLag, 231-306, 1966.
Treshow, M. Fluorides as air pollutants affecting plants. Annual Review of Phytopathology,
   9:2243, 1971.
Treshow, M. & Pack, M. R. Fluoride. In: Jacobson, J. S. & Hill, A. C., eds., Recognition of
   Air Pollution Injury on  Vegetation: A Pictorial Atlas. Pittsburgh: Agricultural Commit-
   tee, Air Pollution Control Association, Informative Report 1, D-l-D-17, 1970.
Weinstein, L. H. & McCune, D. C. Effects of fluoride on agriculture. Journal of the Air
   Pollution Control Association, 21:410413, 1971.
                                      5-18
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Plate 5-1. Citrus Foliage with the Typical Fluoride-Induced Pattern of Chlorosis
Plate 5-2. Blueberry Leaves Showing the Kind of Injury Induced by Atmospheric
         Fluoride
                                   5-19

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  Plate 5-3. Marginal and Intercostal Necrosis of a Grape Leaf
Plate 5-4. Hydrogen Fluoride Injury to Poplar (Field Exposure)
                           5-20
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Plate 5-5. Oregon Grape with Symptoms Mimicking Fluoride Injury, Cause Not Known
              Plate 5-6. Lamb's Quarters Showing HF'-Induced Injury
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Plate 5-7. Leaves of Sweet Corn Showing HF Induced Symptoms and Varietal
         Differences in Tolerance. From Top (Tolerant) to Bottom (Sensitive)
         the Varieties are: Surecross, Go/den  Cross Bantam, Gold Rush,
         Spancross and Marcross
Plate 5-8. Injury Due to HF on Gladiolus, Pine, and Tulip Fumigated Together
                                 5-22
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          Plate 5-9. Fluoride-Induced Injury on Gladiolus Foliage
Plate 5-10. Fluoride-Induced Injury on Fir; Note Several Uninjured Needles
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Plate 5-11. Slash Pine Displaying the Reddish-Brown Disco/oration of Needles
          Injured by Fluoride
  Plate 5-12. Suture Red Spot Syndrome of Peach Fruit Induced by HF on
            Dwarf Elberta
                                 5-24
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Plate 5-13. Fluoride Injury to Ponderosa Pine. Note That
          Only One Tree Exhibits Injury. This is an Illus-
          tration of the Natural Differences in Tolerance
          Found in the Field
                       5-25

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                                Chapter 6
                        MINOR POLLUTANTS
                               Introduction


   This  chapter contains  information  on  a  number of pollutants  generally
referred to as "minor pollutants" because they have not yet resulted in major
social or  economic  problems.  Some of these, such  as ethylene, are  widely
distributed but seldom cause damage because  the concentration is usually too
low. Others, such as carbon monoxide,  do not cause plant damage at concentra-
tions  normally  found even  m polluted  atmospheres. Still  others are  not
ubiquitous but occur only as accidental releases. Sources of the pollutants and
relative  frequence  of injury from  these pollutants are  presented  under each
pollutant.  The same format has been  followed in this chapter as in previous
chapters.
                                   6-1

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                       SECTION 1.  CHLORINE
                               Introduction
   Chlorine (C12) is  a  yellowish-green gas that  is widely  used  commercially
because of its strong oxidizing property.  Nearly  10 million tons  of the gas are
produced annually in  the  U.S.  About 70% of this  amount is  used  by  the
chemical industry in  the  manufacture of myriads of products from plastics to
pesticides.  About 18% is used by the pulp and paper industry, and the balance is
used for sanitary purposes, such as water and sewage purification.

                                  Sources
   There are only 69 industrial plants producing this gas in the U.S. Although
there are a number of potential sources of atmospheric emissions in the manu-
facturing process, the manufacturing process has not been responsible for much
vegetation  damage. Because chlorine  is very hazardous to all forms of life, the
manufacturing, handling, and  shipping processes are carried  out with much
precaution. Even when  tank cars or cylinders are returned to factories for refill,
the containers  are  evacuated, and  this gas is used for products  requiring low
grade gas.  However,  since the gas is so  widely used, there  are a number of
potential user sources.
   Damage to vegetation by this gas has usually resulted from accidental  releases
such  as  breaks  in lines  or  faulty connections in equipment using chlorine.
Accidental leaks usually result in very high concentrations of the gas for short
periods of  time in a limited area. The injury that has been observed in the field
has reflected this pattern, i.e., plants near  the source are severely damaged or
killed, and the severity  of symptom expression decreases with distance. Damage
to  vegetation due  to chlorine gas  was reported to have  occurred over  one
hundred years ago in  Europe near brick and clay product factories and chemical
plants.
   Natural  sources  of this gas include  that  released from sea salt particles in
marine  air, emissions from  volcanic eruptions (about 9  million metric  tons
annually), crustal weathering, and forest fires.

                          Atmospheric Chemistry
   Much of the  chlorine compounds emitted from natural sources is removed
from  the atmosphere in  relatively close  proximity to the point of origin by
precipitation and dry fall-out. For example, about 90% of the chlorine produced
by the oceanic source is returned to the sea, and only 10% is deposited on the
continent.  Chlorine is a very reactive chemical and will undergo changes  very
quickly in  the atmosphere. Chlorine-containing compounds can exist in  gaseous
form, or combined with material in aerosols.
   Chlorine compounds  are dispersed  in the atmosphere just as any other trace
contaminant. The chlorine compounds may react chemically in the atmosphere
and be transformed into materials including oxidized species. The atmospheric
reactions of chlorine compounds have not been studied extensively. However, a
number of photochemical reactions have been postulated.
                                    6-2
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                              Monitoring Data
   Only  a very  few measurements  of gaseous chlorine have been  taken in
uncontaminated atmospheres. In coastal  areas the concentration of chlorine is
usually about 0.001 ppm (2.9 jUg/m3). Since chlorine is not as ubiquitous nor as
abundant as  other pollutants, it is not  measured routinely in cities of the U.S.
The average concentration of total chlorine in large cities such as Baltimore and
Cincinnati is 0.02 ppm (58.0 jug/m3). No information is available in the public
literature on  ambient concentrations near point sources nor on long-term trends.
                             Symptomatology
Acute Injury
   Broad-leaved (Dicotyledonous/ Plants. The  most characteristic symptom on
these plants is a spotting of the leaf. The spots first appear as cooked (very dark)
green areas  that later turn straw-colored or brown  (Plates 6-1, 6-2). These are
sometimes located  between the veins, but  usually they are found close to the
margin, and increase with the intensity of the fumigation and progress towards
the midrib.  In some instances, chlorine injury will result in an upper-leaf surface
flecking  and necrosis similar to ozone  injury (Plate 6-3) or in an interveinal
bleaching similar to sulfur dioxide injury (Plate 6-4).
   Narrowleaved (Monocotyledonous) Plants.  On grasses exposed to chlorine,
the first  symptoms to appear  are marginal necrotic streaks that progress toward
the main vein of the leaf with  time.  Symptoms usually develop in the region
between  the tip and the  point where the grass leaf bends over.
   Coniferous Plants. Tip necrosis (Plate  6-5)  has been  the  most common
symptom observed on  conifers in  artificial fumigations. The necrosis extends
toward the base of the  needle as the severity of exposure increases. The necrosis
may be  tan, brown, or reddish in color. Mottling of the needle may  also be
present (Plate 6-6).
   Exposure  to chlorine often produces somewhat different symptoms. On some
plants, such  as mustard, annual  and Kentucky  bluegrass, chickweed, nettle-leaf
goosefoot, and  lamb's quarter, white to tan  markings may be produced. In some
instances, chlorine  may produce an overall  bleaching without killing the  tissue
and resulting in  a discoloration that may range from pure white to light green or
yellow.

Chronic Injury
   Very little is known about the chronic effects of chlorine gas. In experimental
work that has been reported, epinasty has been reported  to occur without foliar
markings, and sometimes leaf cupping and abscission may be present.

Mimicking Symptoms
   In general, chlorine injury symptoms are  similar to those reported for ozone.
On conifers, chlorine injury  causes a tip necrosis and needle mottle that  looks
very similar to ozone injury.
                                    6-3

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                      Factors Affecting Plant Response
   Very little information is available on the factors that affect plant response to
chlorine.  Plants growing under  low soil moisture conditions  are  less  severely
injured than those grown  under high soil  moisture conditions. The age of the
plants appears  to be important;  for  example,  six-week-old  plants are more
sensitive than three-week-old plants. However,  age interacts with soil moisture,
and plants of different ages will react uniformly  when growing on dry soil.
   The presence of moisture on the leaf does not  affect plant sensitivity. Shade
has a tendency to minimize damage when the shade period follows fumigation.
No effect is noted if the shading precedes  fumigation. Water stress, even slight
wilting, also causes  plants to become tolerant. Hardened vegetation (e.g., pine
trees in winter) is less sensitive than actively growing vegetation.
                           Injury Threshold Doses
   Threshold concentrations for acute injury are reported to be in the vicinity of
0.5 to 1.6 ppm  (1.4 to 4.35 mg/m3) for exposures of one-half to three hours as
summarized in Table 6-1.


Table 6-1
Threshold Concentrations for Acute

Species
Cone.
mg/m3
Buckwheat 1 .6
Peach
Bean
Radish
Rose
1.6
3.8
3.8
4.4
Time,
Hrs.
2
3
0.5
0.5
0.5

Chlorine Injury
Dose
(Cone, x Time)
3.2
4.8
18.0
18.0
22.0
                            Air Quality Standards
   No  air quality standard  has been established for chlorine  in this country.
Russia has established a 24-hour average maximum allowable concentration of
0.01 ppm (29/ug/m3).
                   Relative Sensitivity of Plants to Chlorine
   Several  investigators have provided  information regarding relative sensitivity
of  plants  to  chlorine. Table  6-2  is compiled  from the sources listed  under
Selected References.
                                    6-4
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Relative
Sensitive
Alfalfa
Blackberry
Box elder
Chickweed
Crab apple
Gomphrena
Horsechestnut
Mustard
Pin oak
Radish
Rose
Sugar maple
Sunflower
Sweet gum
Tobacco
Tree-of-heaven
Tulip
Virginia creeper
Wandering Jew
Zinnia
Table 6-2
Sensitivity of Various Plants
Intermediate
Annual blue grass
Buckwheat
Cheeseweed
Corn
Cucumber
Dahlia
Dandelion
Nasturtium
Nettle-leaf goosefoot
Onion
Petunia
Pinto bean
Scotia bean
Squash
Tomato






to Chlorine
Tolerant
Azalea
Balsam fir
Begonia
Cactus
Chenopodium
Chrysanthemum
Cowpea
Field corn
Geranium
Kentucky bluegrass
Lamb's quarter
Mignonette
Myrtle
Oxalis
Pepper
Pigweed
Pine
Polygonum


                             Leaf Tissue Analysis
   Although several  methods are available for detecting  chlorine  from plant
tissue, it has been reported that plants exposed to identical chlorine exposures
will give inconsistent  results.
                                     6-5

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              SECTION 2.  HYDROGEN  CHLORIDE
                               Introduction
   Over 2 million tons of hydrogen chloride (HC1) gas is produced annually in
the U.S. at about  ISO facilities. About 90% of this amount is produced  as a
by-product in the chlorination of organic compounds. This gas is easily removed
from contaminated air streams, and control equipment is available to do so. Up
to 99.5% of the gas can be removed from the gas stream. Because the gas is so
easily scrubbed by relatively  inexpensive and readily  available equipment, the
manufacturing industry has been quick to put controls on their process when air
contamination problems arose. Therefore, very few cases of vegetation  damage
have been reported near industrial manufacturing plants.
   Combustion  of fossil and rocket fuels provides another source of HC1 gas. For
example, an 800 megawatt (MW) power plant burning 0.2% chlorine-containing
coal would discharge  about 25 tons of HC1 gas per day. About 500 pounds of
HC1 are produced per 100,000 persons  per day for domestic  space heating. The
gas is also given off in the burning of municipal refuse because of the  chlorine
compounds contained in paper, salt in  food, grass clippings,  wool, leather, etc.
The HC1 concentration of the gas stream leaving incinerators is normally about
500 ppm (745  mg/m3).  However, it may be higher in  individual incinerators
depending on  the  components of the  trash. Vegetation damage was reported
near a hospital incinerator where paper comprised 80 to 90% of the trash.
   About 25,880  tons of  HC1 are emitted into the atmosphere each year from
the lead chloride additives in motor fuels.

                                 Sources
   The effects of hydrogen chloride were first noted in Europe in trie vicinity of
alkali  plants during the  mid-nineteenth  century. Extensive studies were under-
taken at that time and in subsequent years by several German researchers. As a
result .of  their  effort, air scrubbing devices were installed  at the offending
industries, and  the problem  was essentially  solved. Much  of their  research
however, the descriptive aspects in particular,  is of limited  value  for  present
purposes because most of  the fumigations were performed without adequate air
circulation over the plants.

                          Atmospheric Chemistry
   Some investigators  have postulated that sulfur trioxide formed by the oxida-
tion of  sulfur dioxide may dissolve sea salt particles in marine air, lower  the pH,
and release HC1. However, since ammonia is also given off by the sea, it  appears
unlikely that the pH could become low enough to effect the release of HC1.
   Hydrogen chloride  gas is extremely hygroscopic and probably does not exist
as a gas in ambient air following its release. It is probably quickly changed into
hydrochloric acid aerosol droplets.
                                   6-6
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                              Monitoring Data
   There is no information in the public literature on ambient air concentrations
of hydrogen chloride.

                             Symptomatology
Acute Injury
   Broad-leaved (Dicotyledonous) Plants.  Most commonly, two types of injury
occur on broad-leaved plants. Marginal or interveinal necrosis (Plates 6-7 and 6-8)
is  probably  encountered most frequently.  The necrotic tissue may become
yellowish-brown, brown,  reddish, or nearly  black in color. Brown-orange dis-
coloration of the leaf margin has also been  reported. Severe injury on tomato
leaves may result in bronzing or glazing of the leaf surface. Quite frequently, the
tissue surrounding the brown necrotic tissue is bleached to a cream or pure white
color. The second type of injury  commonly seen is a flecking or spotting of the
upper  leaf surface.  The  spots may be transparent, reddish-brown,  black, or
variously pigmented depending on the species involved (Plate 6-9).
   Narrow-leaved (Monocotyledonous)  Plants.  No  information is available on
monocots.
   Coniferous Plants. On  conifer needles the  only symptom reported has  been a
reddish-brown tip necrosis (Plate 6-10).

Chronic Injury
   The only  information  available on chronic injury is on broad-leaved  plants.
Chlorosis is  the dominant  symptom observed  when  plants are  fumigated re-
peatedly at  very low concentrations. The chlorosis  is generally interveinal and
occurs most frequently  on the  younger leaves and  leaves intermediate in
maturity.  Upward curling of the leaf  and  leaf abscission are also sometimes
present.
   As with  many  other  pollutants, symptom  expression  appears to be quite
variable among different  plant species.  Some of this variability is undoubtedly
related to the hygroscopicity of the  gas. Some of the symptoms that have been
observed in  the field, particularly  leaf spotting,  are  probably  the  result of
hydrochloric acid injury  while other symptoms are more typical of a gas-type
injury.

Mimicking Symptoms
   Under-leaf surface glazing, which may also be caused by hydrogen chloride,
was first noted  as a response to PAN. Marginal  leaf scorch can be caused by a
number of  agents  such   as chlorine,  soluble  salts,  drought  or wind injury,
fluorides, and sometimes sulfur dioxide.

                      Factors Affecting Plant Response
   Only a limited amount of work has been done on the factors that affect plant
response  to  chlorine exposure. Relative humidity appears to be  the dominant
factor in symptom  expression. There appears to be a threshold above  which
injury will be quite  severe and below which the injury is minimal for a given
dose.
                                    6-7

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   Age of tissue appears to be another important factor in symptom expression;
for example, chloride can be translocated in the leaf and accumulate in the tip
much like fluoride so that these tissues may show the greatest injury.

                              Injury Threshold
   Chronic injury  (chlorosis) will develop in tomato when fumigated at 0.7 ppm
(1.04 mg/m3) for ten hours per day for two days. No visible injury results at 0.4
ppm (0.6 mg/m3)  for eight hours per day for six days.
   Acute injury is more variable. About 4 ppm (6.0 mg/m3) for two to four
hours is required  to injure sensitive broad-leaved  plants at relative humidities
conducive to injury. Up to 10 ppm (14.9 mg/m3) for the same time periods is
required to injure those same species at low relative humidity (less than 50%).
   Tolerant  broad-leaved plants, such as chrysanthemum, are injured  at concen-
trations between 4 and 9 ppm (6.0 to 13.4 mg/m3) for three hours.
   Conifers  are injured  at concentrations starting at 8  ppm (11.9 mg/m3). Some
hardwoods (e.g., tulip poplar) are sensitive at 3 ppm (4.5 mg/m3) for four hours,
while others are tolerant even at 13 ppm (19.4 mg/m3) for four hours.

                            Air Quality Standards
   No standard has  been set  for hydrogen  chloride in the  U.S., but Russia has
established 0.009 ppm (13 yUg/m3) as a 24-hour maximum average.

              Relative Sensitivity of Plants to Hydrogen Chloride
   Investigators have provided information regarding relative sensitivity of plants
to  hydrogen  chloride. Table 6-3  is compiled from  the sources  listed  under
Selected References.
                                  Table 6-3
           Relative Sensitivity of Various Plants to Hydrogen Chloride
       Sensitive
       Caespitose phlox
       Columbine
       Cornflowers
       Garden daisies
       Oriental poppy
       Tomato
       Tulip tree
Intermediate
Black cherry
Chrysanthemum
European black alder
Norway maple
Sugar maple
Pinto bean
White pine
Tolerant
Adonis
Arborvitae
Austrian pine
Balsam fir
Douglas fir
Garden iris
Garden lupin
Garden peony
Goldenrod
Larkspur
Lily-of-the-valley
Norway spruce
Paniculate phlox
Plantain lily
Pheasant's eye pink
Red oak
Solidago
Sweet William
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                                      Leaf Tissue Analysis
             Good results have been reported for detecting chloride in plants fumigated
          with hydrogen chloride. Several methods are available, and one should consult
          chemistry references for method of choice and approved methods.
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                      SECTIONS.  ETHYLENE

                               Introduction
   Of all the hydrocarbons  emitted  into the atmosphere by both  natural and
technological sources, ethylene appears to be the only one that poses a direct
threat  as  an air  pollutant to vegetation.  Its effects on plant  life were  first
observed well over a hundred years ago when city trees were killed by illumina-
ting  gas leaking from  underground  mains. It  was not  until the turn of the
century, however, that ethylene was shown to be the causative agent of injury in
illuminating gas. Paradoxically, this  gas (in the form of kerosene smoke from
space heaters) was also being used commercially by the horticultural industry at
that  time to ripen fruit. Subsequent  research showed that ethylene  is produced
by plants and is also an important growth-regulating hormone. The importance
of ethylene as an air pollutant at the present time, however, bears  no relation-
ship  to its original source as a phytotoxicant.

                                 Sources
   Ethylene is a colorless gas  with two carbon atoms joined by  a double bond
and  which  smells somewhat  like ether.  The  natural  sources of  the gas are
principally production  by  plants (estimated at 20,000 tons annually in the U.S.)
and soils, volcanic eruptions, forest and other wild fires, and, to a minor extent,
leaking  natural  gas. However, the  greatest contribution  to  the atmospheric
burden  comes from the activities of  man. Automobile emissions  provide the
greatest volume,  but other motorized transportation vehicles, stationary fuel
combustion units, various industrial processes  such  as  brick kilns, foundries,
coke ovens, gas  works, polyethylene plants, and miscellaneous sources such as
refuse and  agricultural  burning also contribute. It has been estimated that nearly
60,000 tons of ethylene are released to the atmosphere annually in the U.S. as a
result of open burning.
   Research on the phytotoxicity of ethylene in comparison to other pollutants
has been extremely limited. It could be concluded that the low level of activity
is simply a reflection of its  relative economic and academic significance. Al-
though most of the  economic losses due to this pollutant have been limited to
commercial flower  growers,  it  is possible  that  considerably more injury  is
occurring but is not detected or reported. It could likewise be concluded that
the  lack of research on  ethylene as  a phytotoxic air  pollutant  precludes an
accurate evaluation of its relative importance  among  other pollutants. Future
research,  however,  may  reveal  subtle effects not  readily noticed by  field
observation.

                           Atmospheric Chemistry
   Ethylene is continuously  emitted into the  atmosphere by a number of
sources, and has upon occasion accumulated in the air to levels injurious to plant
life.  Ethylene is known to react with other  atmospheric pollutants such as ozone
and  oxides of nitrogen. With ozone, ethylene may form both carbon monoxide
and  carbon dioxide, formaldehyde, water,  and  formic acid. Ethylene also reacts
                                   6-10
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with nitrogen oxide and nitrogen dioxide in the presence of sunlight to form
ozone and formaldehyde.
   Soil microbes are able to consume hydrocarbons, including ethylene. Green
plants, however, do not remove the gas from the atmosphere, although there are
reports of uptake by fruit.

                             Monitoring Data
   Because hydrocarbons are  important  in  the formation of photochemical
smog, they are routinely monitored by regulatory agencies. However, only olefin
hydrocarbons are reactive. Furthermore, since the olefins are  all involved in the
photochemical reactions, it is not important to separate and measure each one in
atmospheric analyses. Most instruments in use at the present  time measure the
hydrocarbon  methane (CtU), which is nonreactive, and total hydrocarbons. The
difference between the two  readings is the fraction  of  interest  in  terms  of
photochemical  smog. Unfortunately, this reading gives no indication of  the
amount of ethylene present in the sample. Consequently, only very few data are
available on ethylene concentrations in ambient air.
   It has been reported that ethylene is normally absent or present only in small
amounts in rural air, less than 5 ppb (5.75 ^ug/m3 ). A number of researchers have
reported concentrations in large cities in excess of 100 ppb (115 ,ug/m3). In the
Washington,  B.C. area  in July  and  August of 1972,  the  average  ethylene
concentration ranged from 700 ppb (805 jUg/m3) downtown, to 39 ppb (44.8
jug/m3)  outside  the  beltway. In Denver, measurements made during  October,
December, and February 1972-73, indicated an average concentration of 37 to
45 ppb (42.6  to 51.8 Mg/m3).

                             Symptomatology
   As a  natural plant hormone ethylene plays a role in abscission, regulation of
growth,  and  other physiological  functions.  Since these are normal functions,
they will not be discussed per  se in this section.  Two types of symptoms are of
interest  here: Those resulting from traumatically-induced  ethylene production,
and those resulting from  exposure to elevated concentrations  of ethylene in the
ambient atmosphere. Although there is overlap, and  the distinction may  be
artificial, they will be discussed separately for convenience.

Traumatically-Induced Ethylene
   Ethylene  production in plants is stimulated by insect infestations,  tempera-
ture  extremes, water stress, diseases, mechanical injury, ozone injury,  chemical
injury, and other stresses. The  symptoms produced  by  such stresses include
senescense and abscission of plant  parts. One well-known example is the abscis-
sion  of cotton bolls following infestations by the cotton boll weevil. Accelerated
or premature  ripening is another  symptom  associated with increased internal
ethylene. The practice of mechanically injuring figs to stimulate fruit develop-
ment and ripening dates back to the Egyptian civilization.
   A number of chemicals are known to increase ethylene production through
hormonal  or phytotoxic reactions. Some  of the chemicals, such as the herbicide
                                   6-11

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Endothal, are used commercially as defoliants. Recently, ozone has been demon-
strated to stimulate ethylene production in certain plants. This may explain why
plants exposed to low concentrations  of  ozone exhibit typical ethylene symp-
toms, namely, epinasty, abscission, and  premature senescence.

Exposure to Ambient Air
   Acute Effects. The best known  acute  symptom caused by ethylene  is "dry
sepal"  of orchid (Plate 6-11). This disorder is characterized  by a drying  and
bleaching of the sepals starting at the apex and  progressing toward the base. The
concentrations required to produce  this symptom are 0.04 to 0.1 ppm (4 to 115
yUg/m3 ) for eight hours, or 0.002 to 0.02 ppm (2.3 to 23 /Jg/m3) for 24 hours.
   There have been  many reports of damage to trees, shrubs, and grasses from
leaking gas mams. This problem was particularly troublesome around the turn of
the century when illuminating gas  was in widespread  use.  The ethylene com-
ponent in illuminating gas was shown to be  the principal cause of damage. The
gas in use at the present time is natural gas and  contains no ethylene. Damage to
vegetation from  leaking natural gas  is presently thought to be the result of roots
drying out and lack of oxygen available  to  roots because the gas fills the pore
spaces in the soil.
   Chronic Effects.  A number of symptoms,  mostly involving growth abnormali-
ties, are associated with exposure to ethylene. These include  epinasty, abscission
(Plate 6-12), hypertrophy, premature bud break, inhibition of leaf expansion,
and leaf curling. Perhaps the best known and  most frequently observed symptom
is  that  on  flowering. Actually, three separate effects have  been  described:
inhibition of flowering, promotion of flowering, and sex reversal. Promotion of
flowering occurs primarily with bromiliads (e.g., pineapples) but concentrations
much greater than would  be encountered  in smoggy  air are  necessary to induce
this  symptom. A six-hour exposure to 100 ppm (115  mg/m  ) is necessary to
induce flowering in pineapples.  However, such elevated  concentrations could
occur in  a closed greenhouse with faulty space heaters, for example. Sex reversal
occurs with cucurbits. Horticulturists have capitalized on this  phenomenon by
treating  plants with ethylene derivatives to  increase  the  number  of female
flowers. Again, the concentration required to induce this symptom is similar to
that required for promotion of flowering.
   Inhibition of flowering, commonly called  "sleepiness" or "bullheading," has
been observed on many species of flowering plants.  It was first described on
carnation,  in  which 0.5 ppm  (575 /ug/m3) of ethylene for 12 hours caused
opened  blossoms to close, and 1 ppm (1150 /ug/m3) for three days  prevented
blossoms from opening.  However, concentrations  as low as 0.03 to  0.06 ppm
(34.5 to 69.0 /ng/m3) for 48  hours can  be  injurious. Differences in sensitivity
have also been noted (Table 6-4).
   Loss of apical dominance, or prostrate growth of normally upright plants, has
also been reported. Although these symptoms are not deleterious to plants, they
may result in economic losses to commercial  growers.
   The  chronic  symptoms described above, in one sense,  represent "typical"
symptoms.  However,  many  of these  symptoms are characteristic  of  natural
6-12
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                                   Table 6-4
                     Dose Response of Plants to Ethylene
        Response
        Abscission
         Cotton squares
         Leaves
         Buds
         Petals
        Chlorosis
         (of leaves)
        Dry Sepal
         (orchids)
        Epinasty
        "Sleepiness"
        Growth Inhibition
        Loss of Apical
         Dominance
46-3,435
345-685
115
575

685-2,290

5.75-115
1.15-3,435
115-1,145
685-3,435

46-3.435
   ppm

0.04-3.0
0.3-0.6
0.1
0.5

0.6-2.0*

0.005-0.1 *
0.001-3.0*
0.1-1.0*
0.6-3.0*

0.04-3.0*
                                                              Time
5-30 days
8 hrs.
1 hr.

1-30 days*

8-24 hrs.*
3-20 hrs.*
20 hrs. -3 days*
up to 30 days*
    *The lower concentration for the longer time period produces a similar effect to the
     higher concentration for shorter time periods.
    Source:
    Adapted from: Air Quality Criteria for Hydrocarbons. Washington, D.C.: Public
    Health Service, Department of Health, Education, and Welfare, 6-6.
senescence  and environmental stresses such as water stress, bacterial wilts, and
root  rots. Consequently, ethylene injury  could easily  be confused with other
disorders. An interesting example of ethylene injury occurred in a cotton field in
Texas in 1957. Ethylene  emissions  from a  polyethylene manufacturing plant
located near cotton fields caused considerable damage to the crop. Abscission of
cotton  squares  on plants within one mile  of the plant was severe, and  loss of
apical dominance resulting in prostrate growth was extensive.
   Some researchers have suggested using orchid, carnation, snapdragon, cowpea,
or cotton as indicator plants to detect the degree of  ethylene pollution. The
epmastic response of peas has been  widely used in laboratory experiments  to
make rough measurements of ethylene concentrations.  The "receptivity" of the
plant, however, is important in this respect, as will be discussed below.

                       Factors Affecting Plant Response
   Physiological  age appears to be important in  the epinastic response of leaf
petioles to ethylene. Only young leaves are affected and  will bend. The ability of
this gas to  cause curvature is also  dependent upon a supply of auxin from the
leaf

                             Air Quality Standards
   There is  no  air quality  standard for ethylene per se.  Ethylene is but one  of
many hydrocarbons  that  participate in  the photochemical reactions of the
                                     6-13

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atmosphere.  Rather than singling out  ethylene,  the  regulatory agencies have
chosen rather to set a collective standard for all non-methane hydrocarbons. The
standard is set at a concentration of 0.3 ppm (200 Mg/m3) during the hours of 6
to 9 a.m. Interestingly, this standard  was not established at that level to preclude
detrimental health or property damage effects by hydrocarbons, but rather
because monitoring data indicated that  if non-methane hydrocarbons were kept
below that level, injurious levels of oxidants would not be reached later during
the day.
   Until  more  monitoring  data  are gathered  specifically  on  ethylene,  it  is
impossible  to state whether this standard is  adequate. Losses of  considerable
economic  consequence have occurred, particularly in the commercial green-
house-flower industry.  However,  because  of the lack of  specific  monitoring
equipment, such losses have been difficult to document.


                   Relative Sensitivity of Plants to Ethylene
   As with other  pollutants,  the duration  of exposure  must  be considered
together with the  concentration in determining  the sensitivity and  impact. This
represents the dose, and provides the best measure of sensitivity (Table 6-5).

Relative Sensitivity
Sensitive
African marigold
Orchid









Table 6-5
of Various Plants to
Intermediate
Pepper
Tomato
Rose
Snapdragon
Cowpea
Carnation
Lily
Cotton
Ageratum
Larkspur
Zinnia

Ethylene*
Tolerant
Dahlia
China aster
Forget-me-not
Lobelia
Sweet pea
Viola
Acacia
Calendula



*This table is an arbitrary classification based on available data.
                            Leaf Tissue Analysis
   Since ethylene is produced internally by the plant, it would be impossible to
determine what fraction was from an external source and what fraction from the
internal source.
                                    6-14
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                       SECTION 4.   AMMONIA
                               Introduction
   Injury to vegetation from ammonia is rare, and has usually resulted from
 accidental spills rather than continuous emissions to the atmosphere. Most of the
 ammonia, about 85%, produced in this country is consumed by the agricultural
 industry as fertilizer either as  anhydrous ammonia or fertilizers derived from
 ammonia. It is also used widely in the synthesis of  organic compounds such as
 drugs, plastics, and dyes.  Recent occurrences of  plant damage from ammonia
 resulted  from spills in the transport of the  gas and from breaks in pipe lines.
 Increased usage of anhydrous ammonia as a fertilizer  may well result in increased
 local incidences of damage. However, since it is a commodity  of economic
 significance, and since methods to control industrial losses are readily available,
 it will probably not become a widespread problem.

                                  Sources
   The major portion of the ammonia present in the ambient air is derived from
 biological processes both on land  and  in  the oceans.  These sources  include
 decomposition of organic matter, such as in the  composting process in mush-
 room production, and from animal wastes, such as near large feedlots. Ammonia
 is also produced in the combustion of fossil fuels; however, no reports of damage
 from this source have ever been  noted.

                          Atmospheric Chemistry
   Ammonia gas is very hygroscopic and probably combines with water  to form
 ammonium  hydroxide very quickly once it enters a  humid  atmosphere.  No
 information is available, however, on the  fate of ammonia gas released into  the
 air  as a pollutant. Ammonia released from biological decomposition is brought
 back to  the earth by rain, where it is reused by  plants. Presumably, the same
 phenomenon  would occur for the ammonia  entering  the atmosphere  from
 industrial releases. If SOj  is present in the atmosphere, reactions occur rapidly
 with ammonia to form ammonium  sulfate particles  which tend to settle out in
 time.


                             Monitoring Data
   The National Air  Surveillance Network made measurements of ammonia in
various cities in the U.S. during  1963 and 1964. There is a background concen-
tration in the lower troposphere of 0.009 ppm (6 ]Ug/m3) in temperate latitudes,
and  0.2 ppm (140 /^g/m3) near the equator. The concentration in cities across
the U.S.  varies between  .00014  ppm (0.1  ,ug/m3) and 0.018 ppm (12.7 Mg/m3).
The  average concentration for urban areas is 0.029 ppm (20 jzg/m3). The highest
concentration  reported  was 0.109  ppm  (75.5 fxg/m3) in Ashland,  Kentucky.
Since ammonia is not  routinely measured  by regulatory  agencies, it is not
possible  to  determine if  there have been  any  trends  in  atmospheric con-
centrations.
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                             Symptomatology
   A very limited amount of work has been done on the effects of ammonia on
plants  and consequently the response to this gas has been described for only a
few species. The concentrations involved in  accidental spills are so great as to
render symptom expression on affected plants meaningless.  Two interesting
observations have emerged, however. The injury caused by ammonia  differs from
that caused by the more common gaseous pollutants. With ammonia, practically
all areas  of  the leaf are affected rather than  a specific area as  is  common with
other gases.  Secondly, under certain conditions ammonia increases the pH of the
leaf tissue and induces a color change in the leaf.

Acute Injury
   This type of injury is characterized by a collapse of tissue without the loss of
chlorophyll. The collapsed tissue appears in spots either at the margin of the leaf
or, occasionally, in  the  center. The chlorophyll  takes on a  dull, dark-green
appearance, and, with time, the tissues die and turn brown or black.
   On grasses, the injury first  develops as an  area of very small spots  where the
leaf bends, giving the leaf a powdery, speckled appearance.
   On  broad-leaved plants such as sunflower, cheeseweed, pigweed, poison ivy
(Plate 6-13), and dandelion, ammonia causes a general browning of the leaf.
   Ammonia has been  reported  to  cause  glazing  and  silvering  on  the lower
surfaces of the leaves of vegetable crops.

Chronic Injury
   Internal pH changes in the leaf and changes in pigmentation have also been
reported which could be considered a chronic response.  Generally,  though, too
little  is  known regarding low-level, long-term responses  to  consider  chronic
effects.

Atypical Symptoms
   Fruits, such as  peach and  apple,  may be  injured by ammonia.  A purple to
black discoloration occurs around the lenticels of  apples when experimentally
fumigated with 400 ppm (278 mg/m3) of ammonia. Peaches are blackened when
exposed to such massive concentrations.
   Other symptoms  include the  response  of  cotton, mustard, lamb's quarter,
annual bluegrass, and Kentucky bluegrass.  With these species the leaf markings
are white to tan in controlled fumigations (Plate 6-14).
   Since  ambient  ammonia  as an air pollutant  has  not been  a generalized
problem, no attention has been given to using plants as natural indicators of the
presence of this gas.

                      Factors Affecting Plant Response
   Very little has been done in the study of environmental variables that might
alter the responses of plants to ammonia exposure. Leaf age is known to be an
important factor. Middle-aged leaves, those that have been at full size for a week
or more,  are  the  most sensitive.  The  youngest leaves  very  rarely  show any
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markings. Soil moisture also modified plant response in that sensitivity increases
with increasing moisture.



                              Injury Threshold
   Tomato  plants exposed to experimental  fumigations of 1,008  ppm (700
mg/m3) for three minutes undergo changes in the pH of the leaf and stem tissue.
This appears to be the lowest concentration at which injury will  occur when
exposed for such a short period of time. Concentrations of 55 ppm (38 mg/m3)
require  one hour  to injure plants such as buckwheat,  coleus, sunflower, and
tomato (Table 6-6).


                            Air Quality Standards
   No standard has been  adopted by regulatory agencies in the United States.
Czechoslovakia, however, has adopted a 24-hour maximum allowable average of
0.14 ppm (100 Mg/m3); Russia, a 24-hour average of 0.28 ppm (200jug/m3); ar-cl
Ontario, Canada, a 30-minute average of 5 ppm (3,500 /ug/m3).
                  Relative Sensitivity of Plants to Ammonia
   Investigators have provided information regarding relative sensitivity of plants
to  ammonia.  Table 6-6  is compiled from  the  sources  listed under Selected
References.
                                  Table 6-6
               Relative Sensitivity of Various Plants to Ammonia*



                   Approximate dose required to cause an effect* *

           8.0                        33.6                    46.0
        Mustard
        Sunflower
        Lamb's quarter
        Cheeseweed
        Annual bluegrass
        Pigweed
Kentucky bluegrass
Dandelion
Chick weed
Nettle-leaf goosefoot
Buckwheat
Coleus
Tomato
        "This table is an arbitrary classification based on available data.
       **Dose = mg x time (hours)
                            Leaf Tissue Analysis
   There have  been no  reports  on methods for analyzing plants' tissues for
ammonia contamination.
                                    6-17

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                SECTION  5.   HYDROGEN SULFIDE
                               Introduction
   Hydrogen sulfide is non-toxic to vegetation at concentrations  encountered
even in very polluted atmospheres. The concentration required to injure even the
most sensitive plants is far above that which is objectionable to humans.
   Hydrogen sulfide is emitted from a  number of technological activities. Per-
haps the most familiar is kraft paper mills. About 64,000 tons of  the gas were
emitted from kraft mills in  1960 on a worldwide basis.  Other anthropogenic
sources  include the petroleum industry, coking operations, burning culm piles,
foundries, and certain chemical  industries  such as the manufacturers of sulfur
dyes, viscose rayon, certain pesticides, and  many other organic sulfur chemicals.
A number of inorganic processes, such as the smelting and refining of zinc evolve
hydrogen  sulfide.  It  is also  generated  by  animal processing plants  in  the de-
composition of sulfur-containing proteinaceous materials.

                                  Sources
   Natural  sources of hydrogen  sulfide  have been estimated to yield between
100  and nearly  300  million  tons  annually  on  a worldwide basis.  Hydrogen
sulfide is released  primarily from bacterial decomposition of sulfur-containing
proteinaceous material.
   The  importance of this gas in relation  to plant  damage is inconsequential
compared to other air pollutants. A brief description of its effects is presented
for academic interest.

                          Atmospheric Chemistry
   Hydrogen sulfide is relatively  stable  and does not react photochemically in
the  atmosphere. However, since it  can be oxidized  chemically in the  sewage
treatment process, it is reasonable to assume that some oxidation might occur in
an oxidant-laden atmosphere.  It reacts readily with paints  containing  metal salts
and with certain metallic surfaces.

                             Monitoring  Data
   Hydrogen sulfide is not  measured routinely  by the  National Air Sampling
Network. Most  cities have average concentrations ranging from 0.0007 to 0.004
ppm (1  to  6 /ug/m3).  Industrial areas may average up to 0.066 ppm (92 ng/m3).
Background  concentrations have been  estimated to be  between  0.0001  and
0.0003 ppm (0.15  to 0.46 jug/m3). No data  are available on long-term trends.

                             Symptomatology
   Leaf markings resulting from  exposure to elevated hydrogen sulfide concen-
trations are  quite  different from those caused  by other phytotoxicants. The
youngest leaves  always show the greatest  amount of injury,  and  the growing
points may also  be killed. Less than fifty plant species have ever been fumigated
under laboratory conditions. Knowledge about the  effects of this pollutant is
limited at best.
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Acute Injury
   Broad-leaved plants develop an interveinal white to tan discoloration. Wilting
without  the  typical discoloration has also been  reported to occur, and this is
followed by scorching of the young tissue. Grasses exposed to this gas develop a
powdery appearance between the tip and the bend of the leaf.

Chronic Injury
   Chronic fumigations with hydrogen sulfide have not been  performed.  Sun-
flowers fumigated with this gas will develop an orange-brown  cast on leaves in
the bud stage, rather than the usual  white to tan chlorosis typical of broad-
leaved plants.

                      Factors Affecting Plant Response
   Tissue age appears to be  the  most important factor in plant response, and,
unlike the situation with other pollutants, the growing points of stems and leaves
are the most sensitive.  Also  unlike  response  to other pollutants,  drought or
moisture stress seems to increase the sensitivity of plants to very high concen-
trations, 1,000 ppm  (1,390 mg/m3), of the gas. At lower concentrations, 200
ppm (278 mg/m3), however, high soil moisture increases sensitivity.

                              Injury Threshold
   Most of the species that have been tested have not been injured at concentra-
tions  less than 86 ppm  (120 mg/m3) in five-hour fumigations. Species such as
Boston fern, apple, cherry, peach and coleus will even withstand concentrations
up to 860 ppm (1,200 mg/m3). Some species, including buckwheat, castor bean,
gladiolus, rose, sunflower, tobacco, cucumber, and tomato have been injured at
concentrations between these two extremes (Table 6-7).
                           Air Quality Standards
   No standard has been established for this gas. The odor threshold is between
0.0007 to 0.03 ppm (1 to 42 ug/m3). The odor becomes offensive at around 7.2
ppm (10,000 Aig/m3).


              Relative Sensitivity of Plants to Hydrogen Sulfide
   Investigators have provided information regarding relative sensitivity of plants
to hydrogen sulfide. Table 6-7  is compiled from the sources listed under Selected
References.

                            Leaf Tissue Analysis
   Since sulfur is  metabolized by plants, it is possible in some cases to detect
increased  sulfur content due to contamination. It would not be possible to
distinguish which form of sulfur the plants  had been exposed to. If other sulfur
sources were present, these would most likely contribute to the body burden.
                                   6-19

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                        Table 6-7
Relative Sensitivity of Various Plants to Hydrogen Sulfide



      Minimum dose at which 50% leaf injury will occur*

      600                                      3,000
Lamb's quarter
Nettle-leaf goosefoot
 *Dose = mg/m  x time (hours).
Chickweed
Dandelion
Sunflower
Kentucky bluegrass
Pitweed
Annual bluegrass
Mustard
Cheeseweed
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                SECTION 6.  CARBON  MONOXIDE
                               Introduction
   Like hydrogen  sulfide, carbon monoxide (CO) is not toxic to vegetation at
concentrations encountered in polluted atmospheres. However,  it is the most
widely distributed and the most commonly occurring air pollutant. Total emis-
sions exceed those of all other pollutants  combined. However, it is important
from the standpoint of human  health. The general public is usually interested in
this  pollutant and, therefore, even plant biologists  should be aware of a few facts
concerning it.

                                 Sources
   Transportation  activities represent the largest anthropogenic source.  Other
sources in  this category  include any activity in which combustion takes  place,
such as steam generating facilities, industrial processes, and combustion of solid
waste. Interestingly  enough, man's contribution  of carbon monoxide  to  the
atmosphere accounts for only about  10%  of  total emissions. The remainder
comes from natural sources. These sources consist of emissions from volcanoes,
natural gas in coal mines, electrical storms,  and forest fires. Carbon monoxide is
also  formed by certain brown  algae (kelps). Concentrations  of up to 786 ppm
(904  mg/m3) have been  measured above  floats  of kelps, colonies of marine
jellyfish, and other ocean-dwelling organisms.
   The estimated worldwide emission of CO from anthropogenic sources is 198
to 231  million tons per year. The amount  theoretically should have raised  the
atmosphere background concentration. That has  not occurred, however,  and a
sink  or removal process must exist in nature. A few years ago researchers  at  the
Stanford Research Institute discovered that soil microorganisms  are capable of
removing  CO from  the soil  atmosphere.  Fungi, such  as  certain species of
Pemcillium, Aspergillus, Mucor, and others are particularly efficient at removing
this gas.
   The  trend in  carbon  monoxide  concentrations  in  large cities,  including
Chicago, Cincinnati, Denver, Philadelphia, and St. Louis, is encouraging. All of
these cities have experienced a decrease in  annual  average CO concentrations
between the period from  1962-66 to 1967-71. This percentage decrease ranges
from  18% for Denver to 46% for Chicago. The average percentage decrease was
31%. A summary of annual averages for these cities is presented in Figure 6-1.

                             Symptomatology
   Carbon  monoxide has not  been found  to produce  detrimental effects on
plants  at concentrations below  100 ppm during exposures ranging from one to
three weeks. Since the standards have been established at 35 ppm (40 mg/m3)
for eight hours and 9 ppm (10  mg/m3) for  one hour, it  appears that vegetation
will be amply protected.
                                   6-21

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   When plants are  fumigated at concentrations that will elicit responses,  the
resulting injury has  been similar  to  that caused by ethylene. Epinasty is  pro-
duced at 500 ppm (575 mg/rn3), while chlorosis and abscission will develop on
sensitive plants at 10,000 ppm (11,500 mg/m3). Tolerant plants can withstand
ten times this concentration.
     10
      0

     20
 £

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 (0
 Ui
 O

 cc
     20
     20
     10
                                                             CHICAGO CAMP
                                                           CINCINNATI CAMP
                                                              DENVER CAMP

                                                 'o     a     U     n
                                                         PHILADELPHIA CAMP
                                                             ST. LOUIS CAMP
                                                 T~T
            1962  1963   1964   1966  1966  1967   1968   1969   1970   1971   1972


                                       YEAR


                           O INDICATES INVALID AVERAGE

                             (AVERAGE BASED ON INCOMPLETE DATA)



          Figure 6-1. Trend Lines for CO Annual Averages in Five CAMP Cities


Source: Air Quality and Emissions Trends Annual Report: Volume I. Research Triangle
       Park, North Carolina: National Air Monitoring Program, Environmental Protection
       Agency, 4-25, 1973.
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                   SECTION 7.   HEAVY  METALS
                               Introduction
   Heavy metals, such as lead, cadmium, zinc, copper, and mercury, represent a
group  of pollutants that are currently receiving a good deal of attention The
pollution potential of some of these is relatively unknown while for some others
considerable  information has already been assembled and is available in review
articles. One  outstanding characteristic of all members of this class of pollutants
is their longevity and stability once they reach the soil. The metals tend  to build
up in the upper soil layers and are not degraded or leached out with time. If the
source of the pollutant persists long enough in an area, the metal(s) accumulate
to levels  which, in come cases, become toxic to plants or a hazard to other forms
of life.

                                   Lead
   Lead  concentrations have been measured in chronological layers of snow
strata in  quiescent ice sheets of the frozen polar regions. Annual ice layers from
the interior of northern Greenland show that lead concentrations increased from
less than  0.005 jug/kg of ice in 800 B.C. to more  than 0.2 M8/kg in 1965 A.D.
Lead started  to increase in 1750 at the beginning of the industrial revolution,
and the lead  concentration at that time was 25 times greater than natural levels.
During the second half of the 18th  century, lead concentrations  tripled, and
from 1935 to 1965, they abruptly tripled again. The sharpest rise occurred after
1940.  Today, lead concentrations in Greenland  snows are about 400  times
earlier levels.
   There  is evidence  also that  lead  is increasing in other ecosystems.  Surface
waters  in some areas of the Mediterranean and the Pacific have ten times more
lead now than  in pre-industnal  times. The soil in rural areas of the U.S. has a
lead concentration usually similar to the average  content in the earth's crust, i.e.,
10 to  15 jUg/g. However,  in many  cities the concentration  of lead in  soil and
street dust is much higher. The concentration of lead in street dust and surface
soil of large  cities in the  Midwest averaged 1,636 fj.g/g for residential sites and
2,413 /ig/g for commercial sites.
   The inorganic  emission  of  lead from  the  combustion  of leaded  gasoline
constitutes approximately  98%  of the total  lead emission, or approximately
181,000  tons annually. The concentration of  lead in  ambient  air is closely
correlated with the density of vehicular traffic in the U.S. The concentration is
largest  in cities,  smaller in suburbs, and  smaller yet in rural areas.  There is
evidence  of diurnal and seasonal cycles. Numerous studies have shown that  the
concentration of lead in depth profiles of soils along highways decreases with
distance from the highway and with depth.
   Effects on Plants.  Lead does not cause visible injury to plant life. However,
plants can become contaminated by lead from three sources: lead in soil, lead in
air, and lead present in rainwater or groundwater. Usually, only trace amounts of
lead  are  absorbed by plants from soils, but this  amount can  be  increased by
increasing the lead content of the soil or by decreasing the  binding capacity of
                                   6-23

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the soil for lead. Some crops, such as lettuce and potatoes, will not translocate
lead readily, and  lead  accumulates  in  the  smaller feeder roots.  It appears,
however, that in spite of the widely varied concentration of lead in soils, the net
effect  on  the lead content of the plant is negligible because the lead is  largely
unavailable to the plant. Lead  in rainwater also  does not appear to cause any
detectable change in the lead content in any part of crops.
   Several studies have shown that lead in air increases the concentration  of lead
on  the  leafy parts of plants near highways.  All of the studies seem to indicate
that lead  accumulates mostly  on the foliage. About 50% of the lead  that is
accumulated  on plants can be washed off.
   Some outbreaks of lead poisoning in  domestic  animals have been reported in
the U.S. in which the apparent source was contamination of pasture or crops by
industrial  lead  operations. Horses  are  more  sensitive  and may die after an
exposure of 2.4 mg/kg per day  for several weeks.  It should be noted that horses
often ingest soil lead because they pull forage out by the roots and eat both
roots and the soil. Cattle rarely do that.
   No injuries to man or animals have ever been reported from consuming crops
grown  near highways. Since unleaded motor fuels  wDl  become more available
with time, perhaps the problem (or potential problem) will have been averted.

                        Zinc, Cadmium and Copper
   Soil contamination from these metals occurs in urban areas, along highways,
near ore smelters and foundries, and from certain pesticides  and phosphate
fertilizers. Contamination by zinc and  copper has  been  known to occur  for
decades. However, cadmium contamination, particularly  that occurring along
highways from automobile tires, has only recently been recognized.
   Zinc deposition rates near a smelter in Pennsylvania were found to be  187 to
561  Ibs. per acre per year in a recent study. Although cadmium deposition rates
were not measured,  they were  calculated to be about 3 Ibs. per acre  per year.
The study also  showed that the soil  downwind  from the source presently
contains 12,000 Ibs.  per acre of zinc and 160 Ibs. per acre of cadmium.  About
85  to 95% of the  zinc and 95% of the cadmium was found to have been retained
in the top  15 centimeters of the  soil in high contamination areas.
   Foliar concentrations of zinc, cadmium, and copper on oak seedlings grown
in contaminated  soils were  2,120, 38, and  33 ppm, respectively,  while those
grown  in  uncontaminated soils were  155, 0, and 16 ppm, respectively. Trees
growing near the source contained up to 4,500  ppm of zinc  and 70 ppm  of
cadmium.  Foliar  symptoms  observed in the same area included interveinal
chlorosis by  the  middle of the  growing season,  followed by  reddening and
yellowing.

                             Mercury Vapors
   The  phytotoxicity of mercury vapor has been known for nearly 200 years.
Reported  incidences of injury  to plants  are very infrequent in spite  of  the
existence  of  many  sources. Unlike  other heavy  metals,  mercury is liquid at
normal  ambient temperatures, and it is its vapors that  are toxic. However, in
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 order  for injurious concentrations to occur, the  metal must be present in the
 same confines as the sensitive vegetation. Thus, many sources that emit directly
 to  the atmosphere  are not important  from  a vegetation damage  standpoint
 because the vapors are quickly dissipated. Examples of such sources include
 primary and secondary ore processing,  manufacture of paints, agricultural
 chemicals,  and  Pharmaceuticals; laboratory  and  instrument sources; and  the
 combustion of coal, oil, and refuse.
   Plant damage has usually occurred as a result of a few very specific emissions.
 For example, flowers in a  commercial greenhouse were injured when  mercuric
 chloride was added  to  the  soil to  kill  earthworms.  In  another greenhouse
 incident, roses were injured because the interior of the greenhouse was painted
 with a mercury-base paint.
   Levels of mercury necessary  to cause injury have rarely been  determined, and
 only a general idea of sensitivity is available  (Table  6-8).  It has  been demon-
 strated that floral parts of plants are more sensitive than leaves, and older leaves
 are more sensitive than  immature ones.
   Mercury injury on red roses consists of brown spots on  the  leaves,  and is
 accompanied  by leaf abscission, especially of older, but still active, leaves. The
 flower  petals  from partially opened buds turn brown while the young buds turn
 brown  and  fall without opening. Fully opened flowers may turn a characteristic
 faded pink, and  stamens may be killed.
   Peach seedlings have  been found  to be very sensitive to mercury vapors.
 Injury first appears as a fading and subsequently a browning of intervemal tissue
 on  older leaves.  The young leaves are the most tolerant. Abscission can  occur,
 sometimes without leaf markings of any kind.

               Relative Sensitivity of Plants to Mercury Vapors
   Investigators have provided information regarding relative sensitivity of plants
to mercury  vapors. Table 6-8 is  compiled from the sources listed under Selected
References.

Relative
Sensitive
Bean
Butterflyweed
Cinquefoil
Boston fern
Holly fern
Hydrangea
Mimosa
Oxalis
Privet
Sunflower
Willow
Table 6-8
Sensitivity of Various Plants to
Intermediate
Azalea
Basswood
Begonia
Camelia
Columbine
Cosmos
Cotoneaster
Forsythia
Fuchsia
Geranium
American holly

Mercury Vapors
Tolerant
Aloe
Jersusalem
Cherry
Croton
Chinese holly
Ivy
Sarcococca




                                   6-25

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                             Table 6-8 (Continued)
             Relative Sensitivity of Various Plants to Mercury Vapors
           Sensitive                 Intermediate                Tolerant

                                   Calla lily
                                   Easter lily
                                   Japanese maple
                                   Oak
                                   Peach
                                   Persimmon
                                   Privet
                                   Salvia
                                   Saxifrage
                                   Strawberry
                                   White Pine
                                   Tobacco
                                   Tomato
                                   Viburnum
                                   Vinca

    Note: Most of the information on mercury was taken from:

    Heck,  W. W., Daines, R. H.  & Hindawi, I. J.  Other phytotoxic pollutants. In:
    Jacobson, J. S.  & Hill, A. C., eds. Recognition of Air Pollution Injury to Vege-
    tation:  A Pictorial Atlas. Pittsburgh: Air Pollution Control Association, F1-F24,
    1970.
                              Leaf Tissue Analysis
   There are several methods available for selectively measuring the presence of
heavy metals in plant tissues. One should consult chemical references for the
method  of choice and approved methods.
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               SECTION 8.   PARTICULATE MATTER
                               Introduction
   A significant fraction of the pollutants found in urban atmospheres consists
of small particles. Such particulate matter varies greatly in chemical composition
and consists of multi-molecular assemblies that may range in complexity from
salt crystals to  living cells.  From the standpoint of vegetation damage, this class
of pollutants is  relatively unimportant.

                                  Sources
   Combustion products and photochemical aerosols make up a large fraction of
the particles in the atmosphere, but these are usually very  small in size.  Larger
particles  are contributed by  local soil,  fine dusts, and sea  salt along the coast.
Industrial sources of dust include incinerators, cement plants, limestone quarries,
industrial  furnaces, paper mills, etc.

                          Atmospheric Chemistry
   Dust particles falling  on leaves seldom cause injury. Particles in the atmos-
phere participate in chemical reactions with the surrounding gases and with each
other. Particles in a humid atmosphere become surrounded by  a water film and
water soluble  gases like HF or SO2 can  become dissolved in this film.  The
presence  of SO2 in the water makes the water acidic and, if the acidified particle
lands  on  a leaf, it may burn  a hole through the leaf tissues. In humid  air,
moisture  droplets containing  dissolved gases reach  a critical size and precipitate.


                             Symptomatology
   Dusts   may  be  harmful,  harmless,  or  indirectly  beneficial to vegetation
depending on   their composition.  Injury may result from  the deposition of a
relatively  thick crust  of  lime and  the toxic effects of alkaline solutions from
cement  dust (Plate  6-15). Dust  may  reduce fruit set by  preventing  pollen
germination on the stigma. Reduction in the number of leaves and stunting of
alfalfa has also  been reported in heavily contaminated fields.  Cement dust may
also result in beneficial effects, however, through changes in the soil reaction.
With the  existing pollution control equipment though, such effects  need not
occur in the U.S.
   Iron oxide dust from  sintering plants  has caused problems during harvest of
vegetable  crops because  of the abrasive effect of the dust  on harvesting ma-
chinery and on  the surfaces of the plant material.
   Limestone dust may accumulate on  vegetation as cement dust does  (Plate
6-16). However, limestone does not adhere to the foliage as  cement does. The
soil pH may  be changed near sources and  cause lime-induced  chlorosis  on
broad-leaved plants.
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                          Air Quality Standards
   The primary standard for particulate matter is 75 jug/m3, annual geometric
mean; the maximum 24-hour concentration not to be exceeded more than once
a year is 260 //g/m3. The secondary standard is 60 yUg/m3 , the maximum 24-hour
concentration not to be exceeded more than once a year is 150 jug/m3.
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                      SECTION 9.  PESTICIDES
                               Introduction
   Pesticides have revolutionized agriculture in the last half of the 20th century
in much the same fashion as mechanization did in the first half. Without the use
of some of  these chemicals today, the production of food and fiber crops would
fall catastrophically short  of demand.  The public would also have  to endure
many  pests  that are not now  nuisances. It  is difficult even to  conceive  of
agriculture  without the use  of such  chemicals when  even now agricultural
production, on a worldwide basis, cannot meet demand.
   Unfortunately, man, in his haste  to increase  production, has inadvertently
introduced  billions of pounds  of chemicals into the  environment, sometimes
with little or no appreciation of  the long-term consequences. As evidence of
their impact on bird and wildlife populations began to  accumulate, the public
began  to question  the  wisdom of having  maximum  amounts of  food at the
lowest possible price without knowing about the hidden costs.
   The use of pesticides will  not decrease; indeed, it will probably increase. It is
urgent, therefore, that the public be better informed of their value but especially
of their potential hazard to  man in his habitat. Pesticides by themselves are not
pollutants; they become pollutants through misuse.
   There are approximately  900 chemical species presently  being used  as pesti-
cides today, with some 45,000 different formulations. Not all of these chemicals
fall within  the purview of  this  book.  In general,  there  are three  types  of
problems associated with  unwanted effects of pesticides: (1) trace contamina-
tion of environmental systems, (2) food contamination; (3) injury to vegetation.
Only the last of the  three will be discussed here.
   There  are also desirable  side effects  associated  with pesticides usage. For
example, the systemic fungicide benomyl has been shown to be very effective in
protecting certain species of plants from ozone injury. Many  pesticides and other
agricultural  chemicals have been shown  to be effective in protecting plants from
air  pollution. These practices have not been adopted commercially yet mainly
because of the cost factor.

                                  Sources
   The class of pesticide most frequently involved in plant  injury is herbicides.
About 50 different herbicides are in use today. Not all have caused  problems.
Damage to  non-target vegetation has been  most frequent with the phenoxy
herbicides, because of their  high volatility and tendency to drift. For example,
2,4-D  has been known  to drift as far as  15 miles from  the site of application.
Other  factors affecting drift include the type of equipment used and the method
of application, the  form of the material being applied (spray or  dust), and the
microclimatology of the area.
   Potential sources of injurious herbicides, in addition to their normal use (or
misuse), include the manufacture, formulation, and packaging processes. No data
are available on emission  rates. The  greatest source is  the  application process
itself. This latter source is interesting because the application of certain classes of
                                   6-29

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pesticides varies  with geographic location.  Crop  insecticides  are  used most
heavily in the southern U.S., while herbicides are used most heavily in the corn
belt.
   A number  of  minor sources exist but are impossible to assess. Such sources
include  garden and  home use,  burning of pesticide containers, leakage from
storage or discarded containers, and transport from other areas via  windblown
soil particles.

                             Symptomatology
   Since  problems have  been associated  mostly with the  phenoxy herbicides
such as 2,4-D; 2,4,5-T; and 2,4,5-TP; the discussion of symptoms will be limited
to these  chemicals. When non-target crop  plants are affected by drift, the most
common symptom is deformation of leaves, fruits or other marketable portions
of the plant. The leaves develop a "lacy" appearance, and the stem or petiole
may become abnormally flattened (Plate  6-17). Discolorations may  also occur.
Cotton  leaves, for  example, take on a yellow-green,  mottled  appearance  or
stippling  and vein-clearing may  be pronounced. Epinasty is another frequently
observed symptom.
   One other problem is  often encountered with the use of herbicides. Farmers
rotate  crops in  their field in  accordance with accepted practices. However,
sometimes  a  crop will become  injured or  contaminated  with  residues from
previous  crop  treatments  (Plate 6-18). This is most frequently encountered
where S-triazine or dieldrin has been used.

                  Relative Sensitivity of Plants to Pesticides
   No relationship has been established  between plant injury and concentrations
required  to  cause such  injury  in the  ambient air. Laboratory  investigation,
however, has provided information on the relative sensitivity of plants to 2,4-D.
These are shown  in Table 6-9. Since symptom expression is usually  of a growth
response  type, it  is difficult to establish threshold concentrations because of the
many factors that affect  growth. In addition, some of these chemicals promote
growth at very low concentrations.

                            Leaf Tissue Analysis
   There are methods available  for detecting pesticide contamination of food-
stuffs. The  methods have  to  be  developed  by the time the  pesticides are
registered. The methods may be quite complex, however, and expensive instru-
ments and training may be required to perform the analysis.
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                                 Table 6-9
               Relative Sensitivity of Various Plants to 2,4-D
    Sensitive
    Apple
    Birch
    Box elder
    Dogwood
    Elderberry
    Forsythia
    Grape
    Hickory
    Lamb's quarters
    Linden
    London plane tree
    Norway maple
    Black oak
    Sorrell
    Sumac
    Tobacco
    Tomato
    Tree-of-heaven
    Wisteria
    Yellow wood
    Zinnia
Intermediate
Aster
Cedar
Cherry
Choke cherry
Corn
Gladiolus
Hemlock
Mulberry
Pin oak
Red oak
Peach
Potato
Privet
Ragweed
Rhododendron
Rose
Spruce
 (Colorado blue)
Sweetgum
Yew
Tolerant
Ash
Bush bean
Cabbage
Eggplant
Pear
Peony
Rhubarb
Sorghum
Source:
Heck, W.W., Daines, R. H. & Hindawi, I. J. Other phytotoxic pollutants. In: Jacob-
son, ]. S. & Hill, A. C-, eds. Recognition of Air Pollution Injury to Vegetation: A
Pictorial Atlas. Pittsburgh Air Pollution Control Association, F1-F24, 1970.
                                   6-31

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                                 Selected References


Abeles, F. B. Ethylene in Plant Biology. New York: Academic Press, 1973.

Air Quality Criteria for Carbon Monoxide. Washington, D.C.:  Public Health Service, Depart-
   ment of Health, Education, and Welfare, AP-62, 1970.

Air Quality Criteria for Hydrocarbons. Washington, D.C.: Public Health Service, Department
   of Health, Education, and Welfare, AP-64, 1970.

Benedict,  H.  M. & Breen, W. H.  The use  of weeds as a  means of evaluating vegetation
   damage caused by  air pollution. Pasadena, California: Proceedings of the Third National
   Air Pollution Symposium,  177-190, 1955.

Brennan, E. &  Leone, I. A. Response of pine trees to chlorine  in the atmosphere. Forest
   Science, 12:386-390, 1966.

Brennan, E.,  Leone,  I. A. &  Daines, R. H. Chlorine as a  phytotoxic  air pollutant. Inter-
   national Journal of Air and Water Pollution, 9:791-797, 1965.

Buchauer, M. J. Contamination of soil and vegetation near a zinc smelter by zinc, cadmium,
   copper, and  lead. Environmental Science and Technology, 7:131-135,1973.

Heck, W. W., Daines, R. H. &  Hindawi, I. J. Other phytotoxic pollutants. In: Jacobson, J. S.
   & Hill, A. C, eds., Recognition of Air Pollution Injury to Vegetation: A Pictorial Atlas.
   Pittsburgh: Air Pollution Control Association, F1-F24,1970.

Lead - Airborne Lead in Perspective.  Washington,  D.C.:  National Academy of Sciences,
   330,1972.

McCallan, S. E. A.,  et al.  Hydrogen sulfide injury  to plants. Contributions  to Boyce
   Thompson Institute. 8:189, 1936.

Miner, S. Preliminary Air Pollution Survey of Hydrogen Sulfide. Washington, D.C.: Public
   Health Service, Department of Health, Education, and Welfare, 91, 1969.

National Inventory of Sources and Emissions: Mercury — 1968. Research Triangle  Park,
   North Carolina: Office of Air and Water Programs, Environmental Protection Agency.

Thornton,  N. C. &  Setterstrom, C. Toxicity of ammonia, chlorine, hydrogen cyanide,
   hydrogen  sulfide and sulfur dioxide gases: volume III, green plants.  Contributions  to
   Boyce Thompson Institute, 11: 343-356, 1940.

Zimmerman,  P. W.  Impurities  in the air and  their influence on plant life.  Pasadena,
   California: Proceedings of the First National Air  Pollution Symposium,  135-141, 1952.
                                        6-32
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 Plate 6-1. Chlorine Injury to Sassafras Showing Reddish-Brown Interveinal Necrosis
Plate 6-2. Chlorine Injury to Witch Hazel Showing Necrotic Lesions Along Veins and
         a Port/on of the Leaf Margins
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Plate 6-3. Chlorine Injury to Italian Prune Showing Upper Leaf Surface Flecking
      Plate 6-4. Chlorine Injury on Wild Mustard Showing Bleaching Effect
                                   6-34
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      Plate 6-5, Chlorine Injury on Pine Showing Reddish-Brown Disco/oration
Plate 6-6. Chlorine Injury on Larch from Chemical Plant Spill. Note Chlorotic Mottle
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Plate 6-7. Hydrogen Chloride Injury to Norway Maple Showing Marginal Necrosis
      Plate 6-8. Hydrogen Chloride Injury to European Black Alder Showing
               Intervemal Necrosis
                                  6-36
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  Plate 6-9. Hydrogen Chloride Injury to Black Cherry Showing Leaf Spotting
Plate 6-10. Hydrogen Chloride Injury on Norway Spruce Showing Tip Necrosis
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Plate 6-11.  Ethylene Injury on Orchid Showing "Dry Sepal" on Flower at the Left
Plate 6-12. Azalea Fumigated with 2 ppm Ethylene for Seven Days. Note Heavy Leaf
          Drop and Loss of Flowers. Control Plant on the Left
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Plate 6-13  Ammonia Injury on Poison Ivy Showing Blackened Appearance
                Plate 6-14.  Ammonia Injury on Cotton
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    Plate 6-15  Cement Dust Deposit on Fir Branch
Plate 6-16. Lime Dust Deposit on Spruce Twigs on the flight
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  Plate 6-17. 2,4-D Injury to Oak Leaves Showing "Lacy" Appearance of Leaves
Plate 6-18. Atrazine Injury on Soybeans. Grain Sorghum was Sprayed with Atrazine
          During Previous Growing Season
                                   6-41

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                               Chapter 7
             INTERACTIONS BETWEEN  POLLUTANTS
        AND BETWEEN  POLLUTANTS AND  PATHOGENS

   More than one air pollutant may be present in the ambient air at the same
time. Thus, plants are often exposed to a mixture of pollutants. The effect of
these mixtures on plants may be less than, equal to, or greater than the effects of
any single pollutant in the mixture. Plant pathogens  and air pollutants may also
interact to modify the disease response of the  plant.  The interaction between
pollutants will be discussed first.

                       Pollutant-Pollutant Interactions
   Mixtures of  gaseous pollutants  affect growing  plants  by:  causing injury
symptoms on the plants; altering the rate or  the type of growth; or altering the
productivity of a particular plant species or  cultivar. Visible symptoms charac-
teristic  of particular  pollutants may be caused by different  pollutant mixtures.
Thus, symptoms produced on various species or cultivars may be confusing.
   The  first report that one pollutant might affect  the response of plants  to
another pollutant was noted in the early  1950's in California. When researchers
equipped greenhouses with water-spray scrubbers to remove  sulfur dioxide from
the ambient air,  they observed increased ambient oxidant  injury to Pinto bean.
The researchers postulated that either the sulfur  dioxide mitigated the effects of
the oxidants or  the plants were more  sensitive  at the higher humidity. A few
years later, it was found that with an SO2 to  O3  ratio of 6:1, symptoms of both
pollutants appeared.  When the  ratio  was lowered  to 5:1, ozone  symptoms
predominated and no  interference  from SO2 was noted. When  the ratio was
lowered to 4:1,  the ozone appeared to interfere with the expected SO2 injury
symptoms. No evidence of increased injury was reported  with  the pollutant
mixtures.  No interacting effects were found  on  gladiolus when fumigated with
combinations of SO2  and  HF  or SO2  and hydrocarbons. Likewise,  propylene
and acetylene did not interfere with the development of foliar symptoms from
products of  irradiated propylene-NO2  mixtures. It  was  found  in  1966  that
certain cultivars of tobacco were slightly injured when fumigated with 0.24 ppm
of SO2  or 0.03  ppm  of O3  for 2  or 4 hours. However, when the tobacco
cultivars were exposed to a mixture of the  two pollutants, the level of injury
increased  to moderate. These  results suggested some  type  of potentiation
mechanism or synergism between the pollutants and stimulated  new research
efforts.
   The field observer should recognize that  several  pollutants may  be present
either simultaneously,  sequentially, or intermittently. Thus in an urban area,
with a number of SO2  sources, plants may be exposed to  SO2 during the early
morning hours  and to oxidants from  photochemical reactions (and possibly
SO2)  later during the day.  Other pollutants  may affect the response if other
industries are  present in or around the urban  area. Only a few of the  more
obvious pollutant combinations have been studied.
                                  7-1

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Sulfur Dioxide and Ozone
   This pollutant combination has received the greatest attention because of the
increase in general  SO2  emissions from mine-mouth power plants and the ubi-
quitous nature  of oxidants (ozone).  Some believe these pollutants are causing
widespread effects at this time.
   In general, foliar symptoms caused by O3 are easily distinguished from those
caused by  SO2. Mixtures of these two gases at concentrations below the injury
threshold  for  SO2  and  in some cases  below the threshold for  O3  produce
symptoms resembling those caused by O3 (Plate 7-1). Usually SO2  symptoms do
not  appear unless the concentration is well above  the injury threshold for SO2
(Plates 7-2, 7-3 and 7-4).
   Table 7-1 contains selected examples of foliar effects of SO2-O3 fumigations.
In some plant species the effect  is additive (equal to the additive effect of the
single pollutants) while in  others the effect is greater or less than additive.  No
general  trend was found to  indicate how  ratios of the  two  pollutants would
affect foliar response.  Symptoms in  these  fumigations frequently appeared on
both leaf surfaces. The undersurface injury was often a silvering and a collapse of
epidermal  tissue (Plate 7-5) while the upper surface was usually an interveinal
necrotic fleck, stipple, and/or pigment accumulation (Plate 7-6).
                                   Table 7-1
                 Selected Examples of Effects of Sulfur Dioxide
                      and Ozone Mixtures on Foliar Injury
       Plant Species
       Broadleaf
         Alfalfa
         Bean
         Onion
         Soybean
         Spinach
         Tobacco
         Tomato
       Narrowleaf
         Hungarian
          brome grass
       Conifer
         White pine
  S02/0,
Cone., ppm

0.1-0.5/0.1
   1.7/0.19
   1.0/0.1
   1.0/0.1
   1.0/0.1
   0.45/0.03
0.1-0.5/0.1
   1.0/0.1

   0.1/0.1
Exposure Time,
     hrs.

      4
      0.5
      4
      4
      4
     2-4
      4
   8 hr./day
   5 day/wk.
   8 wks.
 Mixture
Response *
        *Mixture responses are: + greater-than-additive
                            0 additive
     „                       - less-than-additive
     Source:
     Reinert, R. A., Heagle, A. S. & Heck, W. W. Plant response to pollutant combina-
     tions. In:  Mudd, J. B., ed., Effects of Air Pollution on Plants: Chapter II. New
     York: Academic Press, 1975.
                                     7-2
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Sulfur Dioxide and Nitrogen Dioxide
   This  pollutant  mixture is of concern because  the two gases  are  emitted
simultaneously  in  the combustion of  fossil  fuels  and the  reduction  of ores.
Exhaust emissions from automobiles add considerably to  NO2  levels in large
urban areas.
   The  symptoms resulting from this  pollutant mixture  are  similar to those
caused  by O3,  especially when concentrations of the combined pollutants  are
near or below the injury threshold  of the individual pollutants. Plate 7-7 shows
the effect of  .10 ppm of SO2 and .10 ppm of NO2  on Bel W-3 tobacco on the
upper surface of the leaf. A reddish pigmentation or a silvering, not necessarily
associated with uppersurface injury,  may  develop on  the  lower  surface  of the
leaf as  shown in  Plate 7-8. Since the symptoms associated with this pollutant
mixture are so  similar to those caused  by ozone, and since ozone injury is so
prevalent, identification  of the  causal pollutant is  difficult. It is possible that
foliar injury in  the field previously reported to be caused by O3 may have been
caused by this pollutant mixture.
   Table  7-2  contains selected  examples  of responses of plants to  SO2/NO2
mixtures.
                                  Table 7-2
               Selected Examples of Effects of Sulfur Dioxide and
                  Nitrogen Dioxide Mixtures on Foliar Injury
        Plant Species
        Broadleaf
         Aspen
         Bean
         Radish
         Soybean
         Tobacco
         Tomato
        Narrowleaf
         Oats
    Cone., ppm

0.5-0.7/0.15-0.21
    1.5/1.5
0.05-0.25/0.05-0.25
0.05-0.25/0.05-0.25
    0.1/0.1
0.05-0.25/0.05-0.25

    2.4/1.3
Exposure Time,
     hrs.

      2
     1.17
      4
      4
      4
      4
 Mixture
Response *
        *Mixture responses are: + greater-than-additive
                            0 additive
                            - less-than-additive
    Source:
    Reinert, R. A., Heagle, A. S. & Heck, W. W. Plant response to pollutant combina-
    tions. In: Mudd, J.  B., ed., Effects  of Air Pollution on Plants: Chapter II. New
    York: Academic Press, 1975.
   In studies of plants grown under  semi-arid conditions such as in the south-
western United States, the response of plants to mixtures of SO2 and NO2 has
been  typical of SO2 injury.  The injury, most commonly leaf necrosis, appears
within a  few days  following exposure  in  the field. On broad-leaved species,
injury develops as interveinal patches of bifacial necrotic  tissue. The color varies
with plant species and may appear as tan, gray, brown, yellowish-brown, or rusty
                                     7-3

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brown. Symptoms on narrow-leaved species develop in patches, streaks, or spots
of white, yellow, or light brown necrotic tissue. On conifer species such as pine
and juniper, the injury symptoms develop as brown or reddish-brown necrosis of
the needle  tips and necrotic spots along the needles and scales. Middle-aged and
older leaves are consistently more  sensitive to injury  than the younger  leaves.
These data suggest that there is no  injury  potentiation (i.e., no synergism) with
this gas mixture  under these growing conditions. Much of the injury is due to
SO2.

Sulfur Dioxide and Hydrogen Fluoride
   Sulfur dioxide and  fluorides may occur together in areas where smelters or
aluminum reduction plants  are located near coal-fired power plants or other SO2
sources.
   The effects of both of these gases occurring singly are well known. However,
fumigations with a mixture of these two gases have resulted in injury to some
plant  species  but not  others. Cultivar differences have  been  reported. For
example, continuous fumigation with a mixture of 0.8 ppm SO2 and 2.3 to 17.1
ppb of HF for 23 days resulted in additive  decrease in linear growth of branches
and reduction in leaf area  but no  visible injury  or leaf abscission on Koethen
sweet orange.  When Satsuma orange was exposed to the same mix for 15 days,
however, the fumigation resulted  in  foliar injury that was less than additive and
no growth effects were observed.
   Selected examples of plants' response to this gas mixture are presented below
in Table 7-3.
Table 7-3
Selected Examples of Effects of Sulfur Dioxide and Hydrogen
Fluoride Mixtures on Foliar Injury
SO^/HF Cone.,
Plant Species
Broadleaf
Bean
Koethen
sweet
orange
Satsuma
orange
Tomato
Narrowleaf
Barley
Corn
ppm /ppb

0.08/0.6

0.8/2.5-13

0.8/2.5-13

0.5/5.0

0.08/0.8
0.08/0.6
Exposure Time

27 days

23 days
(10-day interruption)
15 days
(10-day interruption)
4 hrs., 2 day/wk.

27 days
27 days
Mixture
Response *

not defined

0

—

not defined

+
+
*Mixture responses are: + greater-than-additive

Source:
Reinert, R. A., Heagle
tions. In: Mudd, J. B.
York: Academic Press,
0 additive


- less-than-additive
A. S. & Heck, W. W. Plant response to
, ed., Effects of
1975.
pollutant combina-
Air Pollution on Plants. Chapter II. New


                                    7-4
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   Pollutant-pollutant interactions  are  quite  complex  and  our knowledge of
these interactions at the present time is, at best, fragmentary. However, their
importance  may prove to be far greater than the  effects of single pollutants.
Field detection of these interactions may be very difficult. However, many states
now have comprehensive monitoring programs which could provide the type of
information needed to establish pollutant levels at the air basin level.

                        Pollutant-Pathogen Interactions
   Air pollutants may interact with plant pathogens in  two ways: (1) they may
affect the pathogen  during some stage of its life cycle, (2)  they may alter the
susceptibility  of plants  to a given pathogen.  The effects of these interactions
may be harmful or beneficial to the plant. Relatively little is  known about these
interactions. However, the available  literature  on  this subject has  been sum-
marized recently in a review article by A. S. Heagle (see Selected References).
   In general, a decrease in the incidence of  disease in  the presence of SO2 in
ambient  air has been reported.  Sulfur dioxide, for example, can effectively re-
duce the incidence  of black spot of roses, and can also reduce the  size of the
fungus lesions if it does develop. However, it  has also been reported that needle
cast disease on  scotch pine  can be more severe at  some distance from an SO2
source because the fungus can utilize the sulfur in the air.
   Ozone has been shown to decrease wheat rust and powdery mildew  infections
and  increase the incidence of Botrytis  leaf spot on  potato and geranium leaves.
Fluoride as  HF  can inhibit bean rust, bean halo blight,  and tomato early blight
infections.  Preliminary  work with  cement  and limestone dusts indicates that
these two pollutants can enhance bacterial colonization of leaves.
   There is very  little information  that would  be  helpful  in field  diagnosis.
Selected examples of pollutant-pathogen examples are presented in Table 7-4.
                                  Table 7-4
             Selected Examples of Pollutant-Pathogen Interaction
           Disease affected,
             by pollutant
       SO2
        Stem rust of wheat
        Needle casts on larch,
         pine, juniper
        Tan leaf spot (maplel
        Apple scab
        Powdery mildew (oak, lilac)
        Black spot of rose
        Dwarf mistletoe (conifers)
        Armillana root rot
        Needle cast on spruce
Pollutant Dose

   ambient

   ambient
   ambient
   ambient
   ambient
   ambient
   ambient
   ambient
   ambient
                                    7-5
   Changes in
Disease Incidence
    decrease

    decrease
    decrease
    decrease
    decrease
    decrease
    decrease
    increase
    increase

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                              Table 7-4 (Continued)
              Selected Examples of Pollutant-Pathogen Interaction
            Disease affected,
             by pollutant

        °s
         Wheat stem rust
         Powdery mildew (barley)

         Botrytis leaf spot
         Tobacco mosaic virus
           in tobacco
        HF
         Bean rust
         Bean halo blight
         Tomato early blight
         Tobacco mosaic virus
 Pollutant Dose

0.06 ppm, 6 hrs.
0.25ppm,8-12 hrs.
after innoculation
 ambient
Tobacco exposed to
 0.30 ppm, 6 hrs.

300 ppm in leaf tissue
300 ppm in leaf tissue
300 ppm in leaf tissue
100-300 ppm in leaf
 tissue
   Changes in
Disease Incidence

    decrease
    decrease

    increase
   increase on
   pinto beans

    decrease
    decrease
    decrease
   increase on
   pinto beans
     Source:
     Heagle,  A. S. Interactions between air pollutants and plant parasites. Annual Re-
     view of Phytopathology, 11:365-388, 1973.
                                Selected References

Costonis,  A.  C. Injury  to  eastern white pine by sulfur dioxide and ozone alone and in
   mixtures. European Journal of Forest Pathology, 3:50-55,1973.
Grzywacz, A. & Wazny, J. The  impact of industrial air pollutants on the occurrence of
   several important pathogenic fungi on forest trees in Poland. European Journal of Forest
   Pathology, 3(3):129-141, 1973.
Heagle, A. S. Interactions between air pollutants and plant  parasites. Annual Review of
   Phytopathology, 11:365-388,1973.
Hill, A. C., Hill, S.,  Lamb, C. & Barrett, T. W. Sensitivity of native desert vegetation to SO2
   and SO 3 + N01. Journal of the Air Pollution Control Association, 24:153-157,1974.
MacDowall, F.  D. H.  & Cole,  A. F. W. Threshold  and synergistic damage to tobacco by
   ozone and sulfur  dioxide. Atmospheric Environment, 5:553-559, 1971.
Menser, H. A. & Heggestad, H. E. Ozone and sulfur dioxide synergism: Injury to  tobacco
   plants. Science, 153:424425,1966.
Tingey, D. T., Heck, W. W. & Reinert, R. A. Effect of low  concentrations of ozone  and
   sulfur dioxide on foliage, growth and yield of radish. Journal of the American Society of
   Horticultural Science, 96:369-371,1971.
Tingey, D. T., Reinert,  R.  A., Dunning, 1. A. & Heck, W. W. Vegetation injury from the
   interaction of nitrogen dioxide  and sulfur dioxide. Phytopathology,  61:1506-1511,
   1971.
Tingey, D. T., Reinert,  R.  A., Dunning, J. A. & Heck, W. W. Foliar injury responses of
   eleven  plant species  to ozone/sulfur  dioxide  mixtures. Atmospheric Environment,
   7:201-208,1973.
Reinert, R. A., Heagle, A. S. & Heck, W. W. Plant response to pollutant combinations. In:
   Mudd,  J.  B., ed., Effects of Air Pollution on Plants: Chapter If. New York:  Academic
   Press, 1975.
                                       7-6
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Plate 7-1. Bel W-3 Tobacco Exhibiting Injury from Fumigation with .05pprn O^ and
         . 10 ppm of SO 2. Note the Similarity to Ozone Injury
 Plate 7-2. Injury to Bel W-3 Tobacco Fumigated with .05 ppm of O^ and .50ppm of
          SO-2- In This Case the Injury More Closely Resembles SO2 Injury
                                    7-7

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Plate 7-3. Pinto Bean Fumigated with . 15ppm of O3 and .50 ppm of SO2. Note the
         A/most Complete Absence of Bleaching and the Slight Purplish
         Disco/oration
Plate 7-4. Bleaching of Tomato Leaf as a Result of Fumigation with .05 ppm of O3
         and .25 ppm
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Plate 7-5. Lower Surface of Soybean Leaf Fumigated with . 10 ppm ofO$ and .50 ppm
        of SO2- Note the Difference in Symptoms from Plate 7-6
     Plate 7-6. Soybean Leaf Fumigated with . 10 ppm ofO3 and .50 ppm of SO2
                                   7-9

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  Plate 7-7. Bel W-3 Tobacco Fumigated with . 10 ppm of SO2 and . 10ppm of A/O2
Plate 7-8. Lower Leaf Surface of Pinto Bean Leaf Fumigated with .05 ppm of SO-% and
        .10 ppm of NOi
                                  7-10
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                                 Chapter 8
                       MIMICKIMG  SYMPTOMS

   The preceding chapters may suggest that diagnosis of air pollution injury is a
relatively simple matter, particularly if the sources  of pollution are identified in
a given area. In some situations diagnosis  may be simple and straightforward, in
others it may be very perplexing. Plants are affected by biotic and abiotic agents
(Table 8-1).  One must be aware  that some  of the foliar symptoms associated
with  these  agents  may resemble  or "mimic" air  pollution symptoms. Plant
diseases  are  common  and,  even  though  foliar  injury  may not resemble air
pollution injury, it  may be associated with air pollution by the public. The type
of injury depicted  in Plates 8-1,  8-2, 8-3 and 8-4, for example, do not mimic
pollution symptoms. However, an uninformed public  may attribute this injury
to exhaust fumes because  of the proximity of the trees to automotive travel.
                                  Table 8-1
                List of Agents That Can Induce Plant Diseases*
          I. Abiotic Agents
             Lack of or Excess of'
              water
              temperature
              nutrients
              soil acidity
              de-icing salts
              pesticides
              construction injury and
               cultural practices
              air pollutants
 II.  Biotic Agents
     Fungi
     Viruses and
      rnycoplasmas
     Bacteria
     Nernatodes
     Insects
III.  Teratogenic Agents
     Genetic disorders
     'Response to some of these agents may mimic symptoms of air pollution injury.
   To distinguish between air pollution symptoms and mimicking syptoms, one
must have knowledge of plant diseases and their causes.
   A disease is an interaction between a plant, a pathogen, and the environment
which results in an altered or detrimental condition in that plant. Diseases may
be induced by fungi, nematodes, bacteria, viruses, insects, mineral imbalances, or
various  physical stresses.  The purpose of this chapter is to create an awareness
for the many potential causes of disease. Plant disorders are usually grouped into
three categories: those  caused by abiotic agents,  such as air pollutants, mineral
deficiencies,  etc.; those caused by biotic agents, such as fungi, bacteria, etc., and
those caused by teratogens.
                               Abiotic Agents
Water
   The symptoms of prolonged drought are easily recognized and should be easy
                                    8-1

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to diagnose. Complete and permanent collapse of succulent tissues and dieback,
or even death, of entire plants may  occur. Typical wilt symptoms may be in
evidence. Water will correct the situation if the permanent wilting point has not
been reached.
   The  symptoms associated with  short periods of drought or sudden, severe
droughts followed  by adequate  moisture are less easily  recognized. Marginal
scorch  of  foliage will  occur where  adequate moisture  levels have not been
maintained. An orange coloration will occur on affected tissues of maples. Three
separate types of drought-induced necrosis are: (1) leaf tip necrosis with a sharp
demarcation line between  affected and  healthy tissues; (2) leaf tipburn with a
chlorotic area  separating the necrotic from  the  healthy  tissues; and (3) dull
brown or bronzed interveinal lesions that are irregular in outline.
   These same types of symptoms  may occur after fill has been placed around
trees. The  resulting  changes in water flow patterns can cause local "droughts,"
especially for hydrophyllic species such as willow, rhododendron, and sycamore
(Plate 8-5). Purple  coloration of dogwood in July due  to drought, and insect
boring of the  stem  could  be confused with O3 or SO2-induced color changes.
The normal cast of two- and three-year-old needles from conifers has often been
attributed  erroneously to air pollution injury. Symptoms expressed by nearby
pollutant-sensitive species  should  assist  in eliminating natural senescence as a
factor for consideration. Also, natural senescence occurs only toward the end of
the growing season.
   Excessive amounts of water will  also  lead to  plant injury. Symptoms are
usually  associated with man-made  changes in grade levels around construction
sites  or  adjacent to new highways where streams have been blocked without the
use of drainage culverts.  Symptoms include dwarfing of leaves, general chlorosis
of all foliage,  dieback and death.  Affected plants may die gradually and  the
cause can  be  readily identified by an examination of  drainage  conditions in
the area.

Temperature
   Frost, either in the late spring or early  fall, will injure sensitive plant tissues.
Late spring frosts are the most damaging since the  young foliage is succulent at
that  time  of  year.  Diagnosis is  easy because  the  frozen tissues take on  a
blackish-brown  coloration. Mild freezes or even cool  temperatures may cause
slight tissue collapse and/or  chlorosis  that may resemble air pollution induced
symptoms  such as severe SO^ injury (Plate 8-6). Weather records, and personal
observations can assist  in  identifying  injury caused by  late spring frosts. Pre-
mature  autumn coloration  and leaf drop in several species of plants, initiated by
early fall frosts, are common. Green foliage may actually drop from the tree, and
that which remains may have light-brown or other colored margins.
   Many ornamentals, shade  trees,  and forest  tree species are susceptible to
winter  injury.  The  soil water  becomes  frozen  due  to  extended periods  of
sub-freezing temperatures,  and if the  water remains frozen during subsequent
warm periods, the foliage may lose  water and desiccate. The affected leaves may
remain  green  throughout the  winter  months  or turn yellow  and brown  the
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following spring (Plate  8-2). The  entire leaf may be  killed.  On thick-leaved
species, such as magnolia, only the leaf tips may be affected. Deciduous plants
usually suffer less from winter injury, but  orchard trees and even entire forest
stands have been killed.
   Injury may  occur to many plant  species even  though adequate moisture is
available in the soil during periods of extremely high temperature combined with
windy conditions. This type of injury  rarely  occurs in open  fields, but it is
common  in urban areas where  higher than normal  temperatures occur.  The
injury symptoms are characterized by a  marginal  scorch of leaf tissues, with a
fairly sharp  line developing  between affected and healthy areas. The symptoms
appear on the  periphery of the  crown of  trees. The  symptoms may resemble
those induced by fluorides.
   Heat-induced defoliation may  occur near such activities as street paving with
heat-releasing  processes  and refuse burning (Plate  8-1).  Brief exposures to high
temperatures may result in a temporary mild chlorosis  in young foliage. These
symptoms may disappear as the season progresses.  Periods of cool, wet weather
during the spring that  are  followed  by  sudden  extremely high temperatures
commonly lead to increased amounts of heat injury. Heat injury may also occur
on  plants that have  been growing  in  shaded areas that are  either transplanted
into or suddenly exposed to direct sunlight.

Nutrients
   There is a plethora of information on  the symptoms  associated with the lack
or excess of nutrient supply to plants. The effect of either of  these two extremes
is sometimes difficult to diagnose and may require the use of soil  and/or plant
tissue chemical tests (Plates 8-7 and 8-8).
   Symptoms  of a specific nutrient deficiency may occur on all parts of a plant
or on specific parts, such as  on flowers, fruits, or most commonly on the foliage.
The coloration involved  and the plant part  affected are  often the best means of
determining the element involved. Major lists of nutrient disorders are available.
Some of these symptoms are similar to air pollutant symptoms.

Soil Acidity
   Unfavorable soil pH may result in mineral imbalances in the soil solution and
these  imbalances are  usually manifested m  the foliage  as nutrient  excesses or
deficiencies. For example, the presence  of either  low or high  pH may lead to
either the release of  minerals such as aluminum that become toxic to the plant,
or to  the tying up of others, such  as iron or phosphorus, that  are essential  for
plant  growth.  Soil analyses should be conducted in field-grown  crops  where
injury  is  present  and subsequent  comparisons should  be  made with  known
optimum levels for the specific crop involved.
   In  the eastern U.S., soil  acidity is the most common cause  of yellowing of
foliage in some crops, resulting in stunting of overall plant growth, loss of leaves,
and sometimes death of entire plants or crops. Excessively high pH levels, as
found in the alkaline soils of the west, lead to very similar symptom patterns.
   One example of suspected air  pollution injury that was finally and correctly

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attributed  to  improper soil pH  conditions  occurred near a  major source of
several air pollutants in east-central Virginia during 1970. Nearly half of the
seedlings in a large tree nursery of loblolly pines had severe chlorotic mottle. The
nursery is  located near industrial sources of SO2, F, and NO as well as being
located in  the urban center of the state. Symptoms appeared similar to SO2 and
F injury, but soil pH was found to be less than 4.0. Loblolly pine grows best in
soils of pH 5.6 to 6.0 and a simple liming practice alleviated the symptoms.

De-icing Salts
   Many  thousands of miles of highway in sections of the United  States where
winter is severe are salted during snow  storms to melt ice and  snow. During the
summer months, salts are  used to settle  dust on unpaved roads.  Salts such as
calcium chloride (CaCl^) and  sodium  chloride  (NaCl,  common table  salt) are
used  in  this  practice.  When  these  salts accumulate  in the  soil  adjacent to
highways, plants growing there are injured. Hundreds of roadside maples m New
England alone have been severely injured  or killed by salt (Plate 8-3). Salt injury
symptoms  are somewhat similar to  those induced by F or SO2. These include
marginal  leaf scorch of  broad-leaved foliage and needle tipburn of conifers. The
location of the injured plant in relation to the roadside, and knowledge concern-
ing the use of salt along such highways, assist in proper diagnosis of this cause of
injury.
   Salt spray from de-icing salts will also injure evergreens growing adjacent to
roadsides  (Plate 8-4). An uninformed public may attribute  this injury to auto
exhaust simply because  of the location of the plants.

Pesticides
   Certain  pesticides cause symptoms on various plants that also resemble ozone
injury. For example, the  miticide  Kelthane causes injury on soybeans  that
resembles ozone injury (Plate  8-9).  Other ozone-like symptoms may be caused
by fertilizer excess, nutrient deficiencies,  etc. Some  pesticides, when applied in
excess or under improper temperature  or  moisture conditions, may cause burn
of foliage that may resemble air pollution injury. Knowledge of previous pesti-
cide applications, amounts, and  conditions under  which they  were applied
should assist in  diagnosis. Symptoms such as mterveinal necrosis, leaf spotting,
tipburn,  and death are  all  possible.  Lawn fertilizers that contain herbicides are
often  misused as tree  and  shrub  fertilizers, and consequently the  herbicide
ingredient causes foliate symptoms of chlorosis, leaf scorch, and defoliation.

Construction Injury and Improper Cultural Practices
   The construction  of homes in  wooded  areas injures  many trees  that are
retained as shade trees.  Direct  stem  injury is easily diagnosed but the effects of
root injuries and subsequent infection by root-invading fungi may not appear for
several years.  Symptoms of root injury include  dieback of twigs, small leaves,
marginal leaf scorch, premature leaf coloration and defoliation.
   Improper cultural practices such as poor planting procedures, the planting of
species not adapted to specific locations,  and poor maintenance of overall plant
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vigor may  alone  or in combination with many other factors cause symptoms
similar to air pollutant injuries.

Air Pollutants
   The symptoms induced by a specific air pollutant may not be unique to that
pollutant alone.  Several  pollutants, including SO2, F, and  03,  will cause  a
tipburn on conifers depending upon the  dosage and  species of conifer involved.
SO2, O3, C12, and HF all produce similar symptom patterns on many species of
plants. In fact, a  number  of biotic and abiotic agents can produce symptoms on
conifers  that mimic those produced by HF. Necrosis of the tip of the needle can
result from exposure  to other air pollutants, such as Cl?, SO2 or O3, although
the initial stages  of injury may not be the same  as those induced by HF.  Low
temperatures as well as stresses induced by high temperatures and drought also
may produce tipburn. Chemicals applied to, or migrating into, the soil, such as
de-icing salt, boron herbicides, and excess fertilizers, can induce tipburn. Insects,
such as scale insects, can induce a fluoride-like tipburn  of pine needles. Indeed,
when tipburn occurs it is  so non-specific that for  the correct diagnosis one must
rely on  the elimination  of other causes, examination  of symptoms on other
plants, and chemical diagnosis, as well as the likelihood  of an effect of fluorides
from a known source.

                               Biotic Agents
   Plant  diseases  may be  caused  by fungi, bacteria, viruses, mycoplasmas, and
nematodes.  Some of the symptoms associated with these diseases closely re-
semble those caused by some pollutants. Insect  injuries may also be confused
with  air  pollutant-induced symptoms. Only a brief discussion  of the general
symptomatology associated with each will be presented below. Examples of  each
will be  used to illustrate  the importance of recognizing these causal agents.
Although these organisms are capable of causing symptoms on most plant parts,
the  symptoms expressed on  leaves most  often mimic  those  caused by air
pollutants.

Fungi
   Leaf-infecting  fungi may  cause  early symptoms that mimic air pollutant-
caused symptoms. The initial symptoms expressed by needlecast of conifers, oak
and sycamore  anthracnose, early blight of  tomato, and  several  leaf-spotting
diseases of ornamentals are just a few examples  (Plate 8-10). However, as the
disease development progresses, the cause becomes obvious. Initial symptoms of
these diseases  include chlorotic  spots   on  the leaf surface  which eventually
become necrotic.  Fruiting bodies of the organism erupt from the  necrotic tissues
and become visible to the unaided eye.
   Roots invaded by fungi  such as Phytophthora spp.  on vegetables, orna-
mentals,  or Forties annosus and Armillaria mellea on forest and  shade trees will
cause above-ground symptoms such as chlorotic  and necrotic foliage,  dieback,
and death.  Mild  chlorosis may  occur  from a light  infection by root-invading
fungi such as Paicylomyces on boxwood.

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   Wilt-inducing fungi such as Fusarium  oxysporium  f. lycopersici that cause
wilt  of tomato  may  also  induce  symptoms of air  pollutant injury. However,
much of the fungus-caused diseases are  easily distinguished from air pollution
injury by culturing and identifying the fungus.

Viruses and Mycoplasmas
   A number of plant  diseases caused  by viruses  and mycoplasmas  may  be
attributed  to air pollution injury  by untrained persons. Virus-caused  necrotic
symptoms  include spots, mottling, mosaics, and leaf-cupping. These symptoms
should not be a source of confusion. However, tobacco mosaic virus and  tobacco
etch virus may cause symptoms m tobacco that mimic those of O3.
   One of  the most difficult  problems m distinguishing between air pollutant
and  virus-  or mycoplasma-caused  disorders  is the  general lack of knowledge
concerning the host-range of most viruses and the symptoms they may induce on
various minor crop and weed species.

Bacteria
   Bacterial diseases such as halo blight of beans, wildfire of tobacco, wilt of
cucurbits, and leaf  infections  caused by  bacteria such as Pseudomonas  syringae
have symptom patterns that have been well described. Isolation of the suspected
pathogen would eliminate confusion if any  exists.

Nematodes
   The effects of nematodes  on plants  are  almost  identical  to the symptoms
resulting from fungus infections of the root  system. As with bacteria, isolation
procedures will assist  in eliminating or implicating these organisms as a  cause of
the symptom.

Insects
   Sucking insects such as  mites, thrips,  leafhopping scale, and aphids that feed
on leaf and stem fluids may produce symptoms similar to those produced by air
pollutants such as O3, SO2, and F. The  symptoms persist long after the feeding
activity has  ceased, and the  insect causing the injury may therefore not be
present to  assist in  diagnosis although remnants or frass may be present. General
leaf  mottle and chlorosis,  or  local necrotic spots, are typical symptoms of the
feeding activities of sucking insects (Plate 8-11).  Poor overall plant vigor with
associated dieback and even death may occur following heavy infestation (Plate
8-12).  The  presence  of insect carcasses, eggs, exuviae, frass,  and microscopic
examination of damaged areas will assist in  accurate diagnosis.
   Examples of  such insect injury include  mite injury on tomatoes (Plate 8-13)
and soybeans (Plate 8-14). Thrip injury on grass (Plate 8-11), and lacewing injury
on plants such as azalea and dogwood (Plate 8-15) also resemble ozone injury.
Scale insects  on eastern  white  pine  cause  a  needle-browning  that, from a
distance, resembles emergence tipburn (Plate 8-16). However,  in many of the
above  mentioned cases, signs  of the insects'  presence is noticeable with a hand
lens. Examination of infested  leaf material may reveal the  insect itself or insect
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remains, webbing, eggs, or excrement. Also, insect injury on leaf surfaces tends
to be more restricted than does ozone injury. For example, early red spider mite
injury on beans is often  seen  as small patches of symptoms, perhaps 1/2-inch
across, whereas ozone injury on beans may encompass the entire leaf surface.
Certain insecticides, such as Kelthane,  have also been reported to  cause air-
pollution-like symptoms (Plate 8-9).

                             Teratogenic Agents
Genetic Disorders
   Morphological and  pigmentation types of genetically-induced disorders can
easily  be confused with  chronic  exposure to various air  pollutants.  Recent
studies with scotch pines have identified levels of green (or yellow) coloration to
be associated with cultivars of this  species. Such coloration appears to  be similar
to that caused by chronic exposure  to O3.

                                 Summary
   The air pollution diagnostician  must  use extreme care in separating the real
air pollution-caused injury from that caused and/or aggravated by other possible
causes.  A  hypothetical  example  may be  the best method  to  illustrate and
summarize the important points presented throughout this chapter.
   Assume that a  source  of fairly high concentration of  SO2  exists near a
Christmas tree plantation, a forested area,  and an  agricultural area,  as well as
being situated at the edge  of an urban subdivision with well-established and also
recently  constructed homes. The typical SO2 symptoms that have occurred on
nearby  corn plants may  indeed   have  been  induced by  the  pollutant, and
subsequent damage claims may be  sought from the industry involved.  However,
disorders affecting other plants in the area should not be assumed caused by the
SO^.  There may be needlecast on conifers  and  root injury on the large white
oaks near newly constructed homes, salt injury to roadside trees, drought injury
from compacted soil, etc.
   In  this example, the diagnostician involved in  determining the extent  of
damage caused  by SOj should perform a  comprehensive  survey  of the area
because of the obvious other causes of plant  diseases. Consideration of all factors
involved  and accurate and detailed notes will assist in evaluating that damage
caused by  SC>2 and  that  caused  by other  agents.  Table  8-2 should alert the
diagnostician to possible causes other than air pollutants.
                                  Table 8-2
            Cross-Reference of Symptoms Which May Be Confused
                    for Air Pollution Injury by the Layman

       If Symptoms are Similar
         to Those Caused by:            Check These Other Possible Causes
              Cl                  See S02, 03, and F above. Check extent
                                  of affected area.

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                              Table 8-2 (Continued)

              Cross-Reference of Symptoms Which May Be Confused
                     for Air Pollution Injury by the Layman
       If Symptoms are Similar

         to Those Caused by:

             F
             NH
             PAN

             SO,
  Check These Other Possible Causes

De-icing salts; moisture stress; frost; virus
infection; pesticides with oil carriers; Mn,
Zn, K, N deficiency.

Moisture stress; frost.

Virus infection; insects; frost; pesticides;
Mn excess; N, P, Mg, B, Fe deficiency;
moisture stress; leaf diseases caused by
other organisms.

Herbicides; cold injury

Moisture stress; hjgh temperature; frost; de-
icing salts; N, K, Mn, Mg, Ca deficiency,
pesticides; some leaf diseases.
                                Selected References


Anderson, H. W. Diseases of Fruit Crops. New York: McGraw-Hill, 1956.

Bawden,  F. C. Plant Viruses and Virus Diseases, 3rd ed. Waltharn, Mass.: Chronica Botanica,
   1950.

Boyce, J. S. Forest Pathology, 2nd ed. New York: McGraw-Hill, 1948.

Chapman, H.  D., ed.  Diagnostic Criteria  for Plant and Soils. Berkeley and Los  Angeles:
   University of California Press, 1966.

Dickson,  I. G. Diseases of Field Crops, 2nd ed. New York: McGraw-Hill, 1956.

Dowson,  W. J. Manual of Bacterial Plant Diseases. New York: Macmillan, 1949.

McMutrey, J. E., Jr. Diagnostic Techniques for Soils and Crops. Washington, D.C.: American
   Potash Institute, 1948.

Thompson, L. M. Soils and Soil Fertility. New York: McGraw-Hill, 1953

Treshow, M. Environment and Plant Response. New York: McGraw-Hill, 1970.

Walker, J. C. Diseases of Vegetable Crops. New York: McGraw-Hill, 1952.
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Plate 8-1. Heat Injury to Roadside Trees Caused by
         Street Paving

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Plate 8-2. Winter Injury to Boxwood and Deoc/ora Cedar. Many Different Agents
         Could Cause Similar Damage
                                 8-10
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Plate 8-3. Roadside Maples Affected by De-Icing Salts.
         Position of the Trees and the History of Salt
         Application are Keys to Proper Diagnosis
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Plate 8-4. Roadside Shrubs Affected by Salt Spray from Passing Vehicles Following
         Use of De-Icing Salts
        Plate 8-5. Injury to Oaks Caused by Grade Changes in Landscaping.
                 Bronzing of Foliage and Leaf Drop Preceded Death
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Plate 8-6. Frost Injury to White Oak. Note Similarity of Damage Symptoms to SC>2- or
         F-Induced Injury
  Plate 8-7. Nitrogen Deficient Corn Leaves Showing Symptoms That Could Readily
           Be Confirmed Through a Soi/ or Foliage Test

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Plate 8-8. Manganese Deficient Grape Leaves Showing Symptoms Similar to Those
         Induced by Ozone
   Plate 8-9. Miticide (Kelthane) Injury on Soybean Leaves. Note Similarity to
            A ir Pollution Injury
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Plate 8-10. Needlecast of Scotch Pine. Similar Initial Symptoms Could be Caused by
          SO-i, Os, or F
Plate 8-11 . B/uegrass Injured by Thrips (center/. Normal Leaves /right),
          Leaves //eft)
                                     8-15
                                                                      Injured

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Plate 8-1Z Pine Sawfly Damage to Loblolly Pine Stand. Close Examination Would
         Easily Indicate This Cause Unless the Insect Was Not Present
  Plate 8-13. Mite Injury to Tomato Leaflets Grown in the Field. Note Similarity
            to Ozone Injury
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  Plate 8-14. Soybean Leaves. Left, Oxidant Injury (Probably Ozone}; Center,
            Normal Leaflet; Right, Mite Injury
Plate 8-15. Dogwood with Lacewmg Injury. Note Similarity of Insect Damage to
          Air Pollution Injury

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Plate 8-16. Eastern White Pine with Oyster Scale Insect Injury.
           Note Similarity to Air Pollution Injury
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                                Chapter 9
              METEOROLOGY AND  AIR POLLUTION
                      INJURY TO  VEGETATION
   The  atmosphere  is  the  medium in which  air pollutants  are  emitted  and
transported from the source to the receptor. Although this sounds simple on the
surface,  it  is  perhaps  the  most  complex  and least understood facet  of  air
pollution.  Many  variables influence the character of a given  chemical species
from the time it leaves  the source until it reaches the receptor. A few examples
will suffice to illustrate the complexity of the situation.
   First, consider emission. Pollutants can be emitted from a point source such
as a power plant, a line source such as a highway, or an area source such as a city
or large industrial complex. The emission point may be close to the ground (e.g.,
the tailpipe of a car) or over a thousand feet  in height (e.g.,  high stacks of a
power plant). Thus,  elevation  alone has a tremendous influence on how rapidly
the pollutant  will be dispersed and diluted before it  reaches  a receptor. The
relative  size of the  pollution source  is  an obvious variable. Time of emission is
important  because meteorological conditions vary throughout the day. As will
be seen  in  this chapter,  the atmosphere is more stable at night, and less dilution
occurs  then. During the day,  sunlight  plays an important part in  transforming
the chemical species of pollutants.
   Second, consider  the transport phenomenon. Many attempts have been made
to characterize the vertical and horizontal dispersion of pollution from point and
line sources. Many  mathematical equations and models  have  been developed.
Each has deficiencies because of the  variability of sources,  source  strength,
topography, and other  factors.  From  the receptor standpoint, this is the im-
portant  phase  because,  if the  pollutants   are  not  adequately dispersed  and
diluted,  atmospheric insults will occur.
   There are many  factors to  consider and it  should  be kept in  mind that a
nearby source does not necessarily imply that damage  will  result.
   This  chapter will  attempt to point out the salient points about the relation-
ship  between  meteorology  and  air pollution  and  the  effect of weather  on
pollutant dispersion.

                          Sources of Air Pollution
   The sources of pollution have been well characterized over the past few years,
and much public attention has been  focused on the topic. These sources can be
briefly categorized into four groups: industrial, urban, mobile, and rural.

Industrial Sources
   Industrial operations emit  many different types of  pollutants, depending
upon the type  of industry.  One  area of information that can be  useful in the
                                    9-1

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Urban Sources
   This group  includes commercial incinerators  and small furnaces used for
domestic heating purposes. Individually, these sources emit far smaller amounts
of pollutants than industrial sources, but because  of the large number in a given
urban  area,  the sum total of their emissions has become a significant source of
air pollutants.

Mobile Sources
   Mobile sources, of course, include the automobile. This category is responsi-
ble for several pollutants: carbon monoxide, hydrocarbons, and nitrogen oxides.
Nitrogen oxides and hydrocarbons are  the most important of these, since they
are involved in the formation of ozone and peroxyacetyl nitrate, both of which
are major  causes of plant injury.  This source is easy  to  identify, but it  is
impossible to pinpoint a specific polluter responsible for damage because of the
large number of vehicles contributing pollutants to the atmosphere.

Rural Sources
   This group includes pollutants from field spraying of chemicals, agricultural
burning, forest  fires, etc.  Most  of these are isolated sources that tend to be
seasonal.
                   Meteorological Aspects of Air Pollution
   Given the emission of a pollutant from one of the above-named sources, the
next  step in the  chain  of events  leading to pollution injury is transport and
dispersion of the pollutant from the source to the receptor. The major meteoro-
logical factors influencing transport and dispersion of air pollution are: (1) wind
speed and direction, and  (2) atmospheric stability and the temperature.

Wind Speed and Direction
   This is easily understood,  since it  determines the  predominant direction  in
which the pollutants  will move  and the speed at which they will be transported
and  diluted  downwind.  Both speed and direction are concerned  mostly with
horizontal  movement of the air containing the pollutants. When referring  to
wind direction, the direction from which the wind is blowing is the name given
to that wind. Hence,  a northwest wind is one blowing from the northwest to the
                                    9-2
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pinpointing of an industrial  source is the emission inventory developed by the
local  air pollution control agency. These  inventories can be helpful in deter-       |H
mining  which industries in a given area are likely to be emitting a suspected       |j
pollutant. However, in many  industrialized areas, several industries may emit the
same  type  of pollutant. This  can make pinpointing a specific source impossible.
Nevertheless, emission inventories can still  serve as a valuable tool in identifying
the pollutant (or the absence of a pollutant) and probable industrial source(s) of
air pollutants.
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southeast.  The speed of the wind can often influence  the  toxicity of certain
pollutants  by  determining the amount of  time the pollutants  spend in the
atmosphere undergoing chemical changes. Such  changes can cause some pollu-
tants to  become more  toxic and  others to become less toxic. In addition, the
speed of the wind is one factor that determines the volume of air that passes by
the source. The higher the wind speed, the greater the dilution of the effluent,
other factors remaining constant. Thus, the dilution of a pollutant,  once it is
emitted into the atmosphere, is directly proportional to the wind speed. Data on
wind direction and speed can  be used to eliminate possible sources that are
downwind  of the damage  site  at  the  time of the pollution episode or are too
distant either upwind or downwind to be considered probable sources, given the
wind speed at  the  time. Thus,  appropriate sources upwind of an affected area
can be studied more thoroughly to assess their impact.

Atmospheric Stability and Temperature
   The stability of  the atmosphere, as an index of turbulence, can be related to
the vertical mixing  of pollutants. A good deal of the atmospheric turbulence is
associated with thermal  turbulence, in which mixing is enhanced due to tempera-
ture variations between  different altitudes.
   Lapse Rates. On a clear day, when the sun  is shining, the sun warms the
surface of the earth very effectively. This heat is then transferred by  conduction
and radiation to the atmosphere near the ground, increasing the air temperature
as a  result.  This warmer, less dense air then rises and the cooler, denser  air of the
upper atmosphere  descends. Any  pollutants  emitted into the air under  these
conditions  are  caught  in  this  vertical  mixing  and dispersed rather rapidly.
Unfortunately,  these conditions do not always exist.
   Under normal, dry conditions the temperature of the air decreases at the rate
of approximately  1°C per 100  meters (5.4 F per 1,000 feet) of  altitude. This
decrease  in temperature with increasing altitude is  termed  "the  dry  adiabatic
lapse rate." The  dry  adiabatic lapse rate is compared with the "environmental
lapse rate"  (current or actual  temperature  change with altitude) to yield an
index of stability.  Air  is  said  to  be  stable whenever the vertical  decrease in
temperature  —  the  environmental lapse rate — is less than 1 C per 100  m, and
unstable  when  the environmental lapse rate exceeds 1°C per 100 m. As shown in
Figure 9-1,  it follows that an unstable condition, the environmental lapse rate
with the least  slope, represented by the line to the  right of the adiabatic  lapse
rate  line, increases  vertical mixing, and pollutants emitted under this condition
are dispersed relatively quickly. Conversely,  pollutants  emitted  into a stable
atmosphere, represented by the line to the left of the adiabatic lapse  rate line,
are not dispersed as quickly, due to decreased vertical mixing.
   One additional condition exists when the  temperature increases rather than
decreases with  altitude  (Figure 9-2). When the temperature of the air  at higher
altitudes  is  warmer  than that near ground level, a  "temperature inversion" is said
to occur. An inversion  condition  tends  to restrict vertical mixing, keeping the
pollutants trapped in  the inversion layer since cooler, denser air is now below a
warm, less dense layer of air.
                                    9-3

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               Stable Conditions
               Reduced Vertical
               Mixing
Unstable
Conditions
Increased
Vertical
Mixing
      Figure 9-1.  Temperature Variations with Altitude
                                                                 Inversion

                                                                 Layer
                                                                 (0 - 250 ft )
                                                                 (0  762 meters)
Figure 9-2.  Temperature  Variation with Altitude Illustrating
            a  Temperature  Inversion  Based  at  the Earth's
            Surface
                               9-4
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   Figure 9-3 illustrates a set of conditions in which the altitude of an inversion
plays an important role in  the concentration of air pollutants. In the example
given, there are two inversion layers present: one from ground level to approxi-
mately  250 feet (called  a surface-based inversion) and one from about 900 to
1,000  feet  (called an inversion aloft). Figure 9-4  illustrates  the conditions in
Figure 9-3 so that  the effects of these conditions on the dispersion of pollutants
can be  determined more easily. As can be seen, the emissions from the homes
and small industry on the right are being trapped and concentrated beneath the
surface-based  inversion, since vertical mixing  is restricted. The taller industrial
stacks, however, are emitting their pollutants above the  surface-based inversion
and, as  a result, the pollutants may be fairly well mixed, depending on the wind
speed in the layer  from 250 to 900 feet. Remember,  however, that the amount
of pollutants emitted from tall stacks remains the same and that adverse effects
may be  noted at greater  distances downwind.
                                                    h300
         500 -
                                                              Inversion Layer
                                                              900-1000 feet
                                                              274.3 - 304.8 meters
                                                              Unstable Lapse Rate
                                                              250 - 900 feet
                                                              76 2 - 274 3 meters
                                                         aversion Layer
                                                         0 - 250 feet
                                                         0 - 76 2 meters
                             Temperature
            Figure 9-3. Temperature Profile Illustrating Two Inversion Layers
                                     9-5

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   1000 feet   67°F
304.8 meters   194°C
     900 feet  64°F
274.3 meters   17 8°C
Inversion
Aloft
     250 feet  68° F
              »+
76 2 meters    20.0°C
            Figure 9-4. Conditions of Figure 9-3 in a Different Perspective
   Diurnal Temperature Variations.  Another factor that has an  effect on vege-
tation injury  due  to  air pollution  is the diurnal (daily) cycle of temperature
variation through the atmosphere. A typical daily cycle of temperature gradients
over open country  on a cloudless day begins a few hours after sunrise with the
formation of  an unstable lapse rate at the ground; The warm  layer increases in
height during daytime  due  to strong  solar heating  of the ground. This is
associated with a high degree of vertical mixing.
   Shortly before  sunset, the  air near the ground begins to cool rapidly and a
stable lapse  rate begins to develop.  During the  early evening an inversion forms,
reaching maximum intensity  and height near  the time of minimum surface
temperature.  During this period, pollutants are  trapped within the inversion
layer and accumulate  as a result of decreased vertical mixing coupled with low
wind speeds. At this point pollutants emitted at the surface are  not carried aloft,
while pollutants emitted aloft, for example, by tall chimneys,  are not generally
transported  to the ground.
   With the coming of daylight, the ground begins to warm and  the inversion is
destroyed. This may result in "fumigations;" that is, the rapid downward mixing
of pollutants  that  were  released aloft during the night. This wilt often lead to
high pollutant concentrations during the early forenoon before normal, vigorous
daytime  vertical mixing  is resumed. The high concentration of pollutants at
                                     9-6
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ground level during the forenoon may coincide with the opening of the stomata
of plants. As  a result,  this period  becomes a prime time in which  vegetation
injury may occur.

Diagnostic Confusion Caused by Meteorological Conditions
   Temperature, humidity, and precipitation are  meteorological conditions that
can sometimes confuse  diagnosis of injury. Extremes in  temperature  or precipi-
tation can produce visible symptoms similar to and often indistinguishable from
air pollution injury. On the basis of information on these variables, they may be
either included as  possible  causes of the observed symptoms or excluded if the
conditions were near normal at the time.
                    Effects of Topography on Dispersion
   Finally, another factor — the local topography of an area — can interact with
meteorological variables to affect  the  dispersion of pollutants.  Valleys  can
become pockets from  which pollutants  cannot escape,  especially under stable
conditions. The pollutants  can be channeled along the valley, perhaps affecting
areas  many miles  removed  from the source, or  they may simply stagnate in a
sheltered area for a prolonged period of time. Mountains can act as a barrier over
which pollutant-laden  air  cannot flow,  thereby resulting in a  buildup of the
pollutants. An  example of this  is the Los Angeles area,  where the  nearby
mountains form a barrier, and frequent temperature inversions above the surface
allow  "smog" to  accumulate.  On  a much smaller  scale, a row of  trees or
buildings can act as either a barrier or a  channel  for air pollution. Clearly, local
terrain  must  be taken into account  when attempting  to map the  route of
pollutants back to their source.
   Meteorological data for  a given period of time can be obtained from the U.S.
National Weather  Service  Offices. Records  of local  observations may  also be
available from local airports, yacht clubs, agricultural stations, universities,  and
individuals or companies. All available information, including a description of
the local topography, should be examined in order to increase the accuracy of
tracing a suspected pollutant to its likely source.
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                                Chapter 10

                  DIAGNOSIS OF SUSPECTED  AIR
              POLLUTION  INJURY TO  VEGETATION

   Diagnosis of the  nature  and  causes  of suspected  air pollution injury  to
vegetation is usually a complicated process. The factors governing plant growth
are complex and interrelated, and an observer must evaluate as many of them as
possible  when  making a diagnosis.  He must consider all the symptoms that are
present,  separate relevant from irrelevant data, and determine the role of each
possible  causal factor. The observer should understand the basic procedures of
diagnosis, know what background information to seek, and understand how to
interpret information.

                        Diagnosis - Basic Procedure
   The following logical sequence of seven questions forms the basis  of the
diagnosis of suspected air pollution injury to vegetation:
      1.  Is there a pollution source nearby capable of causing injury?
      2.  What are the characteristics of the terrain or location?
      3.  What are the symptoms of injury and what part of the plant is affected?
      4.  What is the distribution of affected plants?
      5.  Are biological agents present?
      6.  Is more than one species of plant affected?
      7.  What is the crop history of the affected area?

1.  Is There a Pollution Source Nearby Capable of Causing Injury?
   The obvious question to ask when air pollution is suspect is whether or not a
source is within range of the affected vegetation. Nothing is served by insisting
that the  observed symptoms were  caused  by a given pollutant if it can be
determined  that no nearby source exists. On the other hand,  one  must keep in
mind that long  distance transport of certain  pollutants is possible. Chapter  3
discusses transport of oxidant from the Los Angeles basin  to the San Bernardino
mountains some 50 miles distant. Dispersion equations for point,  area, and line
sources of pollution  are available to determine ground concentrations at various
distances from the source.

2.  What Are the Characteristics of the Terrain or Location?
   Terrain characteristics of both  the affected area and the area around the
source, and  the location of affected plants in relation to terrain are important
factors to  consider  when  diagnosing suspected air pollution injury. Terrain
influences the dispersion of an air pollutant and, consequently, the geographic
distribution  of affected plants.
   The local terrain may prevent  dispersion of the air pollution if a point source
of air pollution is located in a steep, narrow valley, and vegetation damage will
be  concentrated on  the floor and sides of the valley. Air pollutants are also
trapped by  large terrain features,  such  as  the horseshoe-shaped Los Angeles
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basin, which prevents the dispersion of air pollutants over a wide area.
   The location of plants in relation to local terrain features is another impor-
tant factor to consider in diagnosis.  For example, plants located in a low area in
a field may receive  excessive water during wet periods. The excess water may
drown the roots, leach  out nutrients, or create  conditions that favor disease
development. The low area may be a frost pocket in the spring or early fall.
   Soil conditions also vary within  a local area and must be  considered when
diagnosing plant ailments. The type  of soil may be quite  different in a  low area
compared  with a nearby high  spot.  Soil or plant tissue analyses for mineral
deficiencies are a useful aid to correct diagnosis.
   Location is important in other types of injury  that may be confused with air
pollution  injury.  Plants growing in exposed locations, such as at the corner of a
house or on an open golf course, may exhibit severe winter injury while nearby
protected plants remain uninjured.

3.  What Are the Symptoms of Injury and What Part of the Plant is Affected?
   A  symptom  is a  visible  change  in a plant  caused by some  physiological
abnormality or stress. Although symptoms may appear on any portion of the
plant, those associated with  air pollution injury usually appear on the foliage.
   One of the first steps in  diagnosing suspected air pollution injury to  plants is
to closely examine the foliage. The color of the injured tissue, pattern of injury
on the leaf, which leaf surface is affected, state of maturity of the leaf, and other
such conditions should  be  noted. Foliage that has fallen to  the ground should
also  be examined.  Both detailed  field  notes  describing the symptoms and
photographs are extremely useful, especially if samples are collected to be keyed
out later.  For  comparison  purposes, healthy  foliage from  plants growing in
adjacent areas should be examined.
   Acute symptoms  may appear within 24 hours after an air pollution  episode.
Few other factors  of the  environment cause such rapid  injury and symptom
development. Consequently, many factors can be eliminated as possible causal
agents based solely on this time factor.
   The length of time that  passes between symptom development and  observa-
tion is also important. Leaves with classic air pollution symptoms may fall or
wither on  the  plant over  a period  of  several  weeks, precluding an  accurate
diagnosis.  Also, new growth may hide remaining symptomatic  leaves, especially
on  larger  plants  such as trees.  Decay  fungi and  insects  may  cause additional
damage to injured leaves, thus distorting or obliterating symptoms of air pollu-
tion damage. Therefore,  it should be remembered that the final symptom on a
plant  leaf is the  end result of a series  of complex ecological and physiological
relationships. The longer the time period that occurs between symptom  develop-
ment  and  observation, the more complex  the  diagnosis becomes.  Whenever
possible,  symptoms  should be  evaluated as soon as they are  manifested and
followed through their development if possible.
   Although  the  specific symptom  evaluation  is very important, it  must be
considered in context with many other factors  of the  evaluation to get the
proper perspective of the overall problem. Symptom description must  be com-
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bined with a knowledge of tissues and organs affected, species of plants involved,
time of symptom appearance, and geographic distribution of the problem.
   When air pollution injury is suspected, it should be determined if the entire
plant is  affected or  if only certain stems  or  branches show symptoms.  Air
pollution will often injure a plant rather uniformly, although certain aged leaves
or tissues may be more severely injured than others. If only  one stem or branch
of a plant shows injury, the base of the injured portion should be examined for a
canker, break, or other injury that could cause the entire stem or limb to die
from that point outward. However, it must be remembered  that problems such
as root or basal stem cankers, soil nutrient deficiencies, or water imbalances will
often also affect the aboveground portion  of a plant rather uniformly.
   The approximate  age of affected leaves may be of importance. For example,
whereas  few air pollutants injure the extremely young, immature leaves, recently
matured  leaves may be very sensitive to  air pollution injury. Therefore, severe
injury  on young  foliage just emerging in  the spring may be  more likely due to
frost, herbicides, or something other than  air pollution.
   Sunscald,  winter injury,  or  wind injury  might be suspected if the  injury is
predominantly on one side of a plant. Only  a very local, and probably readily
identifiable, point source  of air pollution would cause such injury on the side of
the plant facing the source.


4.  What is the Distribution of Affected Plants?
   The distribution of affected plants, together with the symptomatology, will
often yield a correct  diagnosis  when dealing with suspected  air pollution injury
around a point source. Damage is usually most severe downwind from the source
and becomes less severe with increasing distance from the source. Less injury is
observed upwind or  at  crosswind locations  with respect  to the source.  The
pattern or distribution of affected  plants will vary  according to terrain, mete-
orology,  and specific source features such  as stack height.
   In the case of a general, widespread source of air pollution, such as a large
urban  area, distribution of affected  plants will be widespread in and adjacent to
the urban area. Pollutants may drift away from urban areas  and cause injury to
vegetation growing in rural areas miles away. As with a point source, damage is
normally most severe  downwind from the  urban area.
   There are  often both tolerant and sensitive individuals within a population of
plant species. A  plant injured  by air pollution  may  be growing  next to  an
uninjured plant of the same species. This confusing situation is more often  the
rule  than not and should be remembered when determining the distribution of
affected  plants.
   If symptomatic plants  are located in a very small area and no local source of
air  pollution  is nearby,  problems directly  associated  with  the  affected  area
should be investigated. For example,  if the area is  in a housing development,
yard care practices involving the use of pesticides, herbicides, fertilizers, or other
chemicals should  be  examined. If the area is rural, natural features such as high
water tables, poor soil, or frost pockets should be considered as possible causes
                                   10-3

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of injury. In addition, if the area is farmed, overfertilization, herbicide spills, or
other accidents must also be investigated.

5.  Ate Biological Agents Present?
   Many biological agents cause symptoms on leaves that mimic those caused by
air pollution. At times, these agents are easily recognized and diagnosis is fairly
simple. The  causal organism or its  remains may be present on  the leaf.  For
example,  mite  injury  on broad-leaved plants closely resembles ozone injury.
However, close  examination of affected tissue with a hand lens may reveal the
mites, their  webs, or  the  skeletons of dead  pests. Also, the specific  tissue
attacked by  mites or insects may  be quite different from  that injured by air
pollution.
   If a fungus is involved, diagnosis may be more complex. Fungi  exist  in or on
the leaf as microscopic, thread-like filaments. Occasionally, fungal fruiting struc-
tures  are visible as small, dark  bumps on  the leaf surface, but the mere presence
of fungi on an  injured plant does not prove  that the injury is fungi-induced.
Many fungi normally inhabit leaves, often sporulating on dead leaf tissue killed
by various other agents. Isolation and correct identification of fungi, viruses, or
bacteria  as causal agents  of  leaf injury  are best performed by  experienced
persons.

6.  Is More Than One Species of Plant Affected?
   Insects, fungi,  and other biotic agents are often quite selective and attack
only certain  plant species.  In  contrast, air pollutants often injure  a wide spec-
trum  of plants,  especially in the case of a severe fumigation. Thus, determining
how  many plant species exhibit injury  can  help  an observer distinguish air
pollution injury from other kinds of injury.
   Grasses, herbs, deciduous trees, and conifers may all show air pollution injury
to various  degrees. Highly sensitive plants  will be most severely injured, while
more  tolerant plants will show  few, if any, symptoms. Symptoms may appear on
only  the  most  sensitive species if  the air  pollution  episode  is not severe. A
combined  knowledge  of the  classic symptom pattern  and  the sensitivity of
various plant species is most helpful in diagnosis. It is important to examine the
highly sensitive "indicator plants" for presence of symptoms, but it is equally
important  to examine species  known to be tolerant to the suspected air  pollu-
tant to confirm the lack of symptoms.
   Other agents of the environment in addition to  air pollution  injure a wide
spectrum of plant species.  Frost, drought, flooding, and other natural  environ-
mental extremes  are  examples. Man-made factors  such as  herbicides, excess
fertilizer, and  improperly-used pesticides may also damage  numerous species.
However, the symptoms and other considerations of the overall syndrome often
aid in separating air pollution injury from other kinds of injury.

7.  What is the Crop History of the Affected Area?
   The symptoms observed  when  making  a diagnosis may actually  have been
caused or  influenced several weeks earlier.  Thus, the crop history prior to  and
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following a suspected  air pollution episode must be carefully considered when
making a  diagnosis.  For example,  if the  injury is  observed on  farm crops,
management practices  such as crop rotation should be investigated.  Information
should be gathered on the type and treatment of crops grown in the soil prior to
the present problem.  Certain crop plants do not grow well following  certain
other crops in the same soil. Continual  cropping of the same species  may also
cause various problems.
   Most farmers keep  good records on crop rotation, amount of fertilizer and
other agricultural chemicals applied, etc., and some keep records on yield. Many
farms have farm plans  prepared by the Soil Conservation Service to prevent soil
erosion,  and  a  fairly  rigid  crop rotation will be  followed on those farms.
However, there are farmers that  keep very few or no records. Also, one must
expect that answers to questions about  over-application of pesticides may not
always be candid.
   The amount and type of fertilizers, pesticides, and herbicides used m the past
should be determined. Certain combinations of these chemicals are incompatible
and may  cause severe  plant  damage resembling air pollution injury. Exceeding
recommended dosages  likewise may cause severe injury. Some chemicals remain
in the soil and build up for years to toxic  levels.
   Pesticides applied to nearby farmlands or to adjacent yards should be investi-
gated as well. Certain herbicides can drift for long distances and cause  injury to
sensitive plants. For example, application of weed killer in a yard, or brush killer
in a right-of-way, may  injure sensitive plants growing as far as half a mile away.

                      Diagnosis — Systematic Approach
   These seven questions are the basic elements of a  proper diagnostic method
for suspected air pollution injury  to vegetation. Not only must these questions
be answered, but  also they must be approached in a systematic fashion. Once  an
observer  trains himself  to  deal  with these questions  in  an orderly fashion,
diagnosis  will become a second-nature  routine that will  come automatically
when confronting a field problem.
   One of the obstacles impeding the accurate  diagnosis of air pollution injury
has been  the failure of  many investigators to utilize a systematic method  of
gathering and analyzing the  information  about an episode. Sometimes investiga-
tors rely too heavily on their past experiences to determine the likely causal
factor. As a result, they have often reached their conclusion  before considering
all the  pertinent  information  available  to them. In other  words, they have
sometimes allowed their individual biases to lead them to an erroneous  diagnosis
of the problem. The remainder of this chapter describes a systematic step-by-
step method of obtaining and handling the pertinent  information in such a way
as to increase the probability of reaching a correct diagnosis of the cause of plant
injury.

Hypothetical Example
   For the purpose of  introducing a systematic  method of gathering and analyz-
ing information concerning  plant injury, a simple, hypothetical example of  an
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incident that appears  to  be air pollution-related is  presented below.  It will
demonstrate that meteorological data,  information from emission inventories,
and information on the relative sensitivities of different plants to different  air
pollutants  are often sufficient  to  determine the likely causal pollutant, if any,
and its probable source.

   Diagnosis of actual  instances of suspected air pollution injury to vegetation is
normally more  complex than this example suggests for two reasons. First, actual
sensitivity ratings  are  not as exact  as  they appear  on the chart, because  re-
searchers have differing opinions about sensitivity and  because different cultivars
of plants listed  often differ in sensitivity to  a pollutant. Second, the  sources in
the example  can also  be  emitting  pollutants other  than the  ones listed. For
example, the  city and  the smelter could both be adding SO-i in addition to  the
pollutants listed. The  field diagnosis of plant injury  thus relies heavily on  the
discrimination of the visible symptoms of injury. However, the combination of
an accurate discrimination of symptoms with a logical approach of assessing  the
meteorological data and source information  will often lead to an  accurate diag-
nosis of the problem.
           Figure 10-1. Topographical Features of the Hypothetical Example
                                     10-6
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   Consider the following example of injury  to  some  vegetation in the area
depicted in Figure 10-1. The  following information is  needed to deduce  the
causal pollutant, if any, and its probable source.
      1. Symptoms observed:
        a. Farm A — Wheat injured
                     Cucumber not injured
        b. Farm B - Oats injured
                     Onion not injured
        c. Farm C — Eastern white pine trees injured
                     Corn not injured
                     Chrysanthemum not injured
        d. Farm D — Alfalfa injured
      2. Meteorological conditions in the city at probable time of plant injury:
        a. Wind from northwest at 2 to 5 mph
        b. Inversion layer base at 500 feet
        c. Sun shining
      3. Possible sources:
        a. Smelter — possible source of fluoride (F)
        b. Generating plant — possible source of sulfur dioxide (SO2 )
        c. Steel mill — possible source of sulfur dioxide (802)
        d. City — possible source of ozone (03), PAN, carbon monoxide (CO)
      4. Topography — Mountain range with farms, factories, and city near river
        in valley to west. See Figure 10-1.
   Given the above information, what pollutant,  if any, probably caused  the
injury,  and what is  the likely source of  the pollutant? The  following is a
step-by-step solution of the problem.
      (1)  Sensitivity charts reveal:
                                     	Pollutants*	
                                     f         SOj         Oa        PAN
           Wheat                    T          S          S          I
           Cucumber                 T          T          T          T
           Oats                      I          S          S          S
           Onion                     +          T          S          T
           Eastern White Pine         S          S          S          +
           Corn                     S          T          S          T
           Chrysanthemum           T          T          S          T
           Alfalfa                    T          S          S          IS**
                 S  =  sensitive
                 I  =  intermediate
                T  =  tolerant
                +  =  not rated in literature
                Note: these are hypothetical ratings
                  *CO not known  to exist in high enough concentrations in
                   ambient air to cause injury.
                 **Different cultivars may vary in  their sensitivity to specific
                   pollutants.
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        This chart reveals the possible pollutants based  on observed injury to
        the plants:
        a. Wheat was injured and is sensitive to  SO2 and  O3. (This tends to
           eliminate F and PAN.)
        b. Cucumber  was not injured and is tolerant to SO2, F, O3, and PAN.
           (Thus, SO2 and  O3 remain suspect, while F or PAN injury becomes
           more unlikely.)
        c. Oats were injured  and are rated sensitive to SO2, O3, and PAN and
           tolerant to F. (No  change in suspicion.)
        d. Onion was  not injured and is sensitive  to O3 and tolerant to SO2 and
           PAN. (Now only  SO2 remains suspect. If O3 were the cause, the
           onion probably would have exhibited symptoms.)
        Continuing down the list of injured plants further supports the con-
        clusion that SO2 was  the likely causal pollutant.
     (2) A survey of possible sources reveals:
        a. Smelter — eliminated (not a source of  SO2)
        b. Generating plant — possible
        c. Steel mill — possible
        d. City — eliminated (not a source of SO2)
     (3) The meteorological and topographical factors reveal:
        a. A  buildup of  pollutants caused by  the  low inversion  layer and
           mountains  to the east, which prevent dispersion.
        b. A low wind speed from the northwest, further restricting dispersion
           and eliminating the steel mill as a possible source.
     (4) Final conclusion:
        a. Probable causal pollutant — SO2
        b. Probable source of pollutant — generating plant

                             Diagnostic Routine
   In order to  structure  a  logical approach  to  the analysis of  the pertinent
information about suspected air pollution injury,  the remainder of this chapter
presents a step-by-step routine to assist in the diagnosis of the cause of plant
injury. The routine utilizes a branching procedure that leads through a series of
steps to  a final  conclusion for a particular set  of circumstances. Before pre-
senting the routine, however, it is advantageous to describe the characteristics of
the branching procedure.
   Each step of the procedure contains a description of what  to look for, or
some other discussion, and  is usually  followed   by  a question  that must  be
answered  in order to  be directed to  the next step. This  question will almost
always list all the alternatives from which to select the appropriate answer. After
selecting  the answer, the next step in the procedure is indicated. This listing of
questions, alternative  answers, and branching procedures, may  tend to appear
too long  and complex to be  of  use, but this is definitely not the case. Figure
10-2  depicts part  of  a  hypothetical  branching   procedure  with one  possible
pathway  through all the steps shaded. This represents the one (and only) correct
path that  leads to the conclusion to one particular problem.
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                       JML   Ml
                       Dnnn
         Figure 10-2. The One Pathway Followed to Solve a Particular Problem

   Only  a  very small portion of  the  entire procedure is used for the example
problem illustrated in  Figure 10-2. By following this  step-by-step branching
procedure  the unused steps would not even be encountered. In following this
path, only five of the procedure's 31  steps to reach a final conclusion are used.
The next time the  procedure is used,  the problem situation will in all likelihood
be  different,  with  a different set  of circumstances, and as a result, a different
pathway will be used.  For this  reason the procedure must  include all possi-
bilities, another factor that adds to the bulk of a branching procedure, but this
increased bulk is far outweighed by the advantage that all possibilities, no matter
how remotely possible, are always taken into consideration.
   The diagnostic routine of this  chapter makes use of a branching technique;
however, for  any  given  situation  only a portion of the entire routine will be
used. The routine contains  100 steps of which  the shortest pathway consists of
only six  steps and the longest 25. The average number of steps required to reach
a final conclusion is 17, and most of those require only very simple yes or no
decisions.
   The diagnostic routine is designed  to do one of two things: (1) lead to a
conclusion that the observed injury was in all likelihood caused by air pollution,
in which case the routine will often indicate the causal pollutant  and its source;
or (2) eliminate air pollution as the cause of the  injury either because of a lack
of conclusive  information or because of a determination  that another factor is a
more likely cause.
   In utilizing the diagnostic routine, several things must be kept  in mind. First,
the scientific study of the effects of air pollution on vegetation is still a young
field and more  research is needed to resolve many unanswered questions. As a
result, gaps in information exist and in some cases must be filled with "educated
guesses." Second, plants are living things with individual differences, and  they
sometimes  react differently to identical stimuli. This entire diagnostic routine is
built on  generalities which may fail when confronted with individual variations.
Third, the  successful completion  of the entire routine depends heavily  on the
successful completion of each individual step. There is nothing to be gained by
eliminating steps or hurriedly finishing the  intermediate steps. Therefore, care
must  be  taken  to  complete each step in the  proper  sequence and  follow all
directions contained within a step.
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1. Observe symptoms on injured plants.
                                               GO TO STEP 2
2. Construct a sensitivity  chart containing both  the affected  and unaffected
   species. This will help  in recalling the symptoms on the different species.
   Use the following format:

Injured Species
1.
2.
3.

Unaffected Species
1.
2.
3.

Pollutant
03









PAN

SO2

F

Enter in these boxes
the relative
sensitivity


rankings found
in Appendix C.



















                                               GO TO STEP 3

3. The  observed injury  can be  attributed  to one of the following causal
   categories.
     a. Insects
     b. Nutrient Deficiency
     c. Environmental Stress
     d. Biotic Disease
     e. Air Pollution
   The following steps in this diagnostic routine will  attempt to resolve the
   confusion of diagnosis as an  air  pollution problem  or one of  the other
   possibilities.

                                               GO TO STEP 4

4. Is there any evidence of an insect pest? Such evidence includes:
     a. the insect
     b. skeletons
     c. excrement
     d. webs
     e. eggs

                                         No - GO TO STEP 7

                                        Yes - GO TO STEP 5
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           5. Is the symptom consistent with the  symptom  normally associated with
              insect evidence present?
                                                 No - GO TO STEP 7
                                                 Yes - GO TO STEP 6

          6. At this point it is reasonable to conclude that the insect is the probable
             cause of the injury.  This  does not eliminate the possibility  of an air
             pollution problem, but at least for the present time air pollution cannot be
             named as a sole causal  factor producing the symptoms.

                                                         STOP

          7. How many different species  of plants are exhibiting symptoms of injury?

                                               One - GO TO STEP 50
                                    More than one - GO TO STEP 8

          8. Are all the affected species rated  sensitive or intermediate to the same
             pollutant or pollutants?

                                                No - GO TO STEP 23
                                               Yes - GO TO STEP 9

          9. Are any native plants affected?

                                                No - GO TO STEP 29
                                               Yes - GO TO STEP 10

         10. The chance of a nutrient deficiency is so slight that it can be assumed there
             is not a deficiency.

                                                      GO TO STEP 11

         11. Consult the local air pollution control agency to obtain information in the
             emission inventories concerning the sources of pollutants in the area and the
             pollutants they can be emitting. Remember that if one of the pollutants
             under consideration is a photochemical oxidant there will not be a source in
             the inventories.

                                                      GO TO STEP 12

         1 2. Are there any sources  in the area that could be emitting pollutants to which
             all the affected plants  are rated sensitive or intermediate? Remember that if
             a photochemical oxidant is under suspicion, the source may be many miles
             away (refer to Chapter 3).
                                                No - GO TO STEP 84
                                               Yes-GO TO STEP 13
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13. Obtain  as  much  data  as  possible  about the following meteorological
    variables:
      a. precipitation
      b. temperature
      c. wind direction
      d. wind speed
      e. inversions
    Collect data for the following time periods:
      a. If the injury appears to be chronic, collect as much as one year's data to
        determine the prevailing wind.
      b. If the  injury  appears to be  acute, collect data from a  day or two
        immediately preceding the onset of symptoms.
      c. If a strong possibility exists that the symptoms are environmental stress
        symptoms, then collect data for the month preceding  the onset of
        symptoms.
    Such  data are available from the U.S. Weather Stations, local airports, yacht
    clubs, Coast  Guard, local air  pollution control agency, agricultural experi-
    ment  stations, universities, companies, and individuals.

                                               GO TO STEP 14

14. Was either  temperature or amount of precipitation extreme in either direc-
    tion during the relevant period?

                                         No - GO TO STEP 17
                                        Yes - GO TO STEP 15

15. Are symptoms consistent with symptoms normally associated with the type
    of environmental stress indicated in step 14?

                                         No - GO TO STEP 17
                                        Yes-GO TO STEP 16

16. Environmental stress is the most likely cause of the observed injury.

                                                  STOP

17. Study the  local topography  of  the  area, noting  terrain  features such as
    mountains, valleys, etc.

                                               GO TO STEP 18

1 8. Using the information collected  on  the meteorological  conditions,  topog-
    raphy, and the emission inventories, is there a possibility that a source(s) in
    the area emitted a pollutant(s) that could have reached the site of injury?

                                         No - GO TO STEP 84
                                        Yes-GO TO STEP 19
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1 9.  How many pollutant sources can be identified?

                                       One - GO TO STEP 32
                            More than one - GO TO STEP 20

20.  Are the  observed symptoms specific for any  of the  pollutants from the
     sources under consideration?

                                        No - GO TO STEP 34
                                        Yes - GO TO STEP 21

21.  How many pollutants still remain suspect?

                                       One - GO TO STEP 35
                            More than one - GO TO STEP 22

22.  At this point a decision as to a causal pollutant depends on the skill applied
     to discriminating between different pollutant symptoms. It is suggested that
     the first half of the handbook be consulted to help in the discrimination and
     also contact a plant specialist.

                                                  STOP

23.  Are any native plants affected?

                                        No - GO TO STEP 47
                                        Yes - GO TO STEP 24

24.  The chance of a nutrient deficiency is so slight that it can be assumed there
     is no deficiency.

                                              GO TO STEP 25

25.  Obtain  as  much  data as possible  about  the  following  meteorological
     variables:
     a. precipitation
     b. temperature
     c. wind direction
     d. wind speed
     e. inversions
     Collect data for the following time periods:
     a. If the  injury  appears chronic, collect as much as one year's data to
        determine the prevailing wind.
     b. If the injury appears acute, collect data from a day or two immediately
        preceding the onset of symptoms.
     c. If a strong possibility exists that the symptoms are environmental stress
        symptoms, then  collect data for the month preceding  the onset of
        symptoms.
     Such data are available from the  U.S. Weather Stations, local airports, yacht
                                 10-13

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    clubs, Coast Guard, local air pollution control agency, agricultural experi-
    ment stations, universities, companies, and individuals.

                                              GO TO STEP 26

26. Was either temperature or amount of precipitation extreme in either direc-
    tion during the relevant period?
                                        No - GO TO STEP 37
                                       Yes - GO TO STEP 27
27. Are symptoms consistent with symptoms normally associated with the type
    of environmental stress indicated in step 26?

                                        No - GO TO STEP 37
                                       Yes - GO TO STEP 28

28. Environmental stress is the most likely cause of the observed injury.

                                                 STOP
29. There is  a chance that a nutrient  deficiency is the cause of injury.  Send
    foliar samples to a university or commercial laboratory for testing.

                                              GO TO STEP 30

30. What were results of tests?

                                 Deficient - GO TO STEP 31
                              Not deficient - GO TO STEP 11

31. The  plants were deficient and this  deficiency is the most likely cause of the
    injury.

                                                 STOP

32. Are the observed symptoms consistent with symptoms normally associated
    with the pollutant from the source discovered in step 18?

                                        No - GO TO STEP 84
                                       Yes - GO TO STEP 33

33. The  causal pollutant and its likely source are now known. However, in order
    to confirm the diagnosis do the following:
      a. Conduct a foliar analysis to rule out a  nutrient deficiency rather than
        just rely on the native plants for an answer.
      b. Definitely rule out a disease either by experience or by sending samples
        to a disease diagnostic laboratory.
      c. Look carefully for an insect pest.
      d. Obtain accurate meteorological data.
    At this point the  state extension service should be  contacted about the
    incident.                                     STOP
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34.  At this point a definitive answer cannot be determined unless the symptoms
     of the various pollutants can be accurately discriminated. It is suggested that
     the first  half of the handbook be consulted to assist in the discrimination
     and that  a plant specialist be contacted for additional assistance.
                                                  STOP

35.  The causal pollutant has just been named. How many of the possible sources
     emit that pollutant?

                                       One - GO TO STEP 33
                             More  than one - GO TO STEP 36

36.  The probable causal pollutant has now been identified, but a single source
     cannot be named unless the meteorological and topographical data eliminate
     all  but one.  It is  suggested  that  an  air pollution specialist and  a  plant
     specialist be contacted at this point.           STOP

37.  Consult the local air pollution control agency to  obtain information in the
     emission  inventories concerning the sources of pollutants in  the area and the
     pollutants they can be emitting.  Remember that if one of the pollutants
     under consideration is a photochemical oxidant there will not be a source in
     the inventory.

                                              GO TO STEP 38

38.  Study the local topography of the area, noting terrain features  such as
     mountains, valleys, etc.

                                              GO TO STEP 39

39.  Using  the information  collected on the meteorological  conditions, topog-
     raphy, and the emission inventory, is there a possibility  that a source(s) in
     the area emitted a pollutant(s) that could have reached the site of injury?

                                        No - GO TO STEP 84
                                       Yes - GO TO STEP 40

40.  A list  of possible sources and  their possible pollutants now exists. Are the
     observed  symptoms specific for any of these pollutants?

                                        No - GO TO STEP 42
                                       Yes - GO TO STEP 41

41.  How many sources  are  possibly emitting this pollutant?

                                       One - GO TO STEP 33
                            More than one - GO TO STEP 36
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42. Reconstruct the sensitivity chart developed in step 2 using only the possible
    pollutants based on the meteorological data and information in the emission
    inventories collected. Is there now any trend?

                                      No - GO TO STEP 45
                                     Yes - GO TO STEP 43              •

43. How many pollutants remain suspect?
                                     One - GO TO STEP 44
                           More than one - GO TO STEP 22
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44.  Are the symptoms consistent with those normally associated with the one       ^^
     remaining pollutant?                                                     II

                                      No - GO TO STEP 45              ™
                                      Yes - GO TO STEP 46

45.  At this point there is no real conclusion you can draw. It is suggested a plant
     specialist be contacted.                     STOP
46.  How many sources could possibly be emitting this pollutant?

                                     One - GO TO STEP 33
                           More than one - GO TO STEP 36
47.  The chance exists that  a nutrient deficiency is the cause of injury.  Send
     foliar samples to a university or commercial laboratory for testing.

                                            GO TO STEP 48

48.  What were results of tests?

                                Deficient - GO TO STEP 49
                            Not deficient - GO TO STEP 25

49.  The plants  are deficient as  indicated in the laboratory results.  This is
     probably the cause of the observed symptoms.

                                               STOP

50.  Since there is just one species expressing symptoms, there is a good chance
     that a disease is responsible for the symptoms. Have you  had considerable
     experience in diagnosing plant disease symptomatology?

                                      No - GO TO STEP 54
                                     Yes - GO TO STEP 51

51.  Do the symptoms resemble any disease known to you?

                                      No - GO TO STEP 54
                                     Yes - GO TO STEP 52
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 52. Would this case be considered a classic example of that disease?

                                        No - GO TO STEP 54

                                        Yes - GO TO STEP 53

 53. At this point convincing evidence exists that a disease is the cause of the
     injury.

                                                  STOP

 54. Send examples of the injured plants to a disease diagnostic laboratory.

                                              GO TO STEP 55

 55. At this point other areas should be investigated for additional species with
     similar symptoms.

                                              GO TO STEP 56

 56. Were there any other species with similar symptoms found?

                                        No - GO TO STEP 60

                                        Yes - GO TO STEP 57

 57. What were the results of disease tests?

                            Disease present - GO TO STEP 59

                                 No disease - GO TO STEP 58

 58. This  choice was  anticipated since other affected species have now been
     located and a disease is not likely to affect more than one species.

                                               GO TO STEP 8

 59. Since additional affected species have now been found, the likelihood of a
     disease  is very low.  It may be worthwhile to send samples of the other
     affected species to a laboratory for disease tests as well as to confirm the
     original test results. If  the tests are negative, go to step 8. If the tests still
     show positive, then a disease must be concluded.
                                              STOP
 60. What were the results of disease tests?

                            Disease present - GO TO STEP 61

                                 No disease - GO TO STEP 62

61. Although there may still be an air pollution problem interacting with the
    disease identified,  the disease must be considered the most likely cause of
    the injury.


                                                 STOP
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62.  Is the affected species rated sensitive or intermediate to any pollutant or
     pollutants?

                                         No - GO TO STEP 65
                                        Yes - GO TO STEP 63

63.  Are any of the unaffected species in the area rated sensitive or intermediate
     to that pollutant or pollutants?

                                         No - GO TO STEP 69
                                        Yes - GO TO STEP 64

64.  Since these plants are unaffected, then air pollution can be ruled out. If air
     pollution was the cause, these plants would have been injured also.

                                               STOP

65.  Are any unusual  events known that could have led to a very high concen-
     tration of a pollutant? (e.g., a leak in a passing  tank car, etc.)

                                         No - GO TO STEP 85
                                        Yes - GO TO STEP 66

66.  Are the observed  symptoms consistent with those normally associated with
     injury  caused by that  pollutant? (Consult  appropriate  chapters in this
     handbook.)

                                         No - GO TO STEP 68
                                        Yes - GO TO STEP 67
67.  The causal pollutant and its source have just been identified.
                                               STOP
68.  At  this point air  pollution must be eliminated as  a possible cause of the
     injury on the basis of the following:
      a.  Since only one species has been affected, and there is  no reason  to
         suspect an accidental fumigation caused the injury, the possibility of an
         air pollution problem is very remote.
      b.  The fact that this species is not  rated sensitive  to  any pollutant
         indicates a lack of research to back up any evidence of an air pollution
         episode.
     The likely cause can be found perhaps in the realm of nutrient deficiency or
     environmental stress.  Both  of  these  possibilities should be explored, but
     such exploration is beyond the scope of this book since the intent here is to
     determine if air  pollution  is the cause.  In this  case,  there is insufficient
     evidence to suspect air pollution.

                                                   STOP
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                                  10-18
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69. Consult with an air pollution specialist to obtain information in the emis-
    sion inventories  concerning the sources of pollutants in the  area and the
    pollutants they can be emitting. Remember that if one of the pollutants
    under consideration is a photochemical oxidant there will not be a source in
    the inventories.

                                               GO TO STEP 70

70. Are  there  any sources in  the  area that could possibly be  emitting the
    suspected pollutant or pollutants? Remember that if a photochemical oxi-
    dant is under suspicion, the source may be many miles  away (refer to
    Chapter 3).

                                         No - GO TO STEP 75
                                        Yes - GO TO STEP 71

71. Obtain  as  much  data as  possible  about the following  meteorological
    variables:
      a.  precipitation
      b.  temperature
      c.  wind direction
      d.  wind speed
      e.  inversions
    Collect data for the following time periods:
      a.  If the injury appears to  be chronic, collect as much as one year's data to
         determine the prevailing wind.
      b.  If the injury  appears  to be  acute,  collect data from a day  or two
         immediately preceding the onset of symptoms.
      c.  If a  strong possibility exists that the symptoms are environmental stress
         symptoms, then collect data for the month preceding  the onset of
         symptoms.
    Such data are available from the U.S. Weather Stations, local airports, yacht
    clubs,  Coast  Guard, local air pollution control agency, agricultural experi-
    ment stations, universities, companies, and individuals.

                                               GO TO STEP 72

72. Was either  temperature or amount of precipitation extreme in either direc-
    tion during the relevant period?

                                        No - GO TO STEP 76
                                        Yes - GO TO STEP 73

73. Are  the symptoms consistent with symptoms normally associated with the
    type of environmental stress indicated in step 72?

                                        No - GO TO STEP 76
                                        Yes - GO TO STEP 74
                                  10-19

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74. Environmental stress is the most likely cause of the injury.

                                               STOP
75. Air pollution can be ruled out since there is no source in the area that could
    be emitting the suspected pollutant(s).
76. Study the  local  topography of the area, noting terrain features such as
    mountains, valleys, etc.
                                            GO TO STEP 77
77. Using the information you have collected on the meteorological conditions,
    topography, and  the emission inventories, is there a possibility that a
    source(s) in the area emitted a pollutant(s) that could have reached the site
    of injury?
                                      No - GO TO STEP 84
                                     Yes - GO TO STEP 78
78. How many sources are under suspicion?
                                     One - GO TO STEP 81
                           More than one - GO TO STEP 79
79. Do all the possible sources emit the same pollutant?
                                      No - GO TO STEP 82
                                     Yes - GO TO STEP 80
80. Are the observed symptoms consistent with symptoms normally associated
    with this pollutant? (Consult previous chapters of this book.)
                                      No - GO TO STEP 84
                                     Yes - GO TO STEP 36
81. Are the observed symptoms consistent with symptoms normally associated
    with the pollutant from that source? (Consult first part of this book.)
                                      No - GO TO STEP 84
                                     Yes - GO TO STEP 33
82. Are the symptoms classical for one of the possible pollutants?
                                      No - GO TO STEP 34
                                     Yes - GO TO STEP 83
83. How many sources could  still be emitting the suspected pollutant?
                                     One - GO TO STEP 33
                           More than one - GO TO STEP 36
                                10-20
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84.  At this point, air pollution injury is very unlikely and as a result, the cause
     of  the  expressed  symptoms should be due to one of  the  other  factors
     mentioned in step 3  (insects, nutrient deficiency, environmental stress, or
     biotic disease). Since  the diagnosis of exactly which of these factors is the
     cause of the injury is beyond  the scope of this book, it is suggested that
     additional expert assistance be obtained to aid in the diagnosis.

                                                STOP

85.  Is the affected species rated tolerant to any pollutant?

                                          No - GO TO STEP 97
                                         Yes - GO TO STEP 86

86.  Consult with an air pollution specialist to  obtain information in the emis-
     sion inventories concerning the sources of  pollutants in the area and the
     pollutants  they  can be emitting. Remember that if one of the pollutants
     under consideration is a photochemical oxidant there will not be a source in
     the inventories.

                                                GO TO STEP 87

87.  Are there any sources of the suspected pollutant(s) in the area? Remember
     that if a photochemical oxidant is under suspicion, the source may be many
     miles away (refer to Chapter 3).

                                          No - GO TO STEP 98
                                         Yes - GO TO STEP 88

88.  Obtain as  much  data as  possible  about the following meteorological
     variables:
      a.  precipitation
      b.  temperature
      c.  wind direction
      d.  wind speed
      e.  inversions
     Collect data for the following time periods:
      a.  If  the injury appears  chronic, collect  as  much as one year's  data to
         determine the prevailing wind.
      b.  If the  injury appears acute, collect data from a day or two immediately
         preceding the onset of symptoms.
      c.  If a strong possibility exists that the symptoms are environmental stress
         symptoms,  then  collect data  for the  month preceding the onset of
         symptoms.
     Such data are available from the U.S. Weather Stations, local airports, yacht
     clubs, Coast  Guard, local air pollution control agency, agricultural  experi-
     ment stations, universities, companies, and individuals.

                                                GO TO STEP 89
                                  10-21

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                                       No - GO TO STEP 92
                                      Yes - GO TO STEP 91
92. Study  the local topography, noting terrain features such as  mountains,
    valleys, etc.

                                             GO TO STEP 93

93. Do the meteorological data and the local terrain suggest a buildup of a very
    high concentration of a pollutant(s) in the area?

                                       No - GO TO STEP 99
                                      Yes - GO TO STEP 94

94. Are the expressed symptoms consistent with symptoms normally caused by
    one of the suspected pollutants?
                                      One - GO TO STEP 33
                            More than one - GO TO STEP 36

97. At this point air pollution must be  eliminated as a possible cause of the
    injury based on the following:
      a. Since  only  one  species has been affected and  there is no reason to
        suspect an  accidental fumigation, the possibility  of an air pollution
        problem is very remote.
      b. The fact that this species is not rated for sensitivity to any pollutant
        indicates a lack of research to  back up any evidence of an air pollution
        episode.
                                 10-22
                                                                              I
                                                                              I
89. Was either temperature or amount of precipitation extreme in either direc-
    tion during the relevant period?

                                       No - GO TO STEP 92
                                      Yes - GO TO STEP 90

90. Are symptoms consistent with symptoms normally associated with the type         Hj
    of environmental stress indicated in step 89?
                                                                              I
91. Environmental stress is the most likely cause of the observed injury.
                                             STOP                            I
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                                                                              I

                                                                              I

                                                                              I
                                      No-GO TO STEP 100
                                     Yes - GO TO STEP 95
95. The probable causal pollutant has now been identified.

                                             GO TO STEP 96                  I
96. How many sources are in the right direction and within range to cause the
    injury?
                                                                               I

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      The likely cause can be found perhaps in the realm of nutrient deficiency or
      environmental stress. Both of these possibilities should be explored, but
      such exploration is beyond the scope of this book since the intent here is to
      determine if air pollution is the cause.  In this case  there is  insufficient

      evidence to suspect air pollution.               STOP


 98.  At this  point air pollution must be eliminated as  a possible cause of the
      injury for the following reasons:
       a.  There is only one species affected and  this species is not known to be
          sensitive to any pollutant.
       b.  This species is tolerant to one or more pollutants, but there is no source
          of the pollutant(s) in the area.
      If air  pollution was, in fact, the cause of  the injury,  there is  insufficient
      evidence to support such a conclusion.
      It is suggested that  the possibility of a nutrient deficiency or environmental
      stress  condition be explored in order to determine a likely  cause. Also, it
      would be beneficial to solicit additional assistance from a  botanist or plant

      pathologist.                                   STOP


 99.  At this  point air  pollution  can  be eliminated as  a cause since a high
      concentration would  be necessary to cause injury to the affected species.
      The cause may be  found in the realm of  nutrient deficiency  or  environ-
      mental  stress. Both  of these  possibilities  should  be  explored, but  such
      exploration is beyond the scope of this book.
                                                   STOP

100.  At this  point, unless the symptoms  can  be accurately  distinguished as
      typical of one pollutant, some outside assistance should be sought.

                                                   STOP
                                    10-23

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                        APPENDIX A

                  CONVERSION FACTORS

        Calculated at Reference Conditions: 25°C., 760 mm Hg



Gas
NH3
HF
CO
CH^CH,,
NO
H2S
HCI
F,
N02
03
S02
ci,
o
CH3COON02



Name
Ammonia
Hydrogen fluoride
Carbon monoxide
Ethylene
Nitric oxide
Hydrogen sulfide
Hydrogen chloride
Fluorine
Nitrogen dioxide
Ozone
Sulfur dioxide
Chlorine

PAN
To convert from
ppm to ng/m3
multiply
ppm by:
696
818
1150
1150
1230
1390
1490
1550
1880
1960
2620
2900

4947
To convert from
tig/m3 to ppm
multiply
ng/m3 by:
14.40x 10-4
12.20x 10'4
8.73 x 10'4
8.72 x 10'4
8.15 x 10""
7.18 x 10"4
6.71 x 10'4
6.44 x 10'4
5.32x10-"
5.10 x 10'4
3.82 x 10'4
3.45 x 10'4

2.02 x 10'4
NOTE: All factors rounded to three significant figures.
or
To convert other gases to ppm

may be used:

                        ppmxMWx 103
                                     , one of the following equations
ppm to /Jg/m3: /zg/m3  =
                          MV
  ,  3              Aig/m3 x MV x 1O'3
Mg/m  to ppm: ppm = 	
                         MW


MW = Molecular Weight

MV = Molar Volume (24.46 8/mole at 25°C., 760 mm Hg)
                            A-l

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                             APPENDIX  B

             NATIONAL  PRIMARY AND  SECONDARY

                    AIR  QUALITY STANDARDS


   Primary standards were set at a level which would prevent health effects from
occurring. They are based on the best information available at the time of their
establishment. Secondary standards  were set at  a level which would  prevent
deleterious effects from  occurring  on vegetation  and materials such as fabrics,
paints, masonry, etc. These standards were also established on the basis of best
available information  at  the time. It  should be noted, however, that the stand-
ards, both  primary and secondary, were established based on data which took
into consideration the presence of only one gas in  the exposure atmosphere.  This
is  seldom  the  case  in nature. Receptors  may  be exposed to a number of
pollutants  of various  concentrations,  simultaneously,  sequentially, or inter-
mittently.  It is  possible that, as more information becomes available, these

standards may need adjustment.
   It should also be noted that these are federal standards, and some states and
municipalities may have  more stringent standards. The  reader is  cautioned to
inquire about state or local regulations.


           National Primary and Secondary Air Quality Standards*
Pollutant
Sulfur Dioxide


Photochemical
Oxidants
Nitrogen
Dioxide
Hydrocarbons

Particulate
Matter



Duration
Annual Arithmetic
Mean
Max. 24 hour
Max 3 hour
Max 1 hour
Annual Arithmetic
Mean
Max. 3 hour con-
centration (6-9 AM)
not to exceed once
per year
Annual Geometric
Mean
Max. 24 hour con-
centration not to
exceed once per
year
Primary
Standard
(0.03 ppm)
365 M9/m3
(0.14 ppm)
	
160/ug/m3
(0.08 ppm)
(0.05 ppm)
160M9/m3
(0.24 ppm)

75 M9/rr'3
260 M9/m3


Secondary
Standard
	
	
1300M9/m3
(0.5 ppm)
Same
Same
Same

60/jg/m3
150M9/m3


                                   B-l

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Pollutant
Carbon
Monoxide



Duration
Max. 8 hour con-
centration not to
exceed once per
year
Max. 1 hour con-
centration not to
exceed once per
year
Primary
Standard
10 mg/m3
(9 ppm)

40 mg/m3
(35 ppm)

Secondary
Standard
Same

Same

*Based on Federal Register, Vol.  36, No. 84, April 30, 1971, pp. 8186-8201. (Secondary
 standards for Sulfur Dioxide revised by Federal Register, Vol. 38, No. 178, September 14,
 1973)
                                        B-2
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                              APPENDIX  D

                           BIO-INDICATORS

   Certain plant species,  or more specifically, certain  cultivars or clones have
been used as sensitive indicators of air pollutants. Their  use has been particularly
useful  for "monitoring"  in remote areas where power for instruments is not
available and for determining  the environmental conditions which are conducive
to  plant  injury. Their major limitations are  lack  of  specificity and lack of
identifiable  growth  and  reproductive  effects.  They have  proven useful,  for
example, in delineating extent and frequency of the Los Angeles photochemical
smog.  In the latter study, annual bluegrass and pinto bean were used. Tobacco
has been  used by  many, and has served as an  excellent index of  oxidants.
Lichens have been used widely in Germany and Canada.
   Examples of bio-indicators used to detect ozone include  Bel W-3 tobacco
(Plate  3-2), certain varieties of pinto beans, white  cascade petunia, white ash
(Plate 3-18), and certain clonal lines of eastern white pine (Plate 3-23).
   A number of researchers have  reported that the centers of many cities and
certain industrial areas are free, or nearly so, of epiphytic lichens and mosses.
The usual situation is to find  these epiphytes increasing in numbers and species,
as well as in vigor, as the distance from the city center or the source of the air
pollution  increases. These city "deserts"  are believed to be due to SO^  phyto-
toxicity, although reduced sunlight and other factors cannot, at present, be ruled
out as causes.
   In  recent years,  procedures have been  developed for  mapping  Index of
Atmospheric Purity (IAP) lines around  city centers or point sources of SOj.
Data for IAP lines are derived from study of the number of lichen species in the
area and examination of individual species at selected stations. For such a study,
a tree species is selected, based on its frequency and distribution in the  area. The
trees should be large (0.5 to 1 meter in diameter), not  shaded by  other objects,
and not located in an area where a harmful local atmospheric factor (other than
the one to be studied) might exert an influence. Usually, data are taken from 10
to 15  such trees at each station. The lichen data should be taken  over the same
areas of the  tree trunks at  all stations (ground to 2-1/2 meters).
   Each lichen species  is  assigned a "frequency-coverage  number" (f) at each
station. This number is usually between 1 and 5, and  is assigned as follows:
     1. Rare occurrence at the site area and a low degree of coverage.
     2. Very infrequent occurrence and a low degree of coverage.
     3. Infrequent occurrence or a medium degree of coverage.
     4. Frequent occurrence or a high degree of coverage on some trees.
     5. Very frequent occurrence and a  high degree of coverage on most trees.
   Each species is also assigned in "ecological index number," q. At each station
where  the species in question  occurs, the number of other  epiphyte  species
present is  determined.  The number of other species  present is  then totalled for
all stations,  and divided by the number of stations,  to find the average number
of other species present. This average is q.
                                    D-l

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           q for a species = average number of other epiphyte species
                          occurring at stations where species
                          under study is found
   For example, a species of lichen in one study occurred at 245 of 349 stations.
The number of  companion  species at  these  245 stations ranged  from 4 to 32,
and averaged 15. Thus, q =  15; q x / (ecological index x frequency-coverage) is
divided by  10 to give a convenient,  manageable  number.  The IAP for  each
station is one-tenth the sum of the q x / values  for each species present at that
station. The IAP for all  stations may  then be plotted  on a map, and isotoxic
zones can be defined by linking stations having indexes within a certain range.
   Since  the  effect of  SO2  seems to  be  to kill or retard growth of these
epiphytes, their  presence and well-being  provides a measure of the total physio-
logical effect of  the pollutant on the epiphytes studied. Table D-l records lichen
species, their occurrence or non-occurrence  in each  of five  IAP zones around
large point-sources of SC>2, and the q or tolerance values of the lichens studied.
High q values mean the lichen is sensitive  to SC>2.
Table D-l
Distribution of Epiphytic Lichens in Various IAP Zones*

A/ectoria americana
A. nidulifera
Bacidia chlorococca
Buellia stilling/ana
Ca/oplaca cerina
Cande/aria concolor
Candelariella vitellina
Cetraria ci liar is
C. pinastri
C. saepmcola
Cladonia coniocraea
C. cristate/la
C. fimbriata
Evernia mesomorpha
Hypogymnia physodes
Lecanora expallens
L. saligna
L. subfusca (coll.)
L. subfusca variolosa
L. subintricata
L. symmicta
Lecidea nylanderi
Lepraria aeruginosa
Parmelia exasperatu/a
P. olivacea
Q
16
22
10
27
19
21
19
27
17
14
12
11

18
16
13
12
20
16
18
21
22
11
18
21
ZONES
I II III IV
x
x
X X X X

X

XXX

XXX
XXX
XXX
X

XXX
XXX
X X
X X X X
X
XXX
X X
X

X X
XXX
X
V

X
X
X
X
X
X
X
X
X
X

X
X
X
X
X
X
X
X
X
X
X
X
X
                                    D-2
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P. rudecta
P. septentrionalis
P. sulcata
P. trabeculata
Parmeliopsis ambigua
Pertusaria multipunctata
Physcia aipolia
P. adscendens
P. farrea
P. grisea
P. orbicularis
P. stellaris
Ramalina fastigiata
Rinodina hallei
R. papillata
Usnea sp.
Xanthoria fa/lax
X. polycarpa
TOTAL
*From LeBlanc, F. The epiphytic
significance as an air pollution i
Journal of Botany, 50:519-528.
Q
19
24
13
28
14
14
24
20
24
20
17
19
28
20
27
21
17
19

vegetation
idicator in

ZONES
I II III IV

X
X X X X

X X
X
X
X

X X

X X

X X

X


4 14 21 23
of Populus balsamifera and
Sudbury, Ontario. Canadian

V
X
X
X
X
X

X
X
X
X
X
X
X
X
X
X
X
X
40
ts


   Bio-indicator plants may be planted (or transplanted in the case of lichens) in
polluted areas and  observed  periodically  for specific symptom  types.  Such
observations may reveal the presence, and perhaps even the relative importance
of various  pollutants in  a given area. If indicator plants are established in "air
pollution  gardens" scattered  over a wide geographic area, the distribution  of
various  pollutants  may  be  determined.  Such gardens are also  useful youth
projects  and  make  good  demonstration  plots  for  showing  examples of air
pollution injury to plants. Table  D-2 shows some of the more frequently used
bio-indicators.

   Certain  types of  plants  may  also  be  used  to indicate  the  amount  of a
pollutant which has been taken in or absorbed by the plant — even though the
plant may  not show injury. This type of sampling followed by chemical analysis
has been used extensively to determine patterns of exposure or dispersion  of
fluorides.
   The  concentration of  fluoride in vegetation can be mapped in order  to
compare one  site with another or to determine fluoride dispersion over a large

area. The considerations  mentioned above concerning superficial fluoride should
be applied. Age, location, and portion of tissue  sampled can also affect the
result. Thus, a uniform method for the selection and preparation of foliage must
                                    D-3

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                                  Table D-2
                List of Common Bio-indicators and Pollutant(s)
                         to Which They Are Sensitive*
               Bio-indicator
                                                    Pollutant
               Alfalfa
               Gladiolus*
               Petunia, white cascade
               Pinto bean
               Tobacco, Bel W-3
               White pine*
               White ash
               Lichens
               Bluegrass
               Aspen
               Bracken fern
   *Certam cultivars or clones only.
S02
HF, F
Oxid., PAN
03,PAN

o'.so,

SO,
Oxid.
S02
SO,
be used.  The same species should be sampled in each area because different
species accumulate atmospheric fluoride at different  rates.  If one species does
not exist  at all stations and two or more species must be used, samples should be
taken  from  all species at  sites  where they overlap to afford  a  comparison
between  them.  The  sites  from which samples are  obtained should be chosen
systematically with respect to the geometry  of the map or the expected or
predicted pattern  of dispersion. More than one  sample should be  collected at
each site  in both  the affected and remote areas during the first visit. Once  the
site for sampling  has  been reached, the cost of additional samples is relatively
small,  and all  samples need not be  analyzed. But should variability or some
analytical problem arise, it is easier and cheaper to obtain another sample from
those stored on the shelf than to resample in the field.

Evaluation of the Fluoride Concentration of Forage
   The most important objective often is to judge whether or not the forage  in a
pasture has accumulated enough fluoride  to constitute a hazard to  livestock or
to violate a legal standard. The methods used for sampling will be determined by
two sets  of criteria: biological and statistical. Biological criteria are more impor-
tant  with respect to obtaining samples that are representative of the vegetation.
If the field contains a mixture of species, the sample should reflect the relative
amounts of the  species present because different species accumulate fluoride at
different  rates.  The same  kind of consideration  is also  appropriate if the crop
contains  plants  of different ages.  The species  eaten should  also be considered;
since  thistle  and certain other species are rarely eaten, sampling  them gives an
erroneous value. Unless care is taken  in cutting the  sample, either at the height
mown or cropped, the inclusion  or exclusion of  older  foliage  may bias  the
results. Unless specified by a standard, the sample should not be washed because
particulate or superficial fluoride is available for ingestion by livestock. However,
care  should be  taken that the presence of road dust or  soil  in the sample does
not bias the results.
                                     D-4
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   Whenever possible, forage should  be sampled just prior to harvest, but if it
cannot be,  owing to the schedule and plan of sampling, the following factors
might be considered in relation to an evaluation of the result. Precipitation can
lower the fluoride content. A period  of slow growth, due to climate or maturity
of the crop, can increase the concentration because of the lack of new foliage,
which is lower in fluoride.  Similarly,  rapid growth may lower the concentration
through growth dilution or  through  senescence  and loss of older fluoride-
containing leaves.
   The actual  plan  of sampling  and number of samples  taken is usually not
known before  the first  sampling time. However, the initial samples should be
taken in such  a way that information can be derived that will allow the most
efficient  schedule and  pattern of sampling to be  employed  for  subsequent
sampling periods.
                               Selected Reference

Heck, W. W. The use of plants as indicators of air pollution. International Journal of Air and
   Water Pollution, 10:99-111, 1966.
                      List of Commonly Used Bio-indicators

For ozone
      Petunia (certain cultivars only)
      Pinto bean
      Tobacco (Bel W-3)
      White pine (certain strains only)

For PAN
      Pinto bean
      Petunia (some white-flowered cultivars)

For Fluorides
      Gladiolus (c.v. Elizabeth the Queen)
      Iris
      Ponderosa pine


For SO,
      Alfalfa
      White pine (certain strains only)
      Bean
      White birch
                                    D-5

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                              APPENDIX  E

                  GLOSSARY  OF AIR POLLUTION

                      AND  BOTANICAL  TERMS


Abaxial	facing away from the axis of stem; usually refers to
                         the undersurface of a leaf blade.

Abscission	dropping of leaves or other plant parts.

Acute injury	injury,  usually  involving  necrosis, which develops
                         within several hours to a few days  after a  short-term
                         exposure  to  a  pollutant,  and expressed  as  fleck,
                         scorch, bifacial necrosis, etc.

Adaxial	facing toward the axis of stem; usually refers to the
                         upper surface of a leaf blade.

Aerosol	particles or liquid droplets usually smaller than 100 fj.
                         in diameter suspended  in air.

Ambient	prevailing condition  of the atmosphere at a given
                         time, the outside  air.

Area source	geographical location from which pollutants originate
                         and  are transported by advection. The Los Angeles
                         basin is an area source of photochemical oxidants.

Axillary	occurring in the angle  formed between  any two plant
                         organs.

Bifacial lesion	foliar injury that extends through the leat.

Bifacial necrosis	death or collapse  of tissue extending through the leaf.

Bio-indicator	plant species or varieties that are particularly sensitive
                         to a specific pollutant so that they provide useful
                         indicators of the presence of a particular pollutant.

Bleaching	complete loss of all pigmentation in leaf.

Bronzing	a brown discoloration  that  usually appears on  the
                         abaxial  surface of leaves, and  is often an advanced
                         stage of the silvering or glazing typical of injury by
                         PAN and other oxidents.

Chloride   	the ionic form of  the element chlorine.

Chlorosis	yellowing or paling of green  parts of the plant due to
                         loss of chlorophyll.

Chronic injury	injury  which  develops only  after long-term or re-
                         peated exposure to an air pollutant, and expressed as
                         chlorosis,  bronzing,  premature senescence, reduced
                         growth, etc.; can include necrosis.

Clone	a group of organisms derived asexually from a single
                         individual.
                                    E-l

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Coefficient of haze
   (COH)	a measurement of visibility based on the quantity of
                         smoke and dust in 1,000 linear feet of air.
Conidium, conidia	spore-like asexual reproductive  structure  of  certain
                         fungi.
Conifer	plant that bears seeds in cones.
Cotyledons	the first leaves (1, 2, or more) of the embryo as found
                         in the seed.
Cuticle, cutin	waxy protective layer covering primary plant parts.
Damage	a measure of the  decrease in economic or aesthetic
                         value resulting from plant injury by pollutants. (Term
                         considered by some to be synonymous with injury).
Deciduous	characteristic of plants that shed leaves at  the end of
                         one growing season.
Defoliate	to cause a loss of foliage, especially prematurely.
Desiccation	drying out of foliage.
Dicot	having two cotyledon leaves.
Disease	an abnormal  condition  of the  plant  caused by a
                         pathogen, or the environment.
Diurnal	occurring during the day; daily.
Dose	concentration  of  the  pollutant multiplied  by  the
                         duration of exposure.
Effluent	waste emitted to the environment.
Enation	growth of a stem or branch in a flattened rather than
                         round condition.
Epidermis	the outer layer of cells on all primary plant parts.
Epinasty	leaf growing at right angle or downward  to  a stem
                         rather than at an acute  upward angle.
Fleck	collapse  of a few cells in isolated areas in the upper
                         layers  of  the  leaf, resulting  in tiny light-colored
                         lesions.
Fluorosis	disease  in cattle, sheep, or  other  grazing  animals
                         brought about by  ingestion  of fluorine-contaminated
                         forage.
Fossil fuel	fuel derived from decayed organic matter from past
                         geological ages, e.g., coal, oil.
Fungus, fungi	organisms that lack the  ability  to manufacture their
                         own food but derive their nourishment by absorption
                         from pre-existing organic sources.
Glazing	silvery appearance on the leaf.
Hypertrophy	refers most commonly to an abnormal enlargement.
Hypha, hyphae	thread-like filament consisting  of vegetative body of
                         some  fungi.
                                    E-2
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Injury	any  change in the appearance and/or function of a
                         plant that is deleterious to the plant.
Inoculation	process  involving  introduction  of disease-causing
                         biological agent in tissues of the host plant.
Lapse rate	the rate  of temperature change with elevation m the
                         atmosphere.
Lesion	superficial injury  or  other  circumscribed  pathologic
                         change in tissue.
Marginal	occurring along the periphery of the leaf.
Mesophyll	the inner ground tissue of a leaf consisting mostly of
                         parenchyma cells.
   spongy mesophyll .... the  loosely  associated irregularly  arranged  paren-
                         chyma cells of the lower mesophyll of a leaf.
   palisade mesophyll. .  . . layer of  mesophyll cells oriented perpendicular to the
                         upper epidermis of the leaf.
Monocot	having only one cotyledon leaf.
Mottle	degeneration of the chlorophyll in certain areas of the
                         leaf giving the leaf a blotchy appearance.
Necrosis	death of tissue.
Palisade	layer of  closely  arranged mesophyll cells below upper
                         epidermis of leaf.
PAN,
   peroxyacetyl nitrate. . . the  principal  constituent in a homologous  series of
                         compounds  referred  to  as peroxyacyl nitrates or
                         PAN's. Formed  by photochemical reactions involving
                         nitrogen dioxide and hydrocarbons.
Parenchyma	tissue composed of parenchyma cells.
Parenchyma cells	usually thin walled, vacuolated, and living, with vary-
                         ing shapes, but most commonly isodiametric.
Pathogen	any  organism, usually fungus, bacteria, virus or para-
                         site, or abiotic agent,  capable of inciting disease.
Pathogenesis	process involving disease development.
Pesticide	any  substance or  mixture of substances intended  for
                         preventing,  destroying, repelling or mitigating any
                         insects, rodents, nematodes, fungi,  weeds and  other
                         forms  of plant or  animal life or viruses, except viruses
                         on or in —  living man or other animals which  are
                         declared to be pests,  and any substance or  mixture of
                         substances intended for use as a  plant  growth regu-
                         lator,  defoliant or  desiccant. (PL  92-516,  Federal
                         Environmental Pesticide Control Act of  1972, Sec. 2
                         t,u).
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Phloem	vascular tissue in plants that transports carbohydrates
                         from leaves to roots.
Photochemical oxidants. . pollutants resulting from the reaction of sunlight on
                         automobile exhaust or other airborne gases.
Photosynthesis	the process carried on by green plants which utilizes
                         light energy to split water, forming O2 and chemical
                         energy, which in  turn  is utilized to convert atmos-
                         pheric CO2 into carbohydrate.
Phytotoxicant	any agent that becomes toxic to plants.
ppb	parts  by weight or volume of pollutants per billion
                         parts  by volume of air (usually refers to  volume of
                         pollutant if not so stated).
pphm	parts  by weight or volume of pollutants per hundred
                         million parts by  volume  of  air (usually  refers to
                         volume of pollutant if not so stated).
ppm	parts  by weight or volume of pollutants per million
                         parts  by volume of air (usually refers to  volume of
                         pollutant if not so stated).
Pustules	pimple-like  bodies enclosing reproductive structures
                         of some fungi.
 Senescence	stage  ot  development  of plants or  parts  of plants
                         encompassing the  time from maturity to death.
 Sepal	the outer, often leaf-like, whorl of a flower.
 Stipple	dark-colored lesions on leaves  resulting from pigmen-
                         tation of injured cells.
 Syndrome	a  combination of symptoms and signs characteristic
                         of an abnormal condition.
 Synergism	the action of two independent factors resulting in an
                         effect which is greater  than the sum of the individual
                         factors.
 Temperature inversion ... a  condition in which temperature  increases rather
                         than decreases with altitude.
 Urediospore	asexual reproductive structure of some fungi.
 Vascular bundle	an organization of tissue in the plant for the transport
                         of food, minerals,  and water.
 Xylem	vascular tissues in plants that transport  water  and
                         minerals from roots to leaves.
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                                      INDEX
Abaxial layer, 2-10
Abiotic causal agents (of
       mimicking symptoms), 8-1
   construction damage, 8-4
   de-icing salts, 8-4
   lack or excess of water, 8-1
   nutrient excesses and
       deficiences, 8-3
   other pollutant-induced
       symptoms, 8-5
   pesticides, 8-4
   soil acidity,  8-3
   temperature - frost or cold
       injury, 8-2
   temperature - heat injury, 8-3
   winter injury, 8-2
Abscission, E-l
Accessory cells, 2-30
Adaxial layer, 2-10
Ammonia, 6-15
   acute injury, 6-16
   air quality standards, 6-17
   atmospheric chemistry, 6-15
   atypical symptoms, 6-16
   chronic injury, 6-16
   factors affecting plant
       response, 6-16
   injury threshold, 6-17
   monitoring data, 6-15
   relative sensitivity, 6-17
   sources, 6-15
   symptomatology, 6-16
Apical meristem, 2-5, 2-7
Assessment of damages,  1-4
Axillary buds, 2-6

Bark, 2-6
Biotic causal  agents (of
       mimicking symptoms), 8-5
   bacteria, 8-6
   diseases, 8-5
   fungi, 8-5
   insects, 8-6
   nematodes,  8-6
   viruses and mycoplasmas, 8-6
Blade,  2-8
Bullheading, 6-12
Bulliform cells,  2-28
Bundle sheath,  2-11
Cadmium, 6-24
Carbon monoxide, 6-21
   air quality standards, 6-21
   sources, 6-21
   symptomatology, 6-21
Cells, 2-1
Cell wall, 2-1
   primary, 2-1
   secondary, 2-1
Chlorine, 6-2
   acute injury, 6-3
   air quality standards, 6-4
   atmospheric chemistry, 6-2
   chronic injury,  6-3
   factors affecting plant
       response, 6-4
   leaf tissue analysis, 6-5
   mimicking symptoms, 6-3
   monitoring data, 6-3
   relative sensitivity, 6-4
   sources, 6-2
   symptomatology, 6-3
       broad-leaved plants, 6-3
       coniferous plants, 6-3
       narrow-leaved plants, 6-3
   threshold concentrations, 6-4
Chlorophyll, 2-2
Chloroplast, 2-2
"Christmas tree" pattern  of
       chlorosis, 5-5
Chromatin, 2-2
Chromosomes, 2-2
Copper, 6-24
Cork cambium, 2-6
Cuticle, 2-10
Cytoplasm, 2-2

Darmous, 5-1
Diagnosis, 10-1
   basic procedure, 10-1
   systematic approach, 10-5
Diagnostic routine, 10-8
Diurnal temperature variations, 9-6
Dry adiabatic lapse rate, 9-3

Ecological index number, D-l
Emergence tipburn of eastern
       white pine, 3-10
Emission inventory, 9-2
                                  Index-1

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Endodermis, 2-4
Environmental lapse rate, 9-3
Epidermis, 2-4
Epiphytes, D-l
Ethylene, 6-10
   acute effects, 6-12
   air quality standards, 6-13
   atmospheric chemistry, 6-10
   chronic effects, 6-12
   factors affecting plant response, 6-13
   leaf tissue analysis, 6-14
   monitoring data, 6-11
   relative sensitivity, 6-14
   sources, 6-10
   symptomatology, 6-11
   traumatically induced, 6-11

Flowers, 2-12
Fluoride, 5-1
   air quality standards, 5-17
   atmospheric chemistry, 5-3
   chemical analysis, D-4
   factors affecting plant
          response, 5-10
   injury threshold, 5-13
   leaf tissue analysis, 5-17
   monitoring data, 5-4
   sources, 5-1
   symptomatology, 5-4
       broad-leaved plants, 5-5
       coniferous plants, 5-9
       fruit, 5-10
       narrow-leaved plants, 5-7
Fluorine, 5-1
Fluorspar, 5-1
Frequency - coverage number, D-l

Grape stipple, 3-10
Guard  cells, 2-9
Guttation, 2-10

Heavy  metals (see also Lead -
       Cadmium - Copper -
       Mercury vapors), 6-24
Herbicides, 6-29
Hydathode, 2-10
Hydrogen chloride, 6-6
   acute injury, 6-7
   air quality  standards, 6-8
Hydrogen chloride (continued)
   atmospheric chemistry, 6-6
   chronic injury, 6-7
   factors affecting plant response, 6-7
   injury threshold, 6-8
   mimicking symptoms, 6-7
   monitoring data, 6-7
   relative sensitivity, 6-8
   sources, 6-6
   symptomatology,  6-7
       broad-leaved plants, 6-7
       coniferous plants, 6-7
       narrow-leaved plants, 6-7
Hydrogen fluoride, 5-1
Hydrogen sulfide, 6-18
   acute injury, 6-19
   air quality standards, 6-19
   atmospheric chemistry, 6-18
   chronic injury, 6-19
   factors affecting plant response, 6-19
   injury threshold, 6-19
   leaf tissue analysis, 6-20
   monitoring data, 6-18
   relative sensitivity, 6-19
   sources, 6-18
   symptomatology,  6-19

Index of atmospheric purity (IAP), D-l
Interactions (see Pollutant -
       pollutant interactions -
       Pollutant - pathogen
       interactions)
Intercalary meristem, 2-7
Internode, 2-6

Lamina,  2-8
Lapse rates, 9-3
Lead, 6-23
   effects on plants, 6-23
   sources, 6-23
Leaf arrangement, 2-8
   alternate, 2-8
   opposite, 2-8
   whorled, 2-8
Leaf function, 2-9
Leaf growth, 2-11
Leaf sheath, 2-8
Leaf structure, 2-10
Leaf types, 2-10
   broadleaf, 2-10
                                   Index-2
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Leaf types (continued)
   compound, 2-8
   narrow leaf, 2-10
   needles, 2-10
   simple, 2-8
Legume, 2-5
Lenticel, 2-6
Lichen, D-l

Median effective dose, 1-6
Median toxic dose, 1-6
Mercury vapors, 6-24
   relative sensitivity, 6-25
   sources, 6-25
   symptomatology, 6-25
Mesophyll, 2-10
Meteorological aspects of air
       pollution, 9-2
   atmospheric stability and
       temperature, 9-3
   wind speed and direction, 9-2
Middle lamella, 2-1
Mimicking symptoms (see Abiotic
       causal agents, Biotic
       causal agents)
Mitochondrion, 2-3

Nitrogen dioxide (see NOX)
Node, 2-6
Nodule, 2-5
NOX, 3-22
   air quality standards, 3-29
   atmospheric chemistry, 3-22
   factors affecting plant
          response, 3-27
       external, 3-27
       internal, 3-28
   injury threshold doses, 3-28
   leaf tissue analysis, 3-31
   monitoring data, 3-23
   relative sensitivity, 3-29
   sources, 3-22
   symptomatology, 3-26
       broad-leaved plants, 3-26
       coniferous plants, 3-27
       narrow-leaved plants, 3-27
Nuclear envelope, 2-2
Nucleus, 2-2

O'Gara, 4-8
Onion tipburn or blight, 3-10
Oxides of nitrogen (see NOX)
Ozone, 3-1
   air quality standards, 3-13
   factors affecting plant
          response, 3-11
   injury threshold doses, 3-12
   leaf tissue analysis, 3-16
   relative sensitivity, 3-14
   symptomatology, 3-8
      broad-leaved plants, 3-8
      coniferous plants, 3-9
      narrow-leaved plants, 3-8
Ozone needle mottle of Ponderosa
      Pine, 3-11

Palisade layer, 2-10
PAN (peroxyacetyl nitrate), 3-17
   air quality standards, 3-19
   factors affecting plant
          response, 3-19
   injury threshold doses, 3-19
   leaf tissue analysis, 3-21
   mimicking symptoms, 3-18
   relative sensitivity, 3-19
   symptomatology, 3-17
      broad-leaved plants, 3-17
      coniferous plants, 3-18
      narrow-leaved plants, 3-18
Particulate matter, 6-27
Peroxyacetyl nitrate (see PAN)
Pesticides, 6-29
   leaf tissue analysis, 6-30
   relative sensitivity, 6-30
   sources, 6-29
   symptomatology, 6-30
Petiole, 2-8
Phloem, 2-4
Photochemical oxidant, 3-1
Photochemical reaction, 3-2
Photosynthesis, 2-2
Pith, 2-6
Plasmalemma, 2-1
Plastid, 2-2
Pollutant - pathogen interactions, 7-5
Pollutant - pollutant interactions, 7-1
   sulfur dioxide and hydrogen
      fluoride, 7-4
   sulfur dioxide and ozone, 7-2
   sulfur dioxide and nitrogen
      dioxide, 7-2
                                  Index-3

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 Ray, 2-6
 Resin duct, 2-6
 Rhizome, 2-7
 Roholm, 5-1
 Root cap, 2-5
 Root growth, 2-5
 Root types, 2-4
    adventitious, 2-4
    fascicled, 2-4
    fibrous, 2-4
    tap, 2-4
 Runner, 2-7

 Silicone tetrafluoride, 5A
 Sleepiness, 6-12
 Smog, 3-1
    photochemical, 3-1
 Sources of air pollution, 9-1
    industrial sources,  9-1
    mobile sources, 9-2
    rural sources, 9-2
    urban sources, 9-2
 Spongy  layer, 2-10
 Stem growth, 2-7
 Stem types,  2-6
    gymnosperm, 2-6
    herbaceous dicot, 2 6
    monocot, 2-6
    woody dicot, 2-6
 Stolon, 2-7
 Stomata, 2-8
 Sulfate ion, 4-4
 Sulfite ion, 4-4
 Sulfur dioxide, 4-1
    air quality standards, 4-10
    atmospheric chemistry, 4-2
    factors affecting  plant
          response, 4-6
    leaf tissue analysis,  4-11
    monitoring data,  4-2
    relative sensitivity,  4-10
    sources, 4-1
    symptomatology, 4-4
      broad-leaved plants, 4-5
      coniferous plants, 4-6
      narrow-leaved plants, 4-6
Sulfuric  acid mist, 4-2
Suture red spot, 5-10
Synergism, 7-1
 Teratogenic causal agents (of
       mimicking symptoms), 8-7
   genetic disorders, 8-7
 Tempeiature inversion, 9-3
 Tonoplast, 2-2
 Topographical effects on dispersion
       of pollutants, 9-7
 Transpiration, 2-9
 2,4-D; 2,4,5-T; 2.,4,5-lP, t,^0
   relative sensitivity, 6-30

 Vacuole, 2-2
 Vascular cambium, 2-5
 Viruses and mycoplasmas, 8-6

Weather fleck of tobacco, 3-10
Wood, 2-6

Xylem, 2-4

Zinc, 6-24
                                  Index-4
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