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
I
I
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
-------
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.
I
I
I
I
I
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.
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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.
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
vui
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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-!
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
Xll
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
Xlll
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
xvn
-------
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
xvm
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
Page
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
-------
I
I
I
I
I
I
I
I
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
I
I
xx
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
xxi
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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.
1-1
-------
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.
1-2
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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.
1-3
-------
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
1-4
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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.
1-5
-------
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.
1-6
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
2-1
-------
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)
2-2
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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.
2-3
-------
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
2-4
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
2-5
-------
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
2-6
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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.
2-1
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
2-9
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
CELL
WALL
Plate 2-2. Portion of Hoot Meristem Cell of Chrysanthemum
Showing Cell Organelles
2-15
-------
" ;*v
CHLOROPLAST
STROMA
Plate 2-3. Sect/on Through Chloroplasts of a Chrysanthemum Leaf
Cell Showing Details of Grana and Lamella
2-16
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
EPIDERMIS
STELE
PERICYCLE
Plate 2-4. Cross Section of a Ranunculus sp. (Buttercup) Root
2-17
-------
Plate 2-5. Cross Sect/on Showing the Stele Area of a Ranunculus sp.
(Buttercup) Root
2-18
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
CAMBIUM
LEM
LOEM
RTEX
STOMA
EPIDERMIS
Plate 2-8. Cross Section of the Herbaceous D/'cot Stem of
Medicago Sativa (Alfalfa)
2-21
-------
BARK
PERIDERM
PHLOEM
VASCULAR
CAMBIUM
RAY
Plate 2-9. Cross Section of the Woody Dicot Stem of Liriodendron
tulipifera (Tulip Poplar)
2-22
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
BARK
Plate 2-10. Cross Section of the Gymnosperm Stem of Pinus sp. (Pine)
2-23
-------
Plate 2-11. Cross Section of the outer area of the Gymnosperm Stem of
Pinus sp. (Pine) Showing Sites of Secondary Growth
2-24
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
EPIDERMIS
Plate 2-12. Cross Section of the Monocot Stem of Zea mays (Corn)
2-25
-------
' ',
. >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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
Plate 2-17. Surface View of a Stoma of Zebrina sp. Wandering Jew]
2-30
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
Plate 2-18. Cross Section of the Outer Bark of Liriodendron
tulipffera (Tulip Poplar) Showing a Lenticel
2-31
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
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
1
1
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
3-8
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
3-10
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
3-12
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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.
3-14
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
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.
I
I
I
I
I
I
I
I
I
I
I
I
I
3-21
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
I
I
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
3-26
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
Plate 3-3. Ozone Injury (Flecking) to White Ash
Plate 3-4. Ozone Injury to Swiss Chard
3-34
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
Plate 3-5. Ozone Injury to Tobacco
Plate 3-6. Ozone Injury to Radish
3-35
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
Plate 3-9. Oxidant Injury to Squash
Plate 3-10. Tomato Leaflet Showing Oxidant Injury (Probably Ozone)
3-37
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
Plate 3-15. Severe Ozone Injury and Bifacial Necrosis of Browallia Leaves
Plate 3-16. Severe Crape Stipple Caused by Ozone
3-40
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
Plate 3-19. Bluegrass Injured by Ambient Oxidant in the Los Angeles Basin
3-42
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
Plate 3-20. Severe Oxidam Injury to Ponderosa Pine
3-43
-------
Plate 3-21. Chronic Ozone Injury of Ponderosa Pine. Note Dif-
ference in Tolerance Between Trees and Tufted
Appearance of Foliage
3-44
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
Plate 3-22. Tipburn of Onion Caused by Ozone
Plate 3-23. Eastern White Pine Displaying Oxidant Injury (Probably Ozone)
3-45
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
Plate 3-28. PAN (Ambient) Injury to Swiss Chard
Plate 3-29. Petunia with PAN or Ozone Injury
3-48
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
Plate 4-3. Acute Sulfur Dioxide Injury to White Birch Foliage
4-13
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
Plate 4-4. Acute Sulfur Dioxide Injury to Trembling
Aspen Leaves. Injured Areas are Reddish-
Brown and Darken with Age
4-14
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
4-16
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
Plate 4-15. Acute Sulfur Dioxide Injury to Sonora Wheat (Ivory-Colored)
4-20
-------
Plate 4-16. Suspected Sulfur Dioxide Injury on Virginia Pine
Crowing 1.5 Miles from a Source
4-21
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
Plate 4-19. Acute Sulfur Dioxide Injury to Tulip. Note Ivory-Colored Injury Occurs
at Leaf Tips and Margins
4-23
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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-
5-1
-------
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.
5-2
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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-
5-3
-------
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.
5-4
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
5-5
-------
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
5-6
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
5-7
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
5-9
-------
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
5-10
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
Plate 5-3. Marginal and Intercostal Necrosis of a Grape Leaf
Plate 5-4. Hydrogen Fluoride Injury to Poplar (Field Exposure)
5-20
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
Plate 5-5. Oregon Grape with Symptoms Mimicking Fluoride Injury, Cause Not Known
Plate 5-6. Lamb's Quarters Showing HF'-Induced Injury
5-21
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
Plate 5-9. Fluoride-Induced Injury on Gladiolus Foliage
Plate 5-10. Fluoride-Induced Injury on Fir; Note Several Uninjured Needles
5-23
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
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.
I
I
I
I
I
I
I
I
I
I
I
I
6-9
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
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.
6-15
-------
I
I
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
6-16
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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.
6-18
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
6-20
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
£
I
(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.
6-22
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
6-24
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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.
6-26
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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.
6-27
-------
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.
6-28
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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.
I
I
I
I
I
I
I
I
6-30
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
6-33
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
6-35
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
Plate 6-9. Hydrogen Chloride Injury to Black Cherry Showing Leaf Spotting
Plate 6-10. Hydrogen Chloride Injury on Norway Spruce Showing Tip Necrosis
6-37
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
Plate 6-13 Ammonia Injury on Poison Ivy Showing Blackened Appearance
Plate 6-14. Ammonia Injury on Cotton
6-39
-------
Plate 6-15 Cement Dust Deposit on Fir Branch
Plate 6-16. Lime Dust Deposit on Spruce Twigs on the flight
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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.
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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.
-------
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.
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
Plate 8-1. Heat Injury to Roadside Trees Caused by
Street Paving
-------
Plate 8-2. Winter Injury to Boxwood and Deoc/ora Cedar. Many Different Agents
Could Cause Similar Damage
8-10
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
8-11
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
Plate 8-16. Eastern White Pine with Oyster Scale Insect Injury.
Note Similarity to Air Pollution Injury
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
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.
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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.
9-7
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
10-1
-------
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-
10-2
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
10-4
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
10-5
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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.
10-7
-------
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.
10-8
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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.
10-9
-------
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
10-10
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
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
10-11
-------
I
I
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
I
I
I
I
I
I
I
10-12
I
I
I
-------
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
-------
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
10-14
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
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
10-15
-------
I
I
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
I
I
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
10-16
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
10-17
-------
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
I
I
I
I
I
I
I
I
10-18
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
I
I
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
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
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
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------An error occurred while trying to OCR this image.
-------An error occurred while trying to OCR this image.
-------An error occurred while trying to OCR this image.
-------An error occurred while trying to OCR this image.
-------An error occurred while trying to OCR this image.
-------An error occurred while trying to OCR this image.
-------An error occurred while trying to OCR this image.
-------An error occurred while trying to OCR this image.
-------An error occurred while trying to OCR this image.
-------An error occurred while trying to OCR this image.
-------An error occurred while trying to OCR this image.
-------An error occurred while trying to OCR this image.
-------An error occurred while trying to OCR this image.
-------An error occurred while trying to OCR this image.
-------An error occurred while trying to OCR this image.
-------An error occurred while trying to OCR this image.
-------An error occurred while trying to OCR this image.
-------An error occurred while trying to OCR this image.
-------An error occurred while trying to OCR this image.
-------An error occurred while trying to OCR this image.
-------An error occurred while trying to OCR this image.
-------An error occurred while trying to OCR this image.
-------An error occurred while trying to OCR this image.
-------An error occurred while trying to OCR this image.
-------An error occurred while trying to OCR this image.
-------An error occurred while trying to OCR this image.
-------An error occurred while trying to OCR this image.
-------An error occurred while trying to OCR this image.
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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).
E-3
-------
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.
I
I
I
I
I
I
I
I
I
I
I
E-4
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
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
-------
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
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
-------
Q<
o
1 £
cc
Cub _j
W«> o.
s
§00
o
Q.
03
*
c
f- o 2-c
0.2 »* £
Silo
»-.>.£ z
OQ E -
z g |-
O § -g
1° I
£ |
IX
LU
3
CL
§1
m?
_i a:
< O
08:
°
2
I
I
I
I
O)
Ql
CO o
'C C
a>
1 S>
E §>
« (0
£
*n
u
o|
hi <1>
Z 0)
-§»
o «
>£
t T3
^ (0
o.
UJ
O
Z
z
o
<
o
MM
_J
CO
a
^
1
1
I
1
1
1
1
1
I
I
1
------- |