United Slates Science Advisory EPA-SAB-CASAC-LTR-92-017
Environmental Board (A-101) August, 1992
Protection Agency
EPA CASAC REVIEW COMMENTS
DRAFT "AIR QUALITY
CRITERIA FOR OXIDES OF
NITROGEN"
CLEAN AIR SCIENTIFIC ADVISORY
COMMITTEE COMMENTS ON DRAFT "AIR
QUALITY CRITERIA FOR OXIDES OF
NITROGEN" DEVELOPED BY THE
ENVIRONMENTAL CRITERIA AND
ASSESSMENT OFFICE (ECAO), RESEARCH
TRIANGLE PARK, N.C.
-------
SUMMARY
The Clean Air Scientific Advisory Committee met on April 27-28 to
review the draft "Air Quality Criteria for Oxides of Nitrogen." The
Committee's general reaction to this draft was favorable and is of the
opinion that this air quality criteria document with appropriate revision
will provide a scientifically adequate basis for regulatory decisions on
NOX.
The Committee provides substantial written comments and
suggestions for use by this Agency in revising the draft criteria document.
-------
TABLE OF CONTENTS
General Comments
Page Number
Chapter 1 1-2
Chapter 2 2
Chapters 2
Chapter 4 3
Chapter 5 3
Chapters 3
Chapter 7 4
Chapter 8 4
Chapter 9 4
Chapter 10 4
Chapter 11 4
Chapter 12 4-10
Chapter 13 10-14
Chapter 14 14-26
Chapter 15 26-27
Chapter 16 28
Summary
Chapter 1: Summary
1.1 Critical Issues 29
1.1.2 Organization of the Document 29
1.2 Chemistry, Sources, Transport 29
1.2.1 Chemical and Physical Properties 29
1.2.2 Sources of Nitrogen, Oxides Influencing 30
1.2.3.1 Ozone Production 30
1.2.3.2 Production of Odd Nitrogen Species 30
1.2.3.4 Oxides of Nitrogen and the Greenhouse Effect 30
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Summary (Continued) Page Number
1.2.5.1 Ambient Concentration 30
1.3 Effects of Nitrogen Oxides on Vegetation 31
1.3.1 Effects of Nitrogen Oxides on Vegetation 31
1.3.1.1 Introduction 31
1.3.1.2 Nitrogen Dioxide 31-32
1.3.2 The Effects of Nitrogen Oxides 32
1.3.2.1 Ecosystems: Structure, Function, Response 32
1.3.2.2 Nitrogen Deposition 32-33
1.3.2.3 Effects of Deposited Nitrogen 33
1.3.2.4 Effects of Nitrogen on Sensitive Terrestrial 33
1.3.2.5 Nitrogen, Saturation, Critical Loads 33-34
1.4 Health Effects on Oxides of Nitrogen 34
1.4.2 Epidemiology Studies of Oxides of Nitrogen 34
Chapter 2: Introduction
2. Introduction 35
Chapter 3: General Chemical and Physical Properties
of NOX Derived Pollutants
3.1 Introduction and Overview 36
3.2 Nitrogen Oxides 36
3.2.1 Nitric Oxide (NO) 37
3.2.2 Nitrogen Dioxide (NO2) 37
3.2.4 Nitrogen Trioxide (NO3) 38
3.2.6 Dinitrogen Tetroxide (^04) 38
3.3 Nitrates, Nitrites, and Nitrogen Acids 38
3.4 Ammonia (NH^) 38
3.5 N-NITROSO Compounds 38
3.6 Summary 39
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Page Number
Chapter 4: Sources of Nitrogen Oxides Influencing
Ambient and Indoor Air Quality
4.1 Introduction 40
4.2 Ambient Sources of Nitrogen Oxides 40
4.2.1 Combustion Generated NOX Emissions 40
4.2.1.2 Generation of NOX From Lightning 40
4.2.1.3 Generation of NOX From Soils 40
4.2.2 Removal of NOX From The Atmosphere 41
4.2.3 Global Budgets for NOX 41
4.2.4 Major Sources of NOX Emissions in the U.S 41
4.2.5 Conclusions 42
4.3.2 Formation of Nitrogen Oxides in Combustion 42
4.3.3 Gas Stoves Used For Cooking 42
^
4.3.3.2-4.3.3.8 42
4.3.4 Unvented Space Heaters Fueled With Natural Gas 42
4.3.4.7 Summary of Emissions from Unvented Gas 42
4.3.8 Comparison of Emissions from Sources 42
4.4 Summary of Emissions of NOX 43
Chapter 5: Transport and Transformation of
Nitrogen Oxides
5.1 Background 44
5.2 The Role of NOX in Ozone Production 44
5.2.1 NOX-Rich Chemistry 44
5.2.2 Ozone Production in NOX -Poor Environments 45-46
5.3 Odd Nitrogen Species 46
5.3.1 Nitric Acid 46
5.3.7 Summary of NOy Species 46
5.3.8 Amines, Nitrosamines, and Nitramines 46
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UNITED STATES ENVIRONMENTAL PROTECTION AGENCY
WASHINGTON, D.C. 20460
August 11, 1992
EPA-SAB-CASAC-LTR-92-017
Honorable William K. Reilly THEADM^STRATOR
Administrator
U.S. Environmental Protection Agency
401 M St., S.W.
Washington, D.C. 20460
Subject: Clean Air Scientific Advisory Committee Closure on the
ECAO Air Quality Criteria for Oxides of Nitrogen
Dear Mr. Reilly:
The Clean Air Scientific Advisory Committee (CASAC) of EPA's Science
Advisory Board (SAB) met on April 27-28, 1992 to review the draft document
Air Quality Criteria for Oxides of Nitrogen (NOx). During this session, the Committee
concentrated on assessing the document's adequacy with regard to reviewing the
available scientific data and relevant studies of oxides of nitrogen. It was the
consensus of the Committee that the document is generally well prepared and with
appropriate revision will provide an adequate scientific basis for regulatory decision
on oxides of nitrogen. To facilitate further development of the document criteria, the
Committee has provided detailed comments by chapter for the Agency's consideration
(see attached report).
On behalf of the CASAC, I would like to thank the EPA staff for their efforts in
preparing the first draft of the NOx document. The CASAC looks forward to
commenting on the next draft and on the related staff position paper.
Sincerely
Roger O. McClellan, D.V.M.
Chairman
Clean Air Scientific Advisory Committee
Printed 01
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-------
United States Science Advisory EPA-SAB-CASAC-LTR-92-017
Environmental Boars (A-101) August, 1992
Protection Agency
EPA CASAC REVIEW COMMENTS:
DRAFT "AIR QUALITY
CRITERIA FOR OXIDES OF
NITROGEN"
CLEAN AIR SCIENTIFIC ADVISORY
COMMITTEE COMMENTS ON DRAFT "AIR
QUALITY CRITERIA FOR OXIDES OF
NITROGEN" DEVELOPED BY THE
ENVIRONMENTAL CRITERIA AND
ASSESSMENT OFFICE (ECAO), RESEARCH
TRIANGLE PARK, N.C.
-------
SUMMARY
The Clean Air Scientific Advisory Committee met on April 27-28 to
review the draft "Air Quality Criteria for Oxides of Nitrogen." The
Committee's general reaction to this draft was favorable and is of the
opinion that this air quality criteria document with appropriate revision
will provide a scientifically adequate basis for regulatory decisions on
NOX.
The Committee provides substantial written comments and
suggestions for use by this Agency in revising the draft criteria document.
-------
TABLE OF CONTENTS
General Comments
Page Number
Chapter 1 1-2
Chapter 2 2
Chapter 3 2
Chapter 4 3
Chapter 5 3
Chapters 3
Chapter 7 4
Chapter 8 4
Chapter 9 4
Chapter 10 4
Chapter 11 4
Chapter 12 4-10
Chapter 13 10-14
Chapter 14 14-26
Chapter 15 26-27
Chapter 16 28
Summary
Chapter 1: Summary
1.1 Critical Issues 29
1.1.2 Organization of the Document 29
1.2 Chemistry, Sources, Transport 29
1.2.1 Chemical and Physical Properties 29
1.2.2 Sources of Nitrogen, Oxides Influencing 30
1.2.3.1 Ozone Production 30
1.2.3.2 Production of Odd Nitrogen Species 30
1.2.3.4 Oxides of Nitrogen and the Greenhouse Effect 30
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Summary (Continued) Page Number
1.2.5.1 Ambient Concentration 30
1.3 Effects of Nitrogen Oxides on Vegetation 31
1.3.1 Effects of Nitrogen Oxides on Vegetation 31
1.3.1.1 Introduction 31
1.3.1.2 Nitrogen Dioxide 31-32
1.3.2 The Effects of Nitrogen Oxides 32
1.3.2.1 Ecosystems: Structure, Function, Response 32
1.3.2.2 Nitrogen Deposition 32-33
1.3.2.3 Effects of Deposited Nitrogen 33
1.3.2.4 Effects of Nitrogen on Sensitive Terrestrial 33
1.3.2.5 Nitrogen, Saturation, Critical Loads 33-34
1.4 Health Effects on Oxides of Nitrogen 34
1.4.2 Epidemiology Studies of Oxides of Nitrogen 34
Chapter 2: Introduction
2. Introduction 35
Chapter 3: General Chemical and Physical Properties
of NOX Derived Pollutants
3.1 Introduction and Overview 36
3.2 Nitrogen Oxides 36
3.2.1 Nitric Oxide (NO) 37
3.2.2 Nitrogen Dioxide (NO2) 37
3.2.4 Nitrogen Trioxide (NO3) 38
3.2.6 Dinitrogen Tetroxide (N2O4) 38
3.3 Nitrates, Nitrites, and Nitrogen Acids 38
3.4 Ammonia (NH3) 38
3.5 N-NITROSO Compounds 38
3.6 Summary 39
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Page Number
Chapter 4: Sources of Nitrogen Oxides Influencing
Ambient and Indoor Air Quality
4.1 Introduction 40
4.2 Ambient Sources of Nitrogen Oxides 40
4.2.1 Combustion Generated NOX Emissions 40
4.2.1.2 Generation of NOX From Lightning 40
4.2.1.3 Generation of NOX From Soils 40
4.2.2 Removal of NOX From The Atmosphere 41
4.2.3 Global Budgets for NOX 41
4.2.4 Major Sources of NOX Emissions in the U.S 41
4.2.5 Conclusions 42
4.3.2 Formation of Nitrogen Oxides in Combustion 42
4.3.3 Gas Stoves Used For Cooking 42
X
4.3.3.2-4.3.3.8 42
4.3.4 Unvented Space Heaters Fueled With Natural Gas 42
4.3.4.7 Summary of Emissions from Unvented Gas 42
4.3.8 Comparison of Emissions from Sources 42
4.4 Summary of Emissions of NOX 43
Chapter 5: Transport and Transformation of
Nitrogen Oxides
5.1 Background 44
5.2 The Role of NOX in Ozone Production 44
5.2.1 NOX-Rich Chemistry 44
5.2.2 Ozone Production in NOX-Poor Environments 45-46
5.3 Odd Nitrogen Species 46
5.3.1 Nitric Acid 46
5.3.7 Summary of NOy Species 46
5.3.8 Amines, Nitrosamines, and Nitramines 46
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UNITED STATES ENVIRONMENTAL PROTECTION AGENCY
WASHINGTON, D.C. 20460
August 11, 1992
EPA-SAB-CASAC-LTR-92-017
Honorable William K Reillv OFFICE OF
liUiiuiauic vviuiain r\. noiny THE ADMINISTRATOR
Administrator
U.S. Environmental Protection Agency
401 M St., S.W.
Washington, D.C. 20460
Subject: Clean Air Scientific Advisory Committee Closure on the
ECAO Air Quality Criteria for Oxides of Nitrogen
Dear Mr. Reilly:
The Clean Air Scientific Advisory Committee (CASAC) of EPA's Science
Advisory Board (SAB) met on April 27-28, 1992 to review the draft document
Air Quality Criteria for Oxides of Nitrogen (NOx). During this session, the Committee
concentrated on assessing the document's adequacy with regard to reviewing the
available scientific data and relevant studies of oxides of nitrogen. It was the
consensus of the Committee that the document is generally well prepared and with
appropriate revision will provide an adequate scientific basis for regulatory decision
on oxides of nitrogen. To facilitate further development of the document criteria, the
Committee has provided detailed comments by chapter for the Agency's consideration
(see attached report).
On behalf of the CASAC, I would like to thank the EPA staff for their efforts in
preparing the first draft of the NOx document. The CASAC looks forward to
commenting on the next draft and on the related staff position paper.
Sincerely,
Roger 0. McClellan, D.V.M.
Chairman
Clean Air Scientific Advisory Committee
Printed on Recycled Paper
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AIR QUALITY CRITERIA FOR OXIDES OF NITROGEN (NOX) REVIEW
CLEAN AIR SCIENTIFIC ADVISORY COMMITTEE
SCIENCE ADVISORY BOARD
CHAIRMAN AND MEMBERS
Dr. Roger O. McClellan, Chairman, Chemical Industry Institute of Toxicology
Research Triangle Park, NC
Dr. Glen R. Cass, California Institute of Technology, Pasadena, CA
Dr. Joe Mauderly, Inhalation Toxicology Research Institute, Albuquerque, NM
D r. Marc B. Schenker, University of California, Davis, CA
Dr. Mark J. Utell, University of Rochester Medical Center, Rochester, NY
Dr. George T. Wolff, General Motors Research Laboratories, Warren, Ml
CONSULTANTS
Dr. William C. Adams, University of California, Davis, CA
Dr. John Balmes, San Francisco General Hospital, San Francisco, CA
Dr. Douglas Dockery, Harvard School of Public Health, Boston, MA
Dr. James Renters, IIT Research Institute, Chicago, IL
Dr. Gareth Green, Harvard School of Public Health, Boston, MA
Dr. Robert Mercer, Duke University Medical Center, Durham, NC
Dr. John Skeliy, Pennsylvania State University, University Park, PA
Dr. Michael Symons, University of North Carolina, Chapel Hill, NC
Dr. Warren White, Washington University, St. Louis, MO
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SCIENCE ADVISORY BOARD STAFF
Mr. Randall C. Bond, Designated Federal Official
Clean Air Scientific Advisory Committee, Science Advisory Board
U.S. Environmental Protection Agency
Ms. Janice Jones, Staff Secretary, Clean Air Scientific Advisory Committee
Science Advisory Board, U.S. Environmental Protection Agency
Dr. Donald G. Barnes, Director, Science Advisory Board
U.S. Environmental Protection Agency
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Page Number
5.4 Transport 47
5.4.1 Transport of Reactive Nitrogen 47
5.4.2 Transport and Chemistry in NOX -Rich Plumes 47
5.4.3 Regional Transport 47
5.5 Oxides of Nitrogen and the Greenhouse Effect 48
5.5.2 Nitrous Oxide Greenhouse Contributions 48
5.6 Stratospheric Ozone Depletion by Oxides 48-49
5.7.1 Dry Deposition of Nitrogen Oxides 49
5.7.2 Methods of Determining V,j 49
5.7.2.1 Eddy Correlation 49
5.7.2.2 Vertical Gradient Methods 49
5.7.3 NOX Deposition 49
5.7.5 PAN Deposition 49
5.7.6 Wet Deposition of Nitrogen Oxides 50
5.8 Summary and Conclusions 50
5.8.2 Production of Odd Nitrogen Species 50
5.8.3 Transport 50
5.8.4 Oxides of Nitrogen and the Greenhouse Effect 50
5.8.5 Deposition of Nitrogen Oxides 51
Chapter 6: Sampling and Analysis for Oxides of
Nitrogen and Related Species
6.10 Paniculate Nitrate (PN) 52
6.7 Nitric Acid (HNO3) 52
6.7.3 Chemiluminescence (CLM) 52
Chapter 7: Ambient and Indoor Concentrations of
Nitrogen Dioxide
7.2.4.2 Diurnal Patterns 53
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Page Number
7.3.2 Residences Without Indoor Sources 53
7.3.3.1 Average Indoor Concentrations and Estimated 53
7.4 Nitric and Nitrous Acids Concentrations 53
Chapter 8: Assessing Total Human Exposure to
Nitrogen Dioxide
8.1 Introduction 54
8.2.2 Personal Monitoring 54
8.3 Indirect Methods 55
8.3.1 Personal Exposure Models 55
Chapter 9: Effects of Nitrogen Oxides on Vegetation
9.1 Introduction 56
9.2.1 Experimental Design and Statistical Analysis 56
9.2.2.1 Supply 56
9.2.3 Pollutant Climatology 57
9.2.4 Pollutant Chemistry 57
9.2.5.1 Plant Response 57
9.2.5.2 Pollutant Exposure 57-58
9.3.1.1 External NOX Ratios Around Leaves 58
9.3.1.3 Foliar Uptake of Nitrate 58
9.3.1.5 Access of NOX Into Leaves 58
9.3.1.6 Access of the Products of NOX Into Cells 59
9.3.1.7 Levels of the Products of NOX In Cells 59
9.3.2 Chemical and Biochemical Responses 59
9.3.2.1 Nitrate Reductase Activities 59
9.3.2.2 Nitrate Reductase 59
9.3.2.5 Effects of Ammonia 59
9.3.4.2 Changes Inside Cells and Tissues 60
9.4 Exposure - Response Relationships 60
9.4.1 Foliar Injury and Loss in Aesthetic Value 60
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Page Number
9.4.1.1 Characteristics of Foliar Symptoms 60
9.4.2 Loss in Growth and Yield 60
9.5.1.1 Species of Plant 61
9.5.1.3 State of Development 61
9.5.2 Environmental Conditions 61
9.6 Effects of Pollutant Mixtures 61-62
9.6.4 Field Chamber and Field Studies 62
9.7 Discussion and Summary 62
9.9 Toxic Reactions in the Tissues 62
9.9.1 Concept of Exposure Index 62
Chapter 10: The Effects of Nitrogen Oxides on Natural
Ecosystems and their Components
10.1 Introduction : 63
10.1.2.3 Ecosystem Response: Impairment of Functions 63
10.1.3 The Nitrogen Cycle 63
10.1.3.1 Biological Nitrogen Fixation 64
10.1.3.5 Denitrification 64
10.2 Dry Deposition 64
10.2.1 Types of Measurements 64
10.2.3 Processes Governing Deposition of Gases 64
10.2.4.1 Nitrogen Dioxide 64
10.2.5 Deposition of "N" Forms to Non-Foliar Surfaces 64
10.3 Effects of Vegetation and Soils 65
10.3.1 Introduction 65
10.3.2 Pollutant N Inputs and Nitrogen Cycling 65
10.3.3.2 Fate of N from Pulse Fertilization 65-66
10.3.4 Effects of Pollutant N Inputs on Soils 66
10.3.4.1 Soil Biota 66
10.3.4.2 Soil Chemistry 66
10.3.6 Effects of Pollutant N Deposition 66-67
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Page Number
10.3.6.2
10.3.6.3
10.3.7
10.3.9
10.4.2
10.4.3
10.4.3.1
10.4.3.2
10.5
10.5.1
10.5.2
10.5.4.4
10.5.4.5
10.6.2.3
10.6.3.1
10.6.3.3
10.6.4.3
10.7
10.7.1
10.7.3
10.7.4
10.7.5
10.7.6
Chapter
11.1
11.2
11.3
11.4
11.5
11.5.1
11.5.2
Soil-Mediated Effects on Vegetation
Ecosystem Level Responses to N Deposition
Critical Loads for Atmospheric N Deposition
Conclusions
Indirect Effects
N Saturation, Critical Loads, and Current
Critical N Loads that have been Proposed
Current Rate of Total N Deposition
Ecosystems Effects-Wetlands and Bogs
Introduction
Atmospheric Nitrogen Inputs
Effects on Biotic Diversity
Mechanisms of Nitrogen Control
Nitrogen Saturation
Chronic Acidification
Biological Effects
Evidence for Nitrogen Deposition Effects
Discussion and Summary
Introduction
Nitrogen Deposition
Effect of Deposited Nitrogen on Forest Vegetation
Effects of Nitrogen on Terrestrial Vegetation
N Saturation, Critical Loads
11: Effects of Nitrogen Oxides on Visibility
Overview of Light Scattering and Absorption
Atmospheric Discoloration
Visual Range Reduction
Nitrate Phase Changes and Hygroscopicity
Role of Nitrogen Oxides in Urban Haze
California Urban Areas
Urban Areas in the Western United States
67
67
68
68-69
69
69
69
69-70
70
70
71
71
71
72
72
72
72
73
73
73
74
75
75
76
77-78
79
79
80
80-82
82
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Page Number
11.5.4 Modeling Urban Haze Effects 83
11.6.1 Nonurban Areas of the Western U.S 83
11.6.2 Nonurban Areas of the Eastern U.S 83
11.6.3 Modeling Regional Haze Effects 84
11.7 Role of Nitrogen Oxides in Plume 84
11.8 Contributions of Nitrogen Oxides 84
11.9 Summary of Effects of Visibility 85
11.10.1 Basic Concepts of Economic Valuation 85
11.10.3.2 Economic Valuation Studies for Urban Haze 85
11.10.4 Conclusions 85
References Not Already Cited in Chapter 11 86-87
Chapter 12: Effects of Nitrogen Oxides on Materials
12.1.3 Deposition Process 88
12.1.4 Chemical Interactions of Nitrogen Oxide Species 88
12.2.1 Fading of Dyes by Nitrogen Oxides 89
12.2.2 Degradation of Textile Fibers 89
12.3.1 Chemical Changes Induced by Nitrogen Oxides 89
12.4 Effects of Nitrogen Oxides in the Corrosion Process 89
12.4.2 Effect of Nitrogen Oxides on Economically 89
12.6 Effects of Nitrogen Oxides 90
12.8 Costs of Materials Damage 90
Chapter 13: Studies of the Effects of Nitrogen Compounds
on Animals
13.1 Introduction 91
13.2.1.2 Principles of Gas Uptake and Dosimetry Models 91
13.2.1.3 Dosimetry of Nitrogen Oxides 92
13.2.2 Mortality 92
13.2.3.1 Host Defense Mechanisms 92-96
13.2.3.2 Lung Biochemistry 96
13.2.3.3 Pulmonary Function 96-97
13.2.3.4 Morphologic Studies 97-99
13.2.4 Extrapulmonary Effects 99
13.2.4.1 Body Weight 99
13.2.4.3 Cardiovascular Effects 100
13.2.4.4 Hepatic Function 100
13.2.4.5 Effects on the Kidney and on Urine Content 100
13.2.4.6 Effects on the Central Nervous System 100
13.2.4.8 Potential Carcinogens 100
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Page Number
13.3 Effects of Mixtures Containing NO2 101
13.4 Nitric Oxide 101-102
13.5 Nitric Acid and Nitrates 102
13.6 Summary 102
13.6.3 Summary Effects on Host Defenses 102-103
13.6.4 Effects of Chronic Exposure 103
13.6.7 Susceptibility of Subpopulations 104
Chapter 14: Epidemiology Studies of Oxides of Nitrogen
14.1 Introduction 105
14.2 Studies of Respiratory Illness 105
14.2.1 United Kingdom Studies 106
14.2.2 U.S. Six Cities Studies 106
14.2.4 Iowa Study 107
14.2.5 Dutch Studies 107
14.2.6 Ohio Studies 107
14.2.8 Connecticut Study 107
142.11 Maryland. Study. 1Q7
14.2.12 Glendora, California Study 107
14.3.3 New York Study 107
14.5.3 Quantitative Analysis 108
14.7 Summary 108-109
Chapter 15: Controlled Human Exposure Studies of
Oxides of Nitrogen
15.1 Introduction 110
15.2.1 Lung Function Effects of NO2 110
15.2.1.1 Concentrations Above 1.0 ppm 110
15.2.3 Effects of NO2-Gas 110
15.2.4 Summary 111
15.3.1 The Effects of NO2 on Asthmatics 111-112
15.3.1.1 Effects of HNO3 Vapor on Asthmatics 112-113
15.3.2 Effects of NO2 on Patients 113
15.3.3 Summary 113
15.4.2 Asthmatic Subjects 113-114
15.6 Effects of NO2 or HNO3 Vapor Exposure 114-115
15.8 Conclusions and Discussion 115-116
Appendix 15A 117
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Page Number
Chapter 16: Health Effects Associated with Exposure
to Nitrogen Dioxide
16.2 Ambient and Indoor Nitrogen Dioxide Levels 118
16.3.1 Airway Reactivity in Asthmatics 118-119
16.3.2 Respiratory Morbidity in Children 119
16.3.3 Biological Bases Relating NO2 Exposure 120
16.3.4 Emphysema and Exposure to NO2 121
16.3.5 Subpopulations Potentially Susceptible 122
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GENERAL COMMENTS
REVIEW DRAFT-AIR QUALITY CRITERIA FOR OXIDES OF NITROGEN--VOL
CHAPTER 1 Summary of Effects of Oxides of Nitrogen and Related
Compounds on Human Health and Welfare
Many chapter summaries fail to act as a sharply written version of the important
facts that are known about the issues at hand as stated in the text of each
chapter.
Chapter 1 is then assembled by gathering together information from these often
inadequate chapter summaries. This in turn results in a version of Chapter
that is not well written nor an adequate summary of the contents of the report.
Recommendation: Examine chapter summaries closely to increase their factual
content and level of reference citation, focusing on positive statements about
what is known about the subjects at hand and make certain it is included in
Chapter 1.
Terminology needs to be standardized throughout the document. There are
many conflicting uses of the symbol NO3, e.g., used as aerosol nitrate,
nitrate radical, nitrate radical called nitrogen trioxide.
Chapter 1 needs total revision. It should not be condensations of the
Chapter summaries. It should highlight the most important issues concerning
NOX. It may benefit from review by the authors of the individual chapters.
Recommendation: Suggest NO3 reserved for nitrate radical and spell out
aerosol nitrate. Settle on single clear definitions for NOX and NOy and use
them consistently.
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o Inconsistent definitions of nitrogen oxides (or oxides of nitrogen) and NOy are
used throughout the text. In addition, the nomenclature for individual species
vary from chapter to chapter.
o Some of the authors, in some of the chapters designate some of the free
radicals with a dot, while most of the time, most of the authors don't use a
dot, and some of the radicals never have a dot.
o Similarly, other chapter summaries need extensive revisions. In most cases,
they do not reflect the main points raised in the body of the chapters, and
and, in some cases, introduce new information.
Recommendation: Chapter authors should write summaries. If this cannot be
accomplished, they should at least review them.
o In reviewing Chapter 1, 36 pages are devoted to ecological effects, 29 pages to
animal and human studies (10 for animal).
o Recommendation: In revising Chapter 1, achieve a better balance in coverages
of ecological effects, animal studies and human studies.
CHAPTER 2 Introduction
No general comments.
CHAPTER 3 General Chemical and Physical Properties of NOx and NOX
-Derived Pollutants
o Gas phase and aerosol phase are not mentioned, but they should be
(e.g., nitro aromatics).
-2—
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CHAPTER 4 Sources of Nitrogen Oxides Influencing Ambient and Indoor
Air Quality
o Overall, the main observation that came out of the committee's discussion
centered on closing the gap between the continental scale discussion of
emissions to the outdoor atmosphere vs. the single flame scale discussion
of indoor emissions. Enough of that discussion is contained in the minutes
of the meeting that it will not be covered again here.
CHAPTER 5 Transport and Transformation of Nitrogen Oxides
o In general, Chapter 5 would benefit from more references. Whenever
a factual statement is made, an appropriate reference should be cited.
o Sections 5.5 and 5.6: EPA should seek another reviewer on this section;
no one on the CASAC panel is an expert in that area.
o The reference list for Chapter 5 should be rechecked to fill in missing
information. Biermann et al. (1988) if submitted four years ago probably]
has been printed by now; Easter et al. 1978 reference is incomplete, as is
Hanson and Mauersberger (1988), etc. There are several others like this.
CHAPTER 6 Sampling and Analysis for Oxides of Nitrogen and Related
Species
No general comments.
-3-
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CHAPTER 7 Ambient and Indoor Concentrations of Nitrogen Dioxide
No general comments.
CHAPTER 8
No general comments.
CHAPTER 9 Effects of Nitrogen Oxides on Vegetation
CHAPTER 10 The Effects of Nitrogen Oxides on Natural Ecosystems
and Their Components
CHAPTER 11 Effects of Nitrogen Oxides on Visibility
CHAPTER 12 Effects of Nitrogen Oxides on Materials
Major points related to both Chapters 9 and 10 and which should also be
considered for the Volume I Summary include:
o A section (somewhere in the whole of the Criteria Document) should be
included and reflect what actual ambient NO, N02, and NOx exposures
are in the US according to the most recent data sets available. Although
perhaps placed into a single section of Chapter 7, such data should be
placed up front in Chapters 9 and 10 so as to offer a quick perspective
of the cited studies concerning agricultural crop, native plant and
"ecosystem" (managed and unmanaged) effects.
o The overall importance of "NOx" as a regional scale air pollutant lies in its role
as a precursor to ambient ozone exposures across much of the eastern US and
west coast air sheds. "NOx" as a phytotoxicant is of minor importance as a
direct phytotoxicant to plants under field conditions anywhere in the US at
current ambient expected doses. Hence, the role of NOx is photochemically
-4-
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produced ozone takes on its greatest significance which losses accountable
in agriculture and forest crops downwind in major urban/industrial centers.
It is this point which should draw most attention to our concerns for continuing
productivity and health of our forest crops and natural ecosystems as brought
about by anthropogenic emissions of "NOx".
Both chapters need some attention to the elimination of conjecture and
subjective statements. Phrases such as "likely to be," "could possibly," "may
be," "could be," and "has the potential to" should be altered to reflect current
scientific knowledge or be eliminated from the document. With today's press
and some science based advocates, any statement which discusses a potential
effect very quickly rolls around to becoming a tort for dispersal to the general
public. Misnomers such as forest decline, acid rain, and the use of subjective
observations should have no place in a Criteria Document.
The conclusions of both chapters should become more precise and reflect the
contents of the chapters as well as be reflected in the Introduction within
Chapter 1 and Volume 1.
As a point raised during the review session, support is given for some additional
reference to the economic considerations of O3 as a direct phytotoxicant with
NOx and VOC's as precursors. Ozone effects to crops and forests is of great
concern in this relationship to nitrogen oxides.
The issue (concept) of critical loads should be removed from the Criteria
Document due to many of the reasons stated within the document. A brief
paragraph describing the concept as employed in central Europe would be
acceptable but the multiple references made o the concept should be
deleted.
Nitric Acid Vapor (HNO3).
The first page of the volume (Chapter 9) lists the principle phytotoxic
compounds as being NO and NO2. This initiation is only partly accurate,
since the last decade has shown that from a vegetation perspective (at least in
North America) that nitric acid vapor (HNO3) is at least as important as NO2 and
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certainly more significant than NO. The chapter on Ecosystems (Chapter 10)
clearly addresses this issue. From a direct effects perspective, NO2 is more
toxic but from an ecological perspective, HNO3 is more important. Its exclusion
seems odd. If not here, in what document is it addressed?
Organization.
The general organization is appropriate. However, there are
innumerable occasions in which the material seems repetitious. The most
obvious is that of nitrogen deposition and the issue of critical loads. In many
cases it was difficult to figure out why the material was being repeated.
Moreover, there were sections being repeated that discussed the concepts
but used different references (e.g., critical loads in the ecosystem and
wetlands section.).
Los Angeles Basin.
Recent studies out of Riverside have indicated that the assumed
ozone-specific effects on forest resources within the LA Basin are not
strictly accountable to ozone. The data indicate that there is a very signifi-
cant nitrogen deposition gradient that co-occurs with ozone; the inference is
the some of the a consequence of co-deposition of ozone and nitrogen oxides
(HNO3). This conclusion has relevance to this document. Interestingly, the
section on deposition notes that Hill calculated rates of nitrogen deposition,
"1 "1
* 100 kg ha" V" for tne ^ Qas^> and Yet tnis information is not discussed.
Given the long periods of dry deposition (little rainfall) and the emissions of
nitrogen compounds from the industrialized LA Basin that forest ecosystems
are experiencing high rates of N deposition and that the rates co-vary with
ozone.
Critical Loads of Nitrogen.
The argument used is that the critical loads concepts is flawed (note:
this flawed aspect is discussed in the forest section which is not embraced in
the section on wetlands and estuaries). However, this document does not go
far enough in emphatically pointing out the problem in using the concept in the
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standard setting process. For example, the following incoherent logic flow:
(i) critical loads of nitrogen might be a low as 1-3 kg N ha"1 y"1 for sensitive
ecosystems,
(ii) nitrogen loads in North America range from 5-26 kg N ha"1 y~1, and
(iii) there is no evidence that the chronic deposition of nitrogen is a problem.
If the critical loads of nitrogen are even close to 1-3 kg ha"1 y"1 as the
European community believes and some sites in North America experience
26 kg ha"1 y"1, the logic in the document is not consistent. The nitrogen loads
concept should be removed. However, since reality dictates its inclusion, the
problem is obvious unless there is a more explicit and quantitative analysis of
the uncertainty in using the critical threshold analysis.
It is also important that the concept be applied similarly across sections of
the document. As currently presented, the uncertainty is well presented in the
section on forests, but the same degree of uncertainty is not applied to wetlands
and estuaries.
Co-occurences of Nitrogen and Ozone.
The document concludes that NC>2 and ozone do not co-occur as
phytotoxicants. However, the document discusses at length the fact that
in natural ecosystems the deposition of HNC>3 is far more important than that
of NO2- The co-deposition of HNO3 and ozone is statistically significant
at least in the eastern part of the United States and this relationship has a
strong first principles basis. Thus, ecosystems experiencing high deposition
rates of ozone also experience high deposition rates of HNQj. From a natural
ecosystem perspective, this is important.
Use of Non-Peer Reviewed Literature.
The section on the Chesapeake Bay is based in large measure on data
that are available in non-refereed documents. Non-refereed publications
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should not be included. Even more disturbing is the fact that the section has
received high visibility in this document. The implicitly stated position is that
the Criteria Documents can now be based on information that has not received
peer review.
One of the problems is that the data in this volume are presented in
deposition units that differ from the remainder of the document. All of the
previous sections use kg ha"1 yV Conversely, this section uses e.g.,
10^ y"1. In order to establish how comparable the numbers are to other parts
of the section, it requires conversion of equivalents to kg and knowledge of the
land use for the area (forests, grasslands, croplands, and surface waters). One
option might be to provide additional columns in the tables that show what are
the rates of N deposition to forest within the Chesapeake Basin in units that can
be presented in a comparable fashion to allow a comparison fashion to allow
comparison among sections.
Uncertainty Analysis of HNO^ Inputs:
For natural ecosystems and the issue of nitrogen loading, the deposition
of HNO3 is the key component since it accounts for approximately 50% of the
total deposition. The fact that HNOs is important is probably the single biggest
difference between this document and its predecessor since none of the
previous efforts even included HNO3- HNO3 deposition is measured
inferentially and there is no existing capability to use micrometerological
eddy correlation techniques using fast-response sensors to establish a
validation exercise. Since the deposition of HNO3 is not measured directly and
must be computed, it seems logical that an uncertainty analysis be performed to
account for all the known sources of variation. Have we erred on the side of
being conservative? If so, by how much? If so, this makes the problem with the
critical loads even more acute. All members of the atmospheric sciences'
community do not endorse the inferential method. If the uncertainty analysis
reveals that the deposition is ± 50%, it lends a different flavor to the chapter
particularly the section on critical nitrogen loading. Interestingly, the chapter
does not present this uncertainty in qualitative terms (e.g., Vol. 1, p 1-27), but
this is not translated to a quantitative analysis.
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Nitrogen Deposition and Elevated CO2
Some recent studies have suggested that nitrogen deposition over the
last several decades is one of the explanations for the biosphere serving as
a sink, for global carbon. The argument is that nitrogen additions to forest via
NO2 and HNOs provides the necessary nitrogen so that increases in
atmospheric CC>2 can result in increases in growth. This information is not
contained in the document.
Nitrogen Deposition and Forest Growth.
In a related study, it has been proposed that the forests in Western
Europe have actually seen an increase in growth over the last several decades
and that this increase is due to nitrogen deposition (Science 1992). This is an
appropriate reference for this document and certainly relates to the discussion
of critical nitrogen loading. If most of the forest in Europe are showing increases
in growth and the levels of N deposition are greater than North America, then
the conclusion might be that N will increase the growth of forests in the States.
As chair of the session on "Ecological and Welfare Effects," I would
like to reiterate a point that became apparent in the session. It was the opinion
of the chapter's author, the primary reviewer, and EPA personnel involved with
Chapter 10 that the concept of "Critical Loadings," deserved some discussion,
but it was not sufficiently evaluated, and the data was woefully insufficient for
the method to be used at this time to develop a secondary NC>2 NAAQS. This
became clear during the discussions, but was not mentioned in Chapter 10.
As a result, it is strongly recommended that it be explicitly stated in the body
of the chapter, the chapter summary, and in chapter 1.
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The author's task in Chapter 11 is complicated by the neglect of participate
nitrate in the earlier chapters. The main shortcoming of the present draft is its
failure to distinguish clearly and consistently between reliable and artifact-
tainted particulate nitrate measurements in its review of field data. State-of-the-
art measurements should be segregated in each discussion, the state-of-the-art
measurements should be emphasized, and inferior measurements should be
treated collectively as qualitative evidence only.
CHAPTER 13 Studies of the Effects of Nitrogen Compounds on Animals
The chapter is generally on target and appears to reach the correct overall
conclusions. There are numerous specific comments, but none that detract
seriously from the present structure or conclusions of the chapter.
Although the animal data do not preclude a potential role of NOX in the develop-
ment of human emphysema, neither do they support such a role. The
literature is fraught with difficulties associated with variations in definitions of
emphysema, approaches to evaluating emphysematous changes, and
the potential for effects of infections in emphysematous changes (older studies).
It is not possible to conclude firmly that NO£ exposure and increased
incidences of respiratory illness due to infectious agents in children. It is not
possible to establish cause and effect for the human response from the animal
data.
Because of high concentrations of NO2 required, the section on animal
mortality is of questionable usefulness for this document.
Because of known species and strain differences in sensitivity to inhaled
oxidants, it is very important to list the strains of rodents in all tables. Age
should also be noted.
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Effort should be exerted to extract all relevant information from published
studies. Authors could be contacted for experimental details not described
in the original reports, if the missing details are critical to present interpretation
of the results.
Overall conclusions probably appropriate, but supporting information needs
some attention.
Generally need more care regarding species, strain and age differences and
their potential impact on response:
These should be given in tables.
Need increased uniformity of terminology for ages.
These factors need to be integrated into each point of synthesis.
Our current understanding of 03 studies indicates several fold
to order of magnitude differences between primates and rodents.
It is reasonable to assume that similar differences might exist for
NO2- This makes the monkey data very important.
Need more cross-review of references among sections for relevant data. For
example, the Mauderly 1990 reference (& 1989) include findings for
emphysema, particle clearance, and lung collagen, but are not mentioned,
although they are referenced for other purposes elsewhere. Similar oversights
might exist for other references.
Need to be more aggressive in getting answers to questions about studies.
Unknowns are stated when a phone call could have resolved the question.
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Mortality data:
Of questionable usefulness overall.
Tables do not indicate whether the references are adequate tests of
mortality effects.
There is mortality information in additional references that could be
relevant.
What about human mortality? Do we have exposure data for any?
Mixtures: Some information can be derived on upper bounds of effects from
exhaust studies, particularly the diesel exhaust chronic studies with soot
filtered out.
Comment on classification of morphological studies.
Morphological classification of the lungs is done at two levels. One
level is concerned with the sites studied (e.g., airways, terminal bronchioles,
alveolar region proximal to the bronchioles, random sampling of alveolar
regions). The second level is concerned with the method (e.g., visual examina-
tion, pathology scoring system or morphometry (i.e., gross physical
examination, light microscopy, electron microscopy). An evaluation of what
has and has not been done by these methods might be useful. For example,
nitric oxide and other oxides of nitrogen have not been evaluated by
morphometry at the electron microscope level, connective tissue fiber
alterations has been evaluated by visual examination with the electron micro-
scope.
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13.1 Introduction, line 12; 13.2.3.2 Lung Biochemistry, lines 18-24; and
13.4 Nitric Oxide, lines 13-23.
In several instances, some toxicologic measure such as alveolar
epithelial hypertrophy, enzyme levels, collagen synthesis, or alveolar
macrophage function is used to determine the toxicity relative to another
toxicant (e.g., ozone versus nitrogen dioxide or nitrogen dioxide versus
nitric oxide.). Toxicity and toxicologic measures cannot be simply equated
across pollutants. While nitrogen dioxide may be one-tenth as toxic. Clearly,
ozone is more potent than nitrogen dioxide in producing hypertrophy of the
alveolar septa. High levels of nitrogen dioxide have shown evidence of
alveolar airspace enlargement and destruction of alveolar septa, while ozone
does not produce such lesions. The determination of which pollutant is more
"toxic" depends on which endpoint you choose. Only if the same toxicologic
measure can be shown to be the principal endpoint for assessing human
health risks can the relative toxicity be addressed by direct comparison.
13.2.3.4 Morphologic Studies, pages 13-106 to 13-117--Emphysema
Following Nitrogen Dioxide Exposure.
Studies which demonstrate destruction of alveolar walls are of particular
importance due to the irreversible nature of the lesion, the destruction of
alveolar walls is also an important criteria in the anatomical definition of human
emphysema. In humans this destructive process develops over a time course of
decades, and when symptoms appears involves either a uniform destruction of
alveolar surface area (panacinar emphysema) or a focal loss in the proximal
regions of the acinus (centrilobular emphysema). The anatomical definition of
human emphysema principally applies to autopsy evaluations of a highly
evolved disease process. In animal studies we are likely to be evaluating the
initial phases of the disease process and, thus, must be concerned with the
accuracy and interpretation of the measurements used to detect destruction
of alveolar walls.
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References to Frampton (1987) and Smeglin (1986) are abstracts.
Should replace with reference to published manuscripts as cited in Chapter
15.
Epithelial permeability is discussed in Chapter 15, page 15-85, lines 14-16.
However, no mention of studies assessing permeability with DTPA after NO2
exposure. Suggest that this discussion be incorporated into "Respiratory
Effects," beginning on page 13-17. One specific reference is: "Oberdoerster, G.
et al.: Decreased lung clearance of inhaled98m Tc-DTPA aerosols after NO2
exposure: indication of lung epithelial permeability change?" J. Aerosol Sci.
17:320-323, 1986.
CHAPTER 14 Epidemiology Studies of Oxides of Nitrogen
The impression from Chapter 14 is that meta-analysis is new. A recent
surge of interest is new on combining evidence from studies reporting
estimates of a particular clinical or epidemiological effect. But, the
ideas of meta-analysis go back nearly 40 years. A pioneering reference
should be given:
Cochran (1954). The combination of estimates from different
experiments. Biometrics. 10:101-129.
This reference sets out the random effects model for the purpose at hand.
The synthesis of NO2 results should be by this model.
In recent years there have been important advances in the estimation
methodology of meta-analysis; see for example the references on the
confidence profile method. But, again, the concepts and basic methods to
back 30-40 years.
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Some additional effort in statistical pedagogy for the NO2 meta-analysis may
be warranted. I would suggest the following points be incorporated:
(a) Studies are not being combined.
(b) Adjusted estimates of an effect from studies are combined.
(c) The adjustments involve accounting for the specific design of
the study, like allowing for multiple cities, and removing the
effects of concomitant variables, like smoking. Some
covariates should be recognized as the best proxies available,
like NO2 exposure for delivered dose. Special difficulties arise
when other variables have synergetic-type relationships with the
measurement of the agent under study. There appeared to be
no such interaction of other variables with NO2 exposure level
or presence.
(d) Similar adjusted estimates of NO2 effect from studies with
very different designs is a strength, indicating a robustness
of the effect estimates.
Recommend for this estimation effort, Dr. Rhonda R. Clark of C
Quantitatives.lnc. (919-493-5408) of Chapel hill, NC. Dr. Clark did her
dissertation work under Professor C.E. Davis of the UNC-CH Biostatistic
Department on errors in variables for logistic regression. Her findings paral
those for normal distributed responses and could be used to quantify the
probable underestimation.
To address the concern that the distributions of NC>2 exposures for gas stove
and electric stove houses differed; only a difference in means has been
considered. Specifically, there was about a 30ppm difference in mean
exposures; concern was expressed about the variation in measurements, or
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distributions, for these two types of stoves. Suppose the random variable Y-j
(Y2) is log- normally distributed for NC>2 exposures in gas stove (electric
stove) houses, the the difference z=ln Y-| - In Y2 is normally distributed with
calculable mean and variance. The concern can be supported by noting
exp(K (z))= exp (z) ,
where £ (•) denotes the expectation operator. In words, the function of a
mean (LHS) is not equal to the mean of a function (RHS), unless the function
is a linear one. There is a strict ordering relationship between the right hand
side (RHS) and left hand side (LHS) of the above equation; RHS is greater
than or equal to LHS.
Such calculations are relevant for evaluating the odds, equal to the
exponential of the logistic regression coefficient, p , for NO2 exposure
as calculated at an increase of 30 ppm with p , the meta-analysis estimate of
the mean (mode) of the distribution of effects from the study estimates being
combined. The calculations on a mean difference of 30 ppm are conservative
if RHS is greater than or equal to LHS.
This chapter makes a laudable attempt to synthesize the epidemiologic
literature instead of reviewing each study in numbing detail. While the
overview of the chapter is appropriate, some of the details need refinement
The section on Health Outcome Measures gets into a convoluted discussion
that seems to be an attempt at self-justification, but does not come across
clearly. It is appropriate for the authors to attempt to explain the combination of
studies with related but different outcomes, but more work is necessary to write
this section more clearly. Sentences such as "In perspective, a question of
similarity exists for other potential outcomes usually considered similar.
(Page 14-43, line 6)" don't say very much.
As noted by the authors, studies have investigated a mixture of outcomes,
including LRI, report of illness and a variety of symptom outcomes. This
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potpourri seems to be recognized in the chapter, although it raises some
cautions regarding much of the initial discussion referring only to LRI, and of the
importance of LRI. The chapter should acknowledge that the different
symptoms combined in the meta-analysis are different, and could indeed
reflect different processes. Thus, caution is necessary in interpreting the
analysis.
The chapter does not clearly distinguish between lower respiratory tract
illness (LRI) and symptoms of LRI. All symptoms are not necessarily LRIs. All
LRIs are not infectious. Also, most bronchitis may be non-infectious. The
difference between wheezing and LRI is not clearly addressed, i.e., all
wheezing is not LRI, nor does all LRI include wheezing. This is important
because of the possible effects of N02 on asthmatics, which are not
directly addressed in the chapter.
The quality and differences in types of epidemiologic studies could be better
addressed in the chapter. Major issues that need to be elaborated or
clarified include:
1. Control for confounding factors or effect modifiers, in particular
cigarette smoking and SES.
2. The difference between cross-sectional and prospective studies.
3. The sensitivity as well as specificity of outcome measurement, e.g.,
remotely recalled events versus recent or prospective events.
Since the quantitative estimates of difference in NO2 levels between gas
stove and non-gas stove houses is for long-term averages, the implications
of a quantitative exposure difference in studies using a surrogate measure of
exposure must related to long term averages. However, it must be recognized
that significant short term peaks are observed from gas appliances. This raises
serious questions for the extrapolation of these studies to ambient standards.
In any case, references to NO2 levels in the chapter should clearly state the
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source of the measurement. In some cases, values are based on assumptions
(e.g., differences between gas and electric homes) and should be so stated.
Several comments on meta-analysis:
1. The inclusion of studies does not appear to strictly conform to the
criteria presented in the chapter, and appears not to be standardized.
Two studies, the Swiss and the Chestnut Ridge studies, were
equivalent or superior to studies that were included in the analysis
but weren't included. While lack of data may have precluded their
inclusion in the analysis, their absence does raise questions about
possible selection or publication bias.
2. There was not consideration of control for important confounding factors
in the studies that were included , e.g., failure to control for cigarette
smoking (active or passive) is a serious deficiency (e.g., Melia, 1977) and
should result in reducing the significance or excluding a study. This
is particularly important when there is some evidence that passive
smoking may interact with NC>2 in it's effect on symptoms.
3. There was no consideration of study type in the full analyses, or the
subsets. Thus, historical, cross-sectional and prospective studies are all
lumped together, when these have very different epidemiologic
significance in their sensitivity. The analysis also lumps together boys
and girls, when these studies and other indoor air pollutant studies all
suggest a difference in effects.
4. The meta-analysis suggests that combining these studies results in
a "true" odds ratio, with a very narrow confidence limit. The preferred
combination of studies are those presented in Table 14-17, which shows
the range of study results by combining (or excluding) similar studies.
From this table a range of odds rations can be summarized for use in
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future regulatory processes. In general, because of the many
uncertainties and other issues discussed, the chapter should focus
on a range and not a single odds ratio.
The inclusion of different model types in Table 14-17 is a little deceptive,
since different models result in a change in Odds Ration or confidence
limits of only 0.01, an insignificant amount. One of the models could be
selected for the table and the others referred to in the text. The table
should include an estimate for all prospective studies.
The issue of controlling for SES is an important one that is only briefly
discussed in the chapter. Gas appliances are commonly associated with
lower SES. Cigarette smoking is increased with lower SES. Other
poorly characterized risk factors for respiratory illness may also be
associated with lower SES (e.g., increased housing density, poorer nutrition,
etc.). Thus, controlling for SES may indeed be over controlling for gas stoves
and NO2 , but failure to control for SES may be failure to control for a
significant confounding factor. It is thus a conservative bias, if any,
to control for SES, but failure to do so raises questions of results that
could be noncausal. It may be possible to dissect out the differences
between SES and gas stove effect, but if such a study has been done, it was
not addressed in this chapter.
The description of the Chestnut Ridge studies is incorrect. All analyses used
gas stove use as a surrogate for indoor NO2 exposure. Most pollutants were
measured at more than one of the monitoring sites, although this is not really
relevant for the gas stove analysis, the ambient air pollution measure for the
analyses varied with the outcome being studies. For the cross-sectional
analysis, ambient pollution was based on estimated NO£ concentrations
modeled from all monitoring stations. For the prospective analysis, exposures
were based on the average exposures for the region. The study is important
because of the sample size (of children), and the rural location of the
population.
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Data are plural, and should be corrected throughout the chapter (and the
document).
Is the strength and consistency of the epidemiologic data base and its analysis
relating NC>2 exposure an an increased rate and/or severity of respiratory
disease and symptoms adequate quantitatively assess whether ambient t
or near ambient levels pose an increased level of risk?
There is a consistent association between small increases in lower respiratory
illnesses and higher indoor concentrations of NC>2 demonstrated in the
epidemiologic studies. These associations appear to extend to the lowest
concentrations measured.
Overall, two important questions related to the meta-analysis in the
epidemiology chapter: (1) is the meta-analysis an acceptable approach
in this situation; and (2) if so, is the analysis presented correct? What
improvements or changes would be appropriate?
The use of meta-analytic techniques are a significant improvement in the
way that epidemiologic evidence is evaluated. It provides a quantitative
method for combining evidence from positive and negative studies adjusting
for the stability of the estimates from individual studies. Possibly more
important than the specific point estimate for the overall effect of NO2
exposure which is provided, the meta-analytic summaries provides a
method for quantitatively evaluating the influence of conjectured confounders
or sources of bias. For example, rather than excluding studies which fail
to control for parental smoking as a confounder, the influence of these
studies alone, and separately for the remaining studies. By comparing the
point estimates and their stability (i.e., 95% Confidence intervals), the
relative influence of such an uncontrolled confounder can be specifically
evaluated. In previous evaluations, such studies might be eliminated from
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consideration for failure to consider a hypothesized covariate. Decisions on
standards would then have to be based on a small number of studies meeting
a set of criteria for acceptability. Meta-analysis provides a quantitative method
for evaluating the weight of the evidence.
Techniques for meta-analysis have been well developed1, and have been
applied extensively in the medical literature, particularly regarding clinical
trials.2 While meta-analysis is currently being applied more frequently to
epidemiologic studies,^ the first epidemiologic application can be found in
1964.4 The methods that have been applied are appropriate. It should be
recognized that approximations must be made in extracting the relevant
data from the published results of each study. There will be small differences
depending on the specific method used for calculating the point estimate and its
variance. Moreover, there are several methods available for combining results
in the meta analysis; two of which, the fixed effect and random effect models,
were applied in the Draft Criteria Document. Thus it should be expected that
different reviewers would obtain slightly different quantitative answers.
However, as shown in the Criteria Document, the results are robust, that
is they are consistent between alternative methods and are not sensitive to the
inclusion or exclusion of any specific study. Thus while it is not appropriate to
characterize the analysis as correct, it can be stated that the meta-analysis
is acceptable, appropriately computed and apparently robust.
1 Light RJ, Pillemer DB. Summing UP: The Science of Reviewing Research.
Harvard University Press, Cambridge, MA, 1984.
2Louis TA, Fineberg HV, Mosteller F. Findings for public health from meta-
analysis. Annual Reviews of Public Health 1985; 6:1-20.
^Greenland S. Quantitative methods in the review of epidemiologic literature.
Epidemiologic Reviews 1987; 9: 1-30.
4MacMahon B, Hutchinson GB. Prenatal x-ray and childhood cancer: a review.
Actas un Int Cancer 1964: 2:1172-1174.
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Specific questions include:
1. The effect of misclassification and measurement error - does it result
in an underestimate or overestimate of the results?
The effect of non-differential misclassification and random measurement
error will be to underestimate and association between NO2 exposure
and adverse health effects. Dr. Neas has reviewed Dr. Roth's comments
on misclassification and has provided a detailed response directly to
Dr. Kotchmar.
2. Is the logistic model used, which assumes a no threshold relationship,
the appropriate model for the analysis of respiratory disease symptoms?
While the logistic model for the prevalence of respiratory symptoms is
non-linear, for the weak effect estimates detected associated with NO2-
In the paper by Neas and other coworkers5 relative odds by categories
of NO2 exposure are presented (Table 5). These data show no
indication of a threshold down to the lowest concentration observed.
3. Not all the epidemiological studies used in the meta-analysis include
all covariates - is it possible that inclusion of additional covariates could
substantially affect the conclusions?
5Neas LM, Dockery DW, Ware JH, Spengler J, Speizer FE, Ferris BG Jr.
Association of indoor nitrogen dioxide with respiratory symptoms and pulmonary
function in children. Am J Epidemiol 1991; 134: 204-19.
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The Neas et al study appears to have been the most complete in
considering potential covariates. In this analysis the estimated odds
ratios adjusting for confounders including SES and parental smoking
were very similar to the crude odds ratios without adjustment. This
suggests that the effects of NO£ are not being confounded by these other
covariates. However, it should be kept in mind that the study design in
this case insured independence of the passive smoking and gas stove
associations. In the other studies which have considered covariates
such as SES and parental smoking, there has not been much evidence
for confounding as indicated by a major change in the effect estimate for
gas stoves or NC^- Note that changes in statistical significance is not an
appropriate indication of confounding.
The meta-analysis provides a technique for evaluating the influence of
potential uncontrolled confounding in the summary results. Studies can
be separated into those which do and do not appropriately consider
some posited confounder, and separate estimates, with and without
adjustment for the potential confounder, provides guidance regarding
the influence of the variable in the analyses.
4. Are the different definitions of respiratory disease too different to allow
for combining evidence?
In compiling the evidence from the various epidemiologic studies, the
reviewer must first define the health end-point of interest. The basis
for selecting the composite lower respiratory illness indicator as the
measure for these studies is convincingly presented based on
animal, clinical and epidemiologic studies.
5. Is the estimate of approximately 30 ug/m3 difference between NO2
levels for gas stove and electric stove homes an appropriate estimate
of exposure?
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Overall, this is an appropriate measure of the difference. However,
there are measured concentrations available from some the the
studies such as those from the United Kingdom, which would allow an
exposure measure different from that observed in the U.S. studies to be
applied. Using an alternative scaling factor for different studies is not a
problem. Ultimately, all studies need to be put on a common basis, and
30 ug/m3 appears to be a reasonable number.
6. To what extent could the effects seen be the result of other
pollutants associated with NO2 such as MONO and others?
The specific causative agent for the observed indoor associations with
NC>2 may indeed be MONO or other decay product of NC^. However,
even if there is an intermediate agent which is responsible for the
damage, control of such exposures would be through reductions in
NO2 concentrations.
The most specific association have been found with indoor NO2
concentrations or indicators of indoor NO2- In part this may reflect
the effect of indoor NO2 sources in producing random misclassifi-
cation of exposure in studies of outdoor ambient NO2 exposures.
Such random misclassification will make it difficult to detect
associations with the ambient outdoor NO2 measurements.
Nevertheless, several studies have shown similar results
with outdoor concentrations.
7. Are there errors in the calculations of the odds ratios?
There were no errors which were identified in the calculated odds
ratios. Extracting estimated odds ratios and their variances from the
published results often requires assumptions and approximations. For
example, in the Criteria Document, it is assumed that the log odds
ratios follow a normal distribution in calculating variances and
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confidence intervals. While there may be subtle differences in calculated
odds ratios depending on the specific approximations made by the
reviewer, the calculations are not sensitive to these differences.
8. Is a two week exposure average adequate to estimate an annual
exposure value?
In designing the Six Cities indoor air pollution study, we considered
the aDpropriate sampling interval for estimating annual exposure.
Spengler et al6 show the distribution of one week integrated NO2
measurements throughout the year. The specific sampling plan was
described by Spengler et al.7 This paper shows very little difference
in the estimates of personal NO2 exposure using two-week measure-
ments in winter, summer, or fall/spring.
Two other related issues for the epidemiology chapter are:
1. If the meta-analysis is considered an acceptable approach, should
the Agency consider using the analysis for measured NO2 studies
with an odds ratio of approximately 1.28 as the best estimate of the effect
as opposed to the odds ratio for all the studies of approximately 1.2,
considering that the measured NO2 studies may have less error
involved.
6Spengler JD, Duffy C, Letz R, Tibbits TW, Ferris BG Jr. Nitrogen dioxide inside
and outside 137 homes and implications for ambient air quality standards and health
effects research. Envir Sci Tech 1983; 17:164.
7Spengler JD, Ware J, Speizer F, Ferris B, Dockery D, Lebret E, Brunnekreef B.
Harvard's indoor air quality respiratory health study. Indoor Air '87, Proceedings of 4th
International Conference on Indoor Air Quality and Climate, 1987; 2; 218-223.
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Given that random misclassification of exposure introduced by
using dichotomous marker of exposure would reduce the estimated
effect estimate of the association between NO2 and lower respiratory
symptoms, it could be argued that the estimate based on the
measured studies is better. However, given the limited number of
available studies, I would think that decisions should be made on the
basis of the weight of the evidence from all studies.
2. Alternatively, should the Agency consider using the Neas et al. (1990,
1991) study (with and odds ratio of approximately 1.4) as the best
estimate of effect, since it studies US children and may be considered
one of the best-conducted studies that takes into account more factors
than other studies. If so, should be meta-analysis be used as a
supportive data base.
Although the Neas et al study appears to have the best design at this
time, any decision should be based on the weight of the evidence
developed from considering all studies.
CHAPTER 15 Controlled Human Exposure Studies of Oxides of Nitrogen
and Appendix 15A
This is a well-written, comprehensive review of clinical studies. It has
done an extremely credible job of developing possible explanations or
hypotheses for the seemingly inconsistent results when comparing high vs. low
level NC>2 exposures. The Chapter is accurate and the Conclusions and
Discussion (pages 15-82 through 15-87) on target. In addition, the effort
at the so-called "meta-analysis" in this Chapter is useful-whether it can
be justified on statistical grounds, should be left to the statisticians.
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Major concern relates to the Chapter Appendix 15A: Severity of Asthma.
Although the concept is reasonable, I will detail my concerns
following the specific comments on Chapter 15.
This chapter is effectively comprehensive, both in breadth and depth. The use
of summary tables of particularly pertinent information, together with appropriate
explanatory text, is very well blended. Further, the essential points of concern,
identified as critical questions on page 2 of the introduction, are effectively
revisited in the conclusions presented on page 87.
A fundamental problem in this review-not readily resolvable--is that controlled
human exposures deal with relatively brief exposures (i.e., less than 4 hours) at
NO2 concentrations well above the annual arithmetic mean standard of 0.053
ppm. Further, several of the critical questions, identified on page 2, can only be
partially answered by controlled human exposure studies.
Little effort has been made to look at observed effects as a function of total
inhaled dose, rather than NO2 concentration alone. Perusal of the data,
however, indicate that this would not be useful for the most part (e.g., Figures 1
and 2, pages 59 and 60).
The "arbitrary" use of 1.0 ppm for conclusions No. 1 and 2 appears somewhat
misleading. There are specific comments regarding this problem in the specific
comments section.
Regarding the three questions posed in Dr. Grant's written handout, the answer
to number 1 is Yes. The answer to the first part of question number 2 is no,
because the results are too inconsistent. Appendix 15A should not be included
in total, though a small part of it might be incorporated into the chapter text as
suggested in the specific comments section.
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CHAPTER 16 Health Effects Associated with Exposure to Nitrogen Dioxide
o The overall organization of the key health effects-namely airway responsive,
increased occurrence of respiratory illnesses, biological basis for the effects
of NOg on the host defense system, and emphysema-are appropriate
parameters. In Section 16.3.3 the authors again stressed the incidence of
mortality in experimental animals is more influenced by the concentration of
N^2 than the duration of exposure.
To support the findings in humans of Goings et al, 1989 (page 16-16, line 1),
refer to our study (referenced on page 13-195, lines 15,16, and 17) using
squirrel monkeys. It was found that monkeys exposed to NO2 showed an
earlier and greater serum neutralizing antibody response to monkey-adapted
influenza virus. We hypothesized that exposure to NO2 may have enhanced
the establishment and multiplication of the virus with the resultant more rapid
and higher antibody response. This agrees with the statement on lines 9 an
10, page 16-16, that "NO2 may play a role in increasing the susceptibility of
adults to respiratory virus infections."
In addition, a quick scan of the text revealed some of the references missing
on pages 16-21 and 16-27. For example, on page 16-21, Abraham (line 2),
Acton (line 6), Adair (line 9), Butler (line 32), Clausing (line 45); page 16-22:
Dorre (line 9), Drye (line 18); page 16-23: Gardner (line 4), Harlos (line 50);
page 16-24: Kleinman (line 23); page 16-25: Miller (line 15), Noy (line 44);
page 16-26: Overton (line 1), Quackenboss (line 17), Richters (line 24),
Schiff (line 49); page 16-27: Schwab (line 1), Stephens (line 17), Wagner
(line 31).
o Many of the biological studies referenced throughout the study were conducted
in the 1960's , 1970's, and early to mid-1980's. Although these studies are
sound and well conducted, recent advances in technology make it possible
to conduct a variety of interesting studies to further evaluate mechanisms of
action. More detailed comments are addressed in the discussion on
Chapter 13.
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CHAPTER 1 Summary
1.1.1 Critical Issues
Page 1-2. line 33. Insert "infectious" before respiratory.
Page 1-3. line 7. If, after consideration of the topic of ecological effects and
critical loads in completed, such findings do not support this concept, how will US EPA
handle this question? That is, will this question be answered by a clear statement
made at the end of the summary section dealing with critical loads?
i. 1.2 Organization of the Document
Page 1-3. lines 17 and 18. More than NO2 is discussed in each of these
chapters; especially in 10 where total N depositions and biological and chemical
transformations are discussed. Should NO2 be changed here (throughout the
paragraph) to Nitrogen oxides?
1.2 Chemistry, Sources, Transport and Transformation, Sampling,
Ambient and Indoor Levels, and Exposure of Oxides of Nitrogen
Page 1-4. The absence of any discussion regarding HNOs is surprising. Most
of the ecological effects are due to HNO3 deposition.
1.2.1 Chemical and Physical Properties of Oxides of Nitrogen
Page 1-4. This section does not actually summarize chemical and physical
properties of NOX but rather lists the several species.
line 10. Eight nitrogen oxides: NO, NO2, N2O, unsymmetrical nitrogen
trioxide (NO^), symmetrical NO3, ^03, N2O4, and ^05. Here and in the section 3.6
summary are the only time the concept of unsymmetrical and symmetrical NO3 is
mentioned. It is not discussed in the text. Here and in Chapter 4, NO3 is called
nitrogen trioxide; in the rest of the document it is referred to as the nitrate radical.
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1.2.2 Sources of Nitrogen, Oxides Influencing Ambient and Indoor
Air Quality
Page 1-5. This section does not list ambient sources, but rather amounts of
NOX; e.g., no mention of automobiles as the predominant source of ambient pollutant.
1.2.3.1 Ozone Production
Does not summarize the role of uv energy in 03 production.
Page 1-5. lines 27-31. At some point in this Introduction/Summary the
importance of NOX as a precursor to ozone and the importance of ozone as a maior
regional scale phytotoxicant of concern to agricultural crops and forest species.
1.2.3.2 Production of Odd Nitrogen Species
Page 1 -6. NOX oxidation products (NOy), include: HNO3, HO2, NO2- HNO2,
PANs, ^05, and inorganic and organic nitrates.
1.2.3.4 Oxides of Nitrogen and the Greenhouse Effect
Page 1-9. line 17. Move Nitrous Oxide title to line 12.
line 25. Stratospheric Ozone Depletion by Oxides of Nitrogen.
Discussion of stratospheric 03 depletion is either unclear or irrelevant.
1.2.5 Ambient and Indoor Concentration of Oxides of Nitrogen
1.2.5.1 Ambient Concentration
Page 1-12. Lines 17-31 and Page 1-13. lines 1-4. This section needs to be
expanded in an effort to relay more information on ambient NOX in areas separate
from California. Data sets are available from statewide networks. Citations with
information on expected NO, NO2, and NOX in agricultural and forested areas should
be included so as to have a reference basis for evaluation of studies done under field
and more artificial exposures.
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line 19. This is the first point at which motor vehicles are mentioned.
This section is far less complete than the indoor section 1.2.5.2.
1.3 Effects of Nitrogen Oxides on Vegetation, Ecosystems, Visibility,
and Materials
Page 1-17. The statement is made that the saturating nitrogen species is NO2-
Is this accurate or is it NO3 via wet and dry deposition?
1.3.1 Effects of Nitrogen Oxides on Vegetation
1.3.1.1 Introduction
Page 1-16. lines 21-26. But most (if not all) of these studies were done at
exposures above ambient expectations. Specifically line 24...in relation to the types of
injury induced by such exposures...at some point, the lack of symptoms expressed
under field conditions and ambient exposures should be presented here. This
paragraph reads as if plant injuries are commonly found.
Page 1-17. lines 13-19. Too much of any compound can be toxic. Do the
studies (at ambient doses) show that plants in general 'take in' sufficient doses of N
(all forms) under ambient exposures to promote toxicity. Lines 16-19 (both sentences)
are not reflective of the bottom line findings of either chapter 9 or 10.
1.3.1.2 Nitrogen Dioxide
Page 1-17. 1-18. and Figure 1-1. The implication of where ambient exposure
expectations fall in relation to these data as graphed in Figure 1-1 would provide a
sense of 'reality' to all of this.
Page 1-17 to 23. Out of balance in the detail of presentation (including data,
and graphs and references to Chapter 9.). The chapter does not conclude with an
assessment of significance in regard to exposure/response.
Page 1-20. lines 12-19. Here, it should be clearly stated that foliar symptoms
are rarely (if ever) noted under field exposure conditions.
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lines 26-31. These studies were all at high dose exposures, especially
Sinn and Pele, 1984 (which used 200 ppb NO2). Why the citation here and no where
else on these pages? Delete or include others.
Page 1-21. lines 20-23. Reference to Figure 1-2B r2 values of .200 (very low).
Where do ambient exposures fit on this curve?
Page 1-23. lines 12-15. "It may be...may be enough to cause ecological
problems. The lack of data makes any conclusion premature." Then why even
suggest that it may be? Why not may not be? Why should the Criteria Document only
offer the negative effect as a potential?
1.3.2 The Effects of Nitrogen Oxides on Natural Ecosystems and their
Components
1.3.2.1 Ecosystems: Structure, Function, Response
Page 1-24. lines 20 and 21. (See comment in Chapter 10 review). Many
"views" emerge, some well founded following good science, others do not. A "view"
does not lend credence to a Criteria Document statement.
line 24. Gorwing concern? By whom?
line 27. See statement made on page 10-79, Chapter 10, lines 23 and
24. As written here (page 1-24), it would appear many ecosystems (soils) have
become N saturated. After all, this is a summary and sentences like this become the
generalized truth rather than as a place to discuss the rare events which are noted.
Page 1-25. lines 1-5. Delete concept of Critical Loads.
line 22. Do Guderian, et al., 1985, actually state that nitrogen loading
can produce perturbations that are not easily reversed? Or is this a general statement
made about air pollutants in general? Really an all important statement for a
Summary and should be as accurate as possible to the pollutant in discussion within
this Criteria Document. This whole paragraph is very general and unless such effects
have been clearly demonstrated as due to N deposition, these should be deleted.
1.3.2.2 Nitrogen Deposition
Page 1 -27. lines 5-6. The prevalence of any one form of nitrogen deposition is
also dependent on the turbulence nature of the atmosphere - canopy interaction. This
is particularly true for the difference between NO2 and HNO3 deposition.
lines 13 and 14. What are ambient doses?
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Page 1-28. line 18. Proposed critical loads? By whom, where in document,
US EPA Policy? Line 19--What changes? Details? Citable studies?
Page 1-29. Table 1-1. Most of these are not natural ecosystems but rather
single sites of managed forest species under uni-crop systems.
1.3.2.3 Effects of Deposited Nitrogen on Forest Vegetation and Soils
Page 1-28 through 29. If high levels of nitrates are good for agriculture, why are
10-100X lower levels harmful to e.g., forests?
Page 1-30 through 31. The discussion of nitrification in non-agricultural settings
needs quantitation, e.g., "high enough inputs" - how high vs. pollutant levels?
Page 1-30. line 31. There are very few proven documented cases...com pare
to line 5, page 1-31. How do these related to each other?
Page 1-31. lines 3 and 4. Conjecture. What are...high enough inputs for a
sufficiently long time? (See comments in Chapter 10 review).
line 19. There is no forest decline in either country. See numerous
comments in review of Chapter 10.
1.3.2.4 Effects of Nitrogen on Sensitive Terrestrial Vegetation
Page 1-32. line 24. This citation is often repeated in Chapter 10 yet no details
of what the clear signs of vegetation change were. Also, is it 20 or 30 Kg N per ha per
year?
1.3.2.5 Nitrogen, Saturation, Critical Loads, and Current Deposition
Page 1-33. lines 16 and 17. Agree, therefore concept of critical loads should be
minimized in this document. Lines 24-27-points to wide range (therefore useless) of
depositions acceptable as critical loads.
line 28. Compare to page 1-32, line 24.
Page 1-34. line 11. Have been suggested? This is far different from clearly
stating such as have been determined.... anyone can suggest anything. Need data
and proof of associations.
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lines 27 and 28. Is it true that there is "little doubt that N deposition in
North America has a pronounced effect on many if not most terrestrial ecosystems"? Is
that speculation rather than hard-fact conclusions?
Page 1-35. lines 6-8. Agree. See previous comments.
lines 23-31 and following lines on page 36. Well done, excellent
summation.
1.4 Health Effects on Oxides of Nitrogen
Page 1-56 through 67. There is no discussion of the ameliorating effect on virus
infection; no studies of airway hyperreactivity are reported.
1.4.2 Epidemiology Studies of Oxides of Nitrogen
Page 1-62. line 30 et sea. Respiratory illness is a vague term; text should
specify infectious respiratory illness since not all respiratory illnesses are aggravated
by NO2.
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CHAPTER 2 Introduction
2. Introduction
Page 2-1. line 7. The words "air quality criteria" are used as if the reader will
automatically know what is meant. This term has a specialized meaning that should
be defined at the beginning of the document.
Organization of the Document
Page 2-6. line 1. Reference is made to basic information contained in earlier
criteria documents that is not in the present document. Are these older studies
incorporated by reference into the present document in a legal sense?
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CHAPTER 3 General Chemical and Physical Properties of NOX
Derived Pollutants
3.1 Introduction and Overview
Page 3-1. line 12. The text states that there are 8 oxides of nitrogen but only 7
are listed.
line 15. NO and NO2 are stated to be the most important species
because they are present in significant concentrations. One should not equate
abundance with importance. The nitrate radical and HN03 are present in lower
concentrations but they are probably as "important" as NO, given their reactivity in the
case of the nitrate radical and given the role of HNO3 in producing aerosols and
strong acids.
Page 3-1. footnote: NOy = NO* + HNO3 + NO3 + N2O3 + N^ + N2O5 + PAN
This is inconsistent with page 1-6.
Page 3-2. 1st paragraph. Ammonia also is important to the fate of nitrogen
oxides because it leads to ammonium nitrate aerosol formation from HNO3-
lines 22-24. These statements would benefit from reference citations.
line 28. It is stated that "most" of the species listed in Table 3-1 cannot be
measured in ambient air. Actually "most" of them can and have been measured in
ambient air; it's just not easy. May such measurements have been made by Pitt's
group at UC Riverside over the years, and probably are documented in the
atmospheric chemistry book by Finlayson - Pitts and Pitts that is cited in Chapter 5.
Page 3-3. Table 3-1. It is not clear whether the column "At Equilibrium" is in the
presence or absence of sunlight, and for both columns, it is not clear whether dry
deposition is included.
Page 3-4. Figure 3-1. More needs to be said about initial conditions. What
latitude and season is this for? Is CH4 and background VOCs considered?
3.2 Nitrogen Oxides
Page 3-5. Table 3-2. (Last Line) Suspect that N2O5 would react with water to
form nitric acid. Please check.
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3.2.1 Nitric Oxide (NO)
Page 3-6. lines 11-14. The Zeldovich mechanism is usually written as:
O2 + M 20 + M
O + N2 NO + N
N + O2 NO + O
See page 83 of Seinfield's text on "Atmospheric Chemistry and Physics of Air
Pollution."
line 29. ...hydrocarbons in the fuel can drive the atomic oxygen
concentration... (insert atomic to distinguish from 02).
3.2.2 Nitrogen Dioxide (NO2)
Page 3-9. lines 24-31. The discussion of these reactions is incorrect. They are
of major importance in the urban situation and are not the reactions that dominate
exhaust gases, the reaction that dominates in exhaust bases is reaction 5-1.
lines 26-29. The series of reactions shown are not of minor importance
in the atmosphere. They are the maior route by which NO2 js produced in the
atmosphere. Therefore, suggest that the wrong reactions are shown. Judging from
the text, the author should have cited the thermal reaction
2NO + O2 2NO2
which is responsible for the NO2 present in combustion exhaust as stated on lines 30-
31, and which is of small importance in the free atmosphere.
Page 3-10. line 14. This reaction involves a third body, M
O + O2 + M O3 + M
(A third body molecule, M, needs to be added to both sides of the chemical equation).
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3.2.4 Nitrogen Trioxide (N03)
Page 3-11. lines 25 and 26. It is likely to be present in the atmosphere at niaht
(during the day, NO3 photolyzes; see top of page 3-12).
Page 3-12. lines 16-17. NO3 also is important because it leads to nitric acid
formation via
3.2.6 Dinitrogen Tetroxide (^04) (Also Known as Nitrogen Tetroxide).
Page 3-13. after Section 3.2.6. This section (3.2) is incomplete since it does not
include a discussion of the physical and chemical properties of some important
species including N2O5 and PAN.
3.3 Nitrates, Nitrites, and Nitrogen Acids
Page 3-13. lines 3-14. Aerosol nitrate formation definitely needs to be
discussed in detail in order to set the stage for the visibility chapter later in the
document.
s
lines 7-10. There are several things wrong with this sentence. I suggest
that the sentence end after "to coalesce into aerosol." The rest of the section should
be replaced with a new sentence: "However, HNO3 can react NH3 gas or aerosols
such as NaCI and alkaline crustal aerosols to produce particulate nitrates." A similar
revision is needed on page 3-18, lines 9-13.
Page 3-14. line 1. It is not clear what the "deleterious effects" are.
3.4 Ammonia (NH3)
Pages 3-14 and 3-15. There is a more recent and comprehensive paper on
NH3 - OH reactions. Stephens, R.D., J. Phvs. Chem. vol. 88, p. 3308-3313 (1984).
The paper indicates that at low NOy, reactions initiated by the NH3 + OH reaction will
lead to the formation of NOX. However, at high NOX, NH3 represents a sink for NOX. A
revision here will need to be reflected on page 3-16, lines 26-29 as well.
3.5 N-NITROSO Compounds
Page 3-15. line 15. Is OH2 + a misprint?
line 26. Strike the words "The election." The spectra described look like
UV spectra.
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3.6 Summary
Page 3-16. lines 9. 10 and 22. Symmetrical and unsymmetrical nitrogen
trioxide are brought up in the summary without much prior discussion.
lines 24 and 25. The text seems to imply that because concentrations
are low that these species are not very important. The nitrate radical and ^0$ are
quite important.
Page 3-17. line 16. ...nitric acid is an important component of acidic rain and is
a maior contributor to the drv deposition flux of acid gases to the earth's surface.
References should be cited regarding photochemical model predictions and
deposition fluxes.
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CHAPTER 4 Sources of Nitrogen Oxides Influencing Ambient and
Indoor Air Quality
4.1 Introduction
Page 4-1. line?. Insert "can" between that directly.
The word should be affect not effect.
line 13. OH is also the a sink for VOCs.
lines 15-17. Agricultural fertilizer use is a trivial source of N20 (see
section 5.5.2).
line 29. NO2 is not produced primarily in combustion processes. It is
formed in the atmosphere from the oxidation of NO.
4.2 Ambient Sources of Nitrogen Oxides
Page 4-2. line 3. ...in terms of the nitrogen content.
4.2.1 Combustion Generated NOX Emissions
This section is not set up correctly. Section 4.2.1 is "Combustion Generated
NOX Emissions," but subsections 4.2.1.2 - 4.2.1.4 are not combustion sources.
Furthermore, discussions of the most important sources, stationary and mobile fossil
fuel combustion sources, are conspicuous by their absence. A major expansion of this
chapter to include these omissions is in order.
4.2.1.2 Generation of NOX From Lightning
Page 4-4 and Table 4-2. It is not clear that all of the emission rates are on a
consistent basis which, in this case, should be tons of N per year.
4.2.1.3 Generation of NO From Soils
Page 4-6. Table 4-3. ...Ammonia (NH4+)...is inconsistent. Ammonia is NH3;
ammonium ion is NH4+, which is intended here?
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4.2.2 Removal of NOX From The Atmosphere
Page 4-7. Although there are more detailed discussions of deposition in
Chapters 5 and 10, for completeness, several additional important points should be
included in this discussion. These include: the importance of dry HNO3 deposition
(Kelly, 1987), and the importance of the NaCI - HNC>3 reaction in marine environments
(Savoie and Prospero, 1982). The Kelly (1987) reference is on page 5-62, the Wolff
(1984) reference is on page 11-64, and the Savoie and Prospero reference is
Geophvs. Res. Let., vol. 9, page 1207-1210.
line 4. ...covering the earth's,surface.
line 8. ...significantly.
line 16. Suggest "deposit velocity" rather than "settling velocity,"
although for large enough particles, the use of settling velocity is not incorrect.
Page 4-8. Table 4-4. Does "Dry Deposition of NOX" include dry deposition of
HNC>3 and particulate NO^?
4.2.3 Global Budgets for NOX
Page 4-9. lines 6 and 9. The symbol NO3 is used. As stated earlier in this
review, NO3 has many different definitions in different places in the document.
Suggest that the words "nitrate" or "inorganic nitrate" be used in place of NO3 here to
avoid possible confusion with the nitrate radical.
4.2.4 Major Sources of NOX Emissions in the United States
Page 4-9. A major expansion of this section is in order. This section should
incorporate the U.S. emissions information contained in EPA's recent reports:
National Air Pollutant Emission Estimates 1940-1990 (EPA-450/4-91-026) and 1990
National Air Quality and Emissions Trends Report (EPA-450/4-91-023).
Page 4-10. Table 4-5. Use most recent estimates from reference in 9.
Page 4-11. Figure 4-1. The shading systems used in these two graphs do not
match up if joined together at the year 1980.
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4.2.5 Conclusions
Page 4-12. line 3. Source: Wagner et al. (1986) is not given in reference list.
4.3.2 Formation of Nitrogen Oxides in Combustion in Gas-fueled
Household Appliances
Page 4-16. line 26. CN, NH + O2 reaction-Is this NH or NH3?
Page 4-17. Figure 4-4. The right y axis (temperature scale) is not labeled.
Page 4-19. line 4. How is the NO produced?
line 8. What is the mechanism for HO2 production?
4.3.3 Gas Stoves Used For Cooking
4.3.3.2 - 4.3.3.8
Is it necessary to give so many details on each study? Couldn't they be
summarized in a Table?
4.3.4 Unvented Space Heaters Fueled with Natural Gas and Propane
Same comment as section 4.3.3.
4.3.4.7 Summary of Emissions from Unvented Gas Space Heaters
Page 4-39 and 4-40. Table 4-16. Has two columns labeled "Emission factor for
NO2mg/kJ"- Should the first of these be for NO?
4.3.8 Comparison of Emissions from Sources Influencing Indoor Air
Quality
Page 4-45. line 28. Table 4-19 data have been excluded...This does not make
sense.
Page 4-47 bottom line and page 4-48. too. There seems to be a large amount
of emissions data available. If you are going to state that more data are needed, then
be more specific. Exactly what additional data are needed?
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4.4 Summary of Emissions of NOX From Ambient and Indoor Sources
Page 4-48. lines 9-12 and lines 13-14. The statements that these emissions are
impacting human health are out of place here, and unfounded based on the material
presented in the health effects chapters. The statement that these emissions are
contributing to global warming is likewise out of place, and erroneously implies that we
have proof that the greenhouse effect is warming the earth now.
line 17. ...differ according to burner type, fuel flow rate and flame
adjustment.
REFERENCES
Page 4-50. lines 19. 35 and 40. Several references are incomplete (i.e.,
Golbally, Graedel, Hofken). Other references to meeting papers or work "in
preparation" etc. should be checked to see if a real reference is now available.
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CHAPTER 5 Transport and Transformation of Nitrogen Oxides
5.1 Background
Page 5-1. lines 18-21. The reference to Figure 5-5 followed by the statement
that multiple study states exist is confusing as Figure 5-5 does not show that. Please
clarify.
5.2 The Role of NOX in Ozone Production
Page 5-7. line 13. The term "phytolysis frequency" is not used commonly,
instead most call this the "photolysis rate."
Page 5-8. lines 4-7: The statement that 63 build up is not observed in "NOX -
rich" power plant plumes is correct in the narrow sense that as long as the plume
remains NOX rich but low in hydrocarbons little 03 will form. However, one could
easily mistake this sentence to mean that power plant plumes don't contribute to 63
formation, which is not true. Once these plumes mix with ambient hydrocarbons, they
can promote 03 formation. Careful qualification of this sentence would be wise.
5.2.1 NOX -Rich Chemistry
It should be pointed out more explicitly that as you move to the left from the 03
maximum in Figure 5-7 (a VOC/NOx ratio of about 10), you enter the NOX -rich
environment (also known as the NOX inhibition regime), and the result is hat additional
NOX will actually decrease 03 primarily because of
NO + O3 NO2 and NO2 + HO + HNO3.
It should also be pointed out that such an environment exists in many large urban
areas and NOX emission reductions in these ares may lead to increased 03
concentrations.
Page 5-9. Figure 5-6. This figure should be proofed very carefully or removed
from the document, the original reactant is a C$ species while some but not all of the
reaction products shown are 04 species, clearly there are errors here.. A reference
should be cited for this figure.
lines 1-11. A reference should be cited for the HCHO chemistry shown.
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Page 5-11. Figure 5-7. The reader should be referred to the source of this
diagram.
5.2.2 Ozone Production in NOX -Poor Environments
Page 5-12. line 36. When first introduced, the notion of a net reaction should
be clarified. Many of the pseudo reactions that follow clearly do not occur directly in a
mechanistic sense.
Page 5-14. line 11. Missouri should be changed to Virginia.
lines 15-17. This statement is incorrect. The Kelly et al. data was
collected at the time of the solar flux maximum (10 a.m. to 2 p.m.) so 63 production
should have been at a maximum. The reason for the lower efficiency, observed by
Kelly et al. could have been due to the higher NOX. However, it is assumed in the
Niwot Ridge analysis that the observed Cg is due to in-situ photochemical production.
That assumption will not be valid on days when the air has been advected from an
urban area, and the result will be an overestimation of the 63 formation efficiency.
Both of these sections are characterized by being NOX -rich and NOX -poor
environments, respectively. The distinction being whether you are to the right or the
left of the 63 maximum in Figure 5-7. (right is NOX -poor, left is NOX -rich). Confusion
arises, however, on page 5-13, lines 1-5. These reactions are said to occur in a NOX
-rich environment, when in fact, they will result in a net 63 production in any
environment to the right (NOX -poor) of the 63 peak in Figure 5-7 as long as the NOX is
greater than 1 0 ppb. To alleviate this confusion, I suggest that three environments be
used: NC^ -rich (as presently defined), NOX -limiting (replaces NOX -poor except
when NOX is less than 10 ppb), and NOX -poor (N(\ less than 10 ppb).
Page 5-16. line 9. Perhaps should read, "The decline in the daily rate of 03
production.
Page 5-1 7. Figure 5-10. Vertical axis should be labeled 63 not O. The circles
with error bars should be defined in the caption.
Page 5-18. lines 2-4. Delete the sentence that suggests that 63 can be
predicted if NOX is known. OQ production depends on an unstated amount of
hydrocarbons too.
line 12. Clarify. How high is the "high 03" level mentioned? Probably
not as high as the "high" levels seen in Los Angeles.
Page 5-20. lines 8 and 9. Remove the ( - ) from NO3-
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Page 5-21. line 4. The statement that the importance of reaction (5-20) as a
sink for HNO3 is not known seems odd. There is a rather large literature on aerosol
nitrate formation and the relative abundance of Nh^NC^ vs. HNO3 concentration in
the atmosphere should be sufficient to show that aerosol nitrate is a significant sink for
HNO3.
5.3 Odd Nitrogen Species
Page 5-19. line 5. This is the first time in the document the term "odd nitrogen
species" is used, so it needs to be defined.
line 7. This definition for NOy is inconsistent with page 1-6. However, it
is stated that Npy are odd oxygen species, but this term is never defined.
5.3.1 Nitric Acid
Page 5-20. lines 8 and 9. Delete the (-) sign after NO3.
line 36. It should be pointed out that this reaction is reversible and
strongly temperature dependent. It should also be pointed out that acid sulfates will
react with NH^NC^ re-releasing HNO3 in the process. At this point a word or two
about the importance of HNO3 dry deposition as a sink for NOX is in order. In addition,
the reactions of HNOq with coarse aerosols should be discussed.
5.3.7
Summary of NOy Species
Should read, "Figure 5-12 shows a plot of the
(NOy) i/NOy ratio versus NOy (NOy) i is the sum..."
page 5-27. Figure 5-12 requires a reference citation.
5.3.8 Amines, Nitrosamines, and Nitramines
Page 5-29. line 2. Refers to the yield o_f triethylnitrosamine in Figure 5-13 while
that figure shows only the yield pldiethylnitrosamine from diethylamine and from
triethylamine.
Page 5-30. line 1-14. The reaction sequence has an obvious error on or about
line 6 of this page, and therefore the entire sequence should be checked very
carefully.
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5.4 Transport
Page 5-31 . line 9. Advection, diffusion, deposition, and chemical
transformations (add deposition).
5.4.1 Transport of Reactive Nitrogen Species in Urban Plumes
Page 5-33. line 12. Is this CFC number 13 or CFCL3?
line 16. Do "nitrogen oxide" depositional losses refer to total NOX or to
NO or what, exactly?
line 21. Clarify "NC>3 products"; the symbol NO3 has too many possible
meanings in this document.
Page 5-34. lines 12 and 14. Avoid use of the symbol NO3; it means different
things in different parts of the document.
5.4.2 Transport and Chemistry in NOX -Rich Plumes
Page 5-36. Table 5-1. Second line from bottom of body of table should read
k *
Footnote (6) should read "...higher aldehydes..."
Footnote (7) ends prematurely; wit should be with ...
k * N2O3 and k * NO3. What is the * for?
Page 5-37. lines 6 and 7. Use particulate nitrate, not particulate NO3, as NO3
means too many different things in various places in the text.
5.4.3 Regional Transport
Page 5-39. Figure 5-14. O3 on August 19 extends above the new zero on the
scale at the left side of the figure.
Page 5-40. line 31. The 4.5 Tg/yr NOX emission rate is in apparent conflict with
the 1 8 x 1 06 tons/yr NOX emission rate of Chapter 4. Is it possible that this is tons N
not tons NOX. In that case, what about numbers given earlier on page 5-40. Please
check.
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5.5 Oxides of Nitrogen and the Greenhouse Effect
Page 5-41. The December 1991 WMO report, "Scientific Assessment of 63
Depletion," makes much of this section obsolete. A summary of the material in
Chapter 7 of the WMO report should replace the present text.
line 2. Oxygenated nitrogen species = NOX + NOy + N2O
lines 23-24. Seems to be in conflict with lines 28-30. In lines 23 and 24,
it is said that stratospheric ozone decrease leads to surface warming while line 29
seems to refer to surface cooling caused by decreases in stratospheric ozone. Please
clarify.
Page 5-43. line 8. Equation (5-42) is wrong in several respects. Presumably
this is an expression for d f 03]. it does not depend on l<5.42, maybe it should be
dt
the rate constant for reaction 5 - 41, and since this is an 03 loss, we should have a
minus sign.
5.5.2 Nitrous Oxide Greenhouse Contributions
Page 5-43. line 28. Should read ... 6.6 x 108 kg not x108 kg.
Page 5-44. line 9. Does this mean that N2O will be 350 x more important than
CO2 as a greenhouse gas in 50 years? Seems hard to believe.
5.6 Stratospheric Ozone Depletion by Oxides of Nitrogen
Page 5-44. line 22. NOy is defined to include CINOs- There are additional
examples which confuse the reader. A consistent nomenclature scheme should be
defined at the beginning and all authors should adhere to it.
Common chemical symbols: For example, sometimes nitrous acid appears in
the text as MONO, and sometimes as HNO^ Be consistent.
Page 5-45. reactions 5-39 to 5-47. The importance of these processes is not
that 2 net 03 are destroyed by these reaction sequences. The importance is that after
the reaction sequences occur, the initial scavengers, NO or CIO, are reformed so the
sequence can continue unabated until something removes them from the sequence
and terminates the reactions. One CIO can destroy 100,000 03 molecules under
normal conditions.
Page 5-45 through 5-47. Several mechanisms for stratospheric 03 depletion
are given. Clarify which mechanisms dominate, if possible.
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Page 5-47. reactions 5-15 to 5-16. The evidence for the importance of these
reactions is stronger now. See Chapter 3 of the O$ depletion report. The same holds
true for the discussion on page 5-48.
5.7.1 Dry Deposition of Nitrogen Oxides
Page 5-49. line 16. Add The deposition velocity ... instead of Deposition
velocity...
line 19. Should read
Vd = 1
Ra + Rb + Re
which is not the same as
5.7.2 Methods of Determining V
-------
5.7.6 Wet Deposition of Nitrogen Oxides
There is some evidence that some of the HNO3 'n ra'n water was found in-situ.
5.8 Summary and Conclusions
line 20. Add importance as an aerosol precursor.
5.8.2 Production of Odd Nitrogen Species
Page 5-54. line 7. Does definition of NOy include or exclude NO and NO2?
lines 12 and 13. Neutralization by NH3 is only part of the story; a key
point is that aerosol formation occurs.
line 21. The nitrate radical is described as a short lived NO*. How does
this square with the distinction between NOX and NOy?
lines 30 and 31. ..^205 provides an important removal mechanism via
HNO3 (not for HNO3).
5.8.3 Transport
Page 5-55. line 16. Insert "and horizontally" after vertically.
Page 5-56. lines 12 and 30 and page 5-57. line 20. Answers to questions
raised earlier about NO3 symbol, 4.5 Tg/yr emission rate and 350 x more efficient
absorption should be reflected here too. (thought 4.5 Tg/yr was equivalent to 4.5 x
1012 g/yr, not 4.5 x 109, and again, is this NOX or N?
5.8.4 Oxides of Nitrogen and the Greenhouse Effect
Page 5-57. paragraph 1. The December 1991 WMO report, "Scientific
Assessment of O3 Depletion," makes much of this section obsolete. A summary of the
material in Chapter 7 of the WMO report should replace the present text.
line 12. Change "sufficiently large" to "significantly higher." This better
reflects Wuebbles statement.
line 18-20. This sentence does not make sense. Why does the
efficiency change?
line 24. ...not destruction of two molecules of O3 per cvcle.
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5.8.5 Deposition of Nitrogen Oxides
Page 5-58. line 14. Symbol NO3 issue arises again.
line 23. Is 2cm sec"1 deposition velocity for PAN based on experiment or
is it just a guess?
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CHAPTER 6 Sampling and Analysis for Oxides of Nitrogen and Related
Species
6.10 Paniculate Nitrate (PN)
There should be some discussion of impactor sampling. The theoretical
framework for comparing volatilization losses in impaction and filter sampling is
presented by Peter McMurry's student Zhang (1990). State-of-the-art impactor
measurements are described by Wall et al. (1988) and Sloane et al. (1991) and
Watson etal. (1991).
6.7 Nitric Acid (HNO3)
Page 6-47. lines 2-8. It should be mentioned up front that filtration and denuder
techniques involve the removal of HNO3 and NO3 species onto a media which will be
discussed later in section 6.10.3.
6.7.3 Chemiluminescence (CLM)
Page 6-51. Aren't wall losses in tubing and in the instrument significant?
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CHAPTER 7 Ambient and Indoor Concentrations of Nitrogen Dioxide
o Title: Why just NC>2 when deposition to the ecosystem is dominated by HNO3?
o The outdoor measurement parts need to be expanded to include data on the
other species discussed throughout this document.
7.2.4.2 Diurnal Patterns
These two sections are poor attempts to characterize the seasonal and diurnal
patterns of NO2- Analysis of more of the data is required, and discussions of the
mechanisms responsible for the observed patterns are in order.
Figure 7-4. This axis labels as well as the %'s are very difficult
to read.
Figure 7-6. These graphs are very difficult to read because you must
use a straight edge. Diurnal plots of the mean values would
be more useful.
x
A discussion of background concentrations of NOX is missing.
7.3.2 Residences Without Indoor Sources
Page 7- 18. lines 8 to 30. All of these 7 points do not follow from Table 7-3.
lines 26-30. Why are the British data different?
7.3.3.1 Average Indoor Concentrations and Estimated Contributions
Page 7-29. line 28. What are geysers and why do they emit more
7.4 Nitric and Nitrous Acids Concentrations
Page 7-54. line 21 . How is MONO formed indoors? Is there a diurnal pattern?
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CHAPTER 8 Assessing Total Human Exposure to Nitrogen Dioxide
8.1 Introduction
Page 8-1. Why is this chapter devoted solely to NO2? Should other species
not be considered?
lines 11 and 12 and 16-18. In lines 11 and 12, it is said that the units of
exposure are concentration times time. Then equation (8-1) on line 16 appears in
which exposure seems to have units of concentration above. This apparent
inconsistency should be corrected or explained.
lines 16 and 21. In equation (8-1), a lower case c is used while in the list
of definitions on line 21, a capital C is used for the same parameter.
Page 8-2. lines 24 and 25. The statement seems to say that health effects are
associated only with long-term exposures to NO2- Please call that line to the attention
of the health effects on the panel to make sure that they agree that this statement is
both necessary and correct.
Page 8-3. line 3. Should this be NO2 than than NO exposure?
8.2.2 Personal Monitoring
Page 8-5. line 18 and 19. "These monitors are passive samplers that utilize
diffusion to control the delivery of gases to the collection medium" would be a better
way to say this.
Page 8-12. line 8. What is a geiser in this context?
Page 8-13. line 14. ...and activity patterns on. NO2 exposure.
line 18. ...NO^ activity patterns...
line 20. Summer needs to be spelled correctly.
Page 8-14. line 1. And elsewhere throughout the chapter the word "variation"
should be replaced by the term "variance" which has a more precise statistical
meaning.
line 3. "alone," not along.
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lines 6 and 7. The sentence beginning "Approximately 15%...is unclear
and should be reworded.
lines 25 - 27. The statement that outdoor concentrations dominate indoor
levels when outdoor concentrations are high, needs to be emphasized strongly here,
and in the chapter summary, and in the document summary, because this is exactly
the case that the ambient standards are set to address.
8.3 Indirect Methods
Page 8-15. line 31 and page 8-16. lines 1-3. One must be careful that
statements such as these are not interpreted to mean that we know so little about such
problems that we can't control NC>2 exposure.
Page 8-15. line 19. Microenvironmental needs to be spelled correctly.
Page 8-16. lines 29-30. Be careful to recognize that as stated on page 8-14
lines 25-27, outdoor concentrations dominate in places where outdoor concentrations
are high (i.e., approaching the ambient standard).
8.3.1 Personal Exposure Models
Page 8-19. lines 10 and 11. ...models...are shown.
line 13. Please check these two sets of numbers for mutual consistency
(i.e., how is 0.12 consistent with 82% of the variance remaining unexplained?).
line 26. estimate, not estimating.
line 30. ...uncertainty associated with modeled personal NO2
exposures...
Page 8-20. Table 8-1. Footnote - "Regression Equation" is stated twice. A plus
sign is needed between the first and second terms on the right side of the equation in
this footnote.
o There are two incomplete references.
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CHAPTER 9 Effects of Nitrogen Oxides on Vegetation
9.1 Introduction
Page 9-1. paragraph 1. This paragraph is very strongly worded--as if the
nitrogen oxides should be considered as a major air pollutant of great concern to plant
life. Lines 14 and 15 serve as an example by inference. No one would argue with
correctness of the statement, but in the context of the lead-in sentence, one would
conclude that we "often" find symptoms of nitrogen oxide as listed on line 15 under
field conditions (i.e., Somewhere in this lead-in paragraph a clear statement of the
infrequent occurrence of visible injuries as due to oxides of nitrogen needs to be
added).
Since NO and NO2 also result in NC>3 depositions to plants (also as described
in Chapter 10), this important phenomenon should be clearly stated as a potential
concern.
line 16. " ...reduced plant growth and yield" may also include increased
growth and yield as some studies have clearly demonstrated. However this should
also carry a caveat that all "fertilization" effects are not necessarily to the good of the
plant.
lines 26 and 27. Add-Since, of these two pollutants, most
available...Inference might be made that of all air pollutants (including OQ and SC>2
and PM) we know most about NO2-
Page 9-1. line 31 and page 9-2. line 1. "Nitrogen oxides are intimately involved
in the formation of ozone and other photochemical oxidants..." This statement should
be more critically expanded as to the reasons NAAQS for the nitrogen oxides. The
major phytotoxicant air pollutant is ozone on a regional scale basis; the role of NOX in
formation as a precursor should not be over looked in this document.
9.2.1 Experimental Design and Statistical Analysis
Page 9-4. line 21. Change oxygen radical to atomic oxygen.
9.2.2.1 Supply
Page 9-7. line 11. "Some studies of forest decline have lead to reports..." At the
outset of this document, the casual use of the term "forest decline" should be avoided.
It is not acceptable to suggest that a real forest decline has taken place. Numerous
authors have started publications with inferences of their studies to a reported "forest
decline." No citations are offered to document a "forest decline," just simply stated as it
was on page 9-7, line 11.
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Suggest-Some studies of the effects of NO and NO2 on forest trees. It is
seriously doubted that whole forests (all components) have been systematically
exposed to NO and NO2 in the cited studies; we have no evidence of a general forest
decline either here in the US or in central Europe or Great Britain.
9.2.3 Pollutant Climatology
Page 9-10. line 8. 80% to 90% of the NO2 is secondary; only the remainder
(10-20%) is secondary. It's production in the atmosphere is linked to meteorology
because 03 or free radicals, formed from photochemical or photochemically-initiated
reactions, are needed and they require sunlight.
lines 7-12. Important to 03 transport and regional 03 induced effects to
vegetation.
Page 9-11. line 1 and 2. "...They become available to the biosphere as toxins."
But what of normal NO^, NO, NO2 emissions and subsequent depositions? Are these
toxins as well? Too dramatic of a statement. Delete.
9.2.4 Pollutant Chemistry
Page 9-11. line 2. Delete "as toxins." Just because some deposits to the
biosphere, it doesn't become a toxin.
9.2.5 Terminology
9.2.5.1 Plant Response
Page 9-11. line 7. Suggest add --... other pollutants. Add -- ...radiation,...
9.2.5.2 Pollutant Exposure
Page 9-14. lines 18-2. Dose-most recently dose has been used as a
determined amount of pollutant taken-uo bv plants, i.e., an internal uptake. Exposure
has been defined here.
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Page 9-15. lines 1-7. Chronic Exposure-Chronic and acute exposure are poor
terms in that they depend upon a symptom (or lack thereof) for definition. Since so
many factors affect symptom development a high exposure mav occur but no
symptoms may follow. An example of drought and high exposure to 63 (above 120pp
for 22 hrs) resulted in no_ symptoms on black cherry, (known sensitive) to O0 in 1988.
"Chronic exposure" if these are sub-injurious "except in very sensitive species
or cultivars" then what is the exposure called when these plants are not present in
the experimental design and/or natural ecosystems? What is injurious? Terms need
to be re-defined and consistent with current literature.
9.3.1.1 External NOX Ratios Around Leaves
Page 9-16. line 7. (At least every five minutes)? Need citation.
9.3.1.3 Foliar Uptake of Nitrate
Page 9-20. lines 15 and 16. The use of the word but here suggests that this
phenomenon may not be of importance.. .however on a season-long basis, with
frequent depositions of NO3, this could be a significant avenue of "N fertilization" for
natural plants and N demanding crops... 60% uptake would appear as significant even
if it does take 14 days.
line 24. Insignificant (statistically?).
lines 25 - 28. Is this reflected in the larger section on forest ecosystems
and red spruce studies of N and winter injury? Remember to check.
9.3.1.5 Access of NO Into Leaves
Page 9-23. lines 5 and 6. Define excess, ambient, chronic or acute exposure.
Field exposure or controlled high dose? Square wave? This is a very dangerous
sentence with implications to natural systems even if at low dose.
line 1 1 . Suggest more readily (two to six fold).
line 21. Is 0.052 ppm NC>2 high, low, or ambient?
line 22. M'2 or CM'2?
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9.3.1.6 Access of the Products of NO Into Cells
Page 9-25: line 10. Confusing sentence... amount to 50-80% air by volume? Of
the leaf or of the air spaces themselves? What else would be in the air paces but air?
Must mean 50-80% of leaf volume is air?
9.3.1.7 Levels of the Products of NOX in Cells
Page 9-26. line 19. Ambient levels? Where is 20ppb NO2 ambient for 5 days
(@ 24 hrs per day?). Exposures need to be defined somewhere in the initial part of
this chapter or reference made to previous chapters of the document which present
pertinent exposure considerations.
This entire paragraph shows the extremes of doses used in various studies, but
readers have not been introduced to what ambient, realistic exposure statistics for NO
and NO2 may bin in situ: in vivo.
Similar comment applies to all of page 28. Example, Sinn and Pell (1984)...
is 200 ppb NO2 ever expected for 5h 2x per week throughout the potato growing
regions of the US?
9.3.2 Chemical and Biochemical Responses
9.3.2.1 Nitrate Reductase Activities
Pages 9-31-39. Relatively high exposures in most studies were needed to elicit
an effect.
9.3.2.2. Nitrate Reductase
Pages 9-36. lines 3 and 4. A criteria document should have no conjecture
present as offered by this sentence beginning with "It is highly likely that..."
9.3.2.5 Effects of Ammonia
Page 9-39. lines 20 and 21 . No citation for such a sweeping statement; once
again some conjecture evident in using the would could. Studies should be cited
which support the phenomenon or delete sentence.
Page 9-46. Exposures for N©2 studies leading to the conclusion on lines 22-26
were high and hence may have influenced results. Conclusion does not necessarily
follow and of great importance to interpreting effects of NOX exposures in northern
latitudes.
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lines 18-28. Confusing. Two years of data presented but a clear
definition of the results for each respective year are not discerned. Specifically, lines
26-28 appear to make something of the lower doses (pooled values for 3 lower
concentrations) even though filtered air and lowest concentration of NO2 were not
different. What does the range average to on a seasonal (290 day) basis? Confusing
paragraph.
Page 9-78. lines 26-29. How was this derived from the data presented in the
previous section? Very generalized and easily mis-intepreted. The nature of the effect
is suggested to be adverse (line 27) but figure 9-12 for instance shows both (-) and
( +) effects on growth of bean at these exposures.
9.5.1.1 Species of Plant
Page 9-82. line 14. Wood volume is only important in commercial timbering
operations. Overall, tree health and bioadversity are of great importance in forested
areas not grown for timber.
9.5.1.3 State of Development
Page 9-89. line 8. Key word here is could.
9.5.2 Environmental Conditions
Page 9-91 through 102. Well written but offers little information of value to
clearly understanding effects of NOy on plants. Results of numerous studies show
( + ),(-), or no effects.
9.6 Effects of Pollutant Mixtures
Page 9-102. lines 16-19. Very true, needs much more emphasis as a major
contributor to OQ formation and then 63 as the major downwind phytotoxicant from
urban sources.
lines 17-27. The reality of finding NOX and SOX at doses above injury
thresholds in situ and together as co-occurrences should be discussed here.
Likewise, 63 and NOx and O3 and 862 co-occurrences should be discussed in light
of injury thresholds before proceeding with this section.
line 30. But 03 alone causes significant "weatherfleck" of Bil W-3
tobacco without the presence of SO2? Confusion which may have been clarified in
later references by Heggestad.
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9.3.4.2 Changes Inside Cells and Tissues
Page 9-49. line 8. Sign, in pathological terms is the visible presence of the
pathogen, i.e., a fruit body of a fungus. Symptom is the correct term here.
lines 12-28. Suggest delete; adds little to discussion, ends with
conjecture, i.e., what else in the "polluted locations outdoors" was not identified?
Drought-nutritional disorders?
General: Much of the previous biochemical and physiological sections are not
relevant to actual field exposure conditions. Although various pathways and
physiological interactions may occur at high doses, implications for long-term low dose
exposure do not necessarily follow. Considerable conjecture is also clearly stated in
these studies.
9.4 Exposure - Response Relationships
9.4.1 Foliar Injury and Loss in Aesthetic Value
Page 9-51. line 25. Absolutely true and very important.
line 2. Order should be ascending, i.e., discoloration (yellowing) pigment
changes, distortions, necrosis, and/or premature senescence of tissues.
lines 3-9. Although most of this is acceptable, we must also recognize
that most plants have a redundancy of foilage and hence the "plants response to NO2
and the effects of various factors upon it" may not be so easily measured.
9.4.1.1 Characteristics of Foliar Symptoms
Page 9-52. lines 11-23. Should add pattern of injury on a spatial and temporal
basis as tied-in to a point source or accidental spill are really the most helpful in a
diagnostic situation.
9.4.2 Loss in Growth and Yield
Page 9-65. lines 23-31 and page 9-67. lines 1-8. Should be moved forward
near the introduction (within introduction) to set the stage for the "high dose" sections
which include many of the biochemical, physiological, foliar effects sections.
Page 9-77. lines 15-17. Need reference by Gupta and Sabaratnam, 1988. A
really amazing effect is reported. Need details before citation should be accepted.
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Page 9-104. lines 4-14. Combine lines 4-14 with initial introduction as
suggested above. More specific detail of MCy and SO2, 03 and the three together
could be presented. Then discussion on following pages (through) 19 would be more
meaningful to document and interpretations therefrom.
9.6.4 Field Chamber and Field Studies
Page 9-124. line 14. It would seem appropriate to give the specific
concentatons here since this appears to be a viable field effect. The data would
complement the details which follow.
9.7 Discussion and Summary
Page 9-127 through 161. Discussion and summary should not present new
information (actually more detailed than text). This is not a summary of the entire
section. What of ambient exposur expectations and effects on plant, productivity,
growth and yield. What of NOX and its important role as a precursor to 03.
This is really another treatise on biochemical and physiological effects.
9.9 Toxic Reactions in the Tissues
Page 155. line 4. Stipple and 03 exposures are very well recognized and
consistent.
line 5. Some chlorotic spots fade.
9.9.1 Concept of Exposure Index
Page 9-158. line 29. It mav be conjecture, delete. The following sentence
negates the conjecture and there is no reason to pre-judge the outcome of future
research efforts.
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CHAPTER 10 The Effects of Nitrogen Oxides on Natural Ecosystems
and their Components
10.1 Introduction
Page 10-1. lines 12-16. These two sentences seem to conflict with one another.
The first suggests impacts of inorganic nitrogen on aquatic and terrestrial ecosystems.
The second reports significant loadings of N compounds, but the latter phrase states
that impacts are generally unknown or considered benign.
The very next sentence points to a growing concern and readers are introduced
to critical loads for nitrogen for various ecosystems.
How can one propose sufficient knowledge exists (generally known or
considered benign) in order to develop Critical Loads as defined in lines 22 to 25,
page 10-1.
10.1.2.3 Ecosystem Response: Impairment of Functions, Changes in
Structure
•\
Page 10-5. lines 22-26. There is a paucity of monitoring data (which is
technically feasible) near and within ecosystems under question for effects of N
depositions. It really isn't difficult to determine accurately, just costly.
As clearly stated here, it is difficult to imagine Critical Loads could be
established for N deposition effects to terrestrial systems at this time.
lines 29 and 30. ...and the possible changes in the nitrogen cycle that
mav result? Is this going to be conjecture? Why not- ... and the defined changes in
the nitrogen cycle that have thus far been demonstrated.
10.1.3 The Nitrogen Cycle
Page 10-6. line 3. Suggest most higher (evolutionary) organisms.
lines 8 and 9. Conjecture ... "may be upsetting"... should be deleted from
Criteria Document.
lines 13. Change pollutant to: anv Nitrogen deposited within an
ecosystem can be...
Page 10-6 through 11. An excellent brief treatise on the N cycle. Many aspects
have little to do with NOX within the Criteria Document but the section adds to the
general understanding and thus serves a very useful purpose.
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10.1.3.1 Biological Nitrogen Fixation
The NOx wetlands section is very thorough and well written. In Vol. II, page 10-
9, top paragraph, the obvious omissions are the blue-green algae which also fix
nitrogen. Otherwise, the document is very good.
10.1.3.5 Denitrification
Page 10-11. lines 12 and 13. Reference to global warming is out of context
within the Criteria Document. Without further citations of proof, this type of single
sentence "silver bullet" should not appear.
10.2 Dry Deposition
Page 10-13. line 6. Suggests change pollutant to Nitrogen forms.
10.2,1 Types of Measurements
Page 10-13. lines 22-24. Suggest deletion since no applications yet made of
significance to understanding pollutant gas deposition.
10.2.3 Processes Governing Deposition of Gases and Particles
Pages 10-16. through 35. Needs a summary to relate depositions, deposition
rates, and differences between receptors and how such findings may further relate to
biologically and meaningfully interpreted effect.
10.2.4.1 Nitrogen Dioxide
Page 10-25. lines 12-15. Very important point to further discussion of forest
ecosystem level effects.
Page 10-30. line 13. micipjneteorologically.
10.2.5 Deposition of "N" Forms to Non-Foliar Surfaces
Page 10-35. line 3Q.Tvpo - NO£ (delete first one).
Page 10-36. Table 10-11. All studies were at > .043 NO2 which is encountered
< 1% of the time in non-urban areas. See Jacobson and McMannus, 1985, Chapter 9.
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10.3 Effects of Vegetation and Soils
10.3.1 Introduction
Page 10-38. lines 5-7 and Figure 10-3. This approach assumes whole
ecosystems will become "toxified" by added nutrients but in reality one or two
organisms may take the brunt of the toxic accumulations. If added nutrient is extremely
high, then it would follow that greater and greater toxicity would be expected to be
observed in even greater numbers of organisms. All substances are poisons, it a
matter of dose. Figure should represent this in its caption.
Page 10-38. line 22. soils.
Page 10-40. lines 1 and 2. How does this relate to the statements (caveats)
found on page 10-5, lines 22-25? Words of caution (caveats) should be stated upfront
as to the current level of understanding N deposition to whole forest ecosystems.
10.3.2 Pollutant N Inputs and Nitrogen Cycling a Natural Ecosystems: A
Brief Review
Page 10-40. lines 22-26. Need citation (immediately and pertinent) to the
suggestion that increased N leads to increased susceptibility to attack by pests and
pathogens (citations) and to climatic change (citations) -- or delete as conjecture.
Page 10-44. line 11. Delete js..
Page 10-51. Single-shot? Single application.
10.3.3.2 Fate of N from Pulse Fertilization vs. Atmospheric Deposition
Page 10-51 through 10-61. "Ecosystems" here are treated as if they are
'natural' ecosystems, at least they are not identified. Picea abies is only found in the
US (on a broad scale) as grown under plantation conditions. Pinus taeda (and many
of the species listed in Tables 10-12 and 10-13) are managed plantation-grown trees
with greatly altered site and understory conditions from both a pre-plant, early growth
stages, thinnings, and final harvested stands. Hence, are these true ecosystem
studies? Are they as defined by Odum and others as cited in the Introduction to
Chapter 10?
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Page 10-59 and 10-60. As based upon statements on 10-59, lines 6-8 and 10-
60, lines 1-4, it would appear that excess N inputs are not taken up by the soil
heterotrophs as much as by higher plants but that N deposited in excess of vegetation
(higher plant, tree) needs is subject to nitrification and nitrate leaching.
This entire section. 10.3.3.2, needs an easily understandable bottom-line type
of summary. Is excess N of importance because of uptake? Excessive leaching?, or
10.3.4 Effects of Pollutant N Inputs on Soils
10.3.4.1 Soil Biota
Page 10-62. lines 13 and 14. ...seem a likely result... Conjecture especially in
light of the next sentence.
lines 28-30. A critical and clear statement of importance to the concept of
Critical Loads and our current lack of knowledge in an important component of the
natural ecosystem.
10.3.4.2 Soil Chemistry
Page 10-65. line 5. Delete We.
Page 10-67. lines 7-14. Following a very well written and easily understood
section, it is difficult to accept the paucity of data under actual field situations. Yet,
once again, the Criteria Document should not accept conjecture as evidenced
particularly on lines 8 and 9. What is a high enough input for sufficiently long term?
On which soils, in what regions, and across or within which ecosystems? More
empirical data is critically needed.
lines 15-21. Within natural systems or are the Douglas fir planted?
Would soils acidified by red alder, naturally be colonized by Douglas fir?
10.3.6 Effects of Pollutant N Deposition upon Vegetation Nutrient Status
Page 10-69. lines 8-19.
lines 8-10. This does not seem to follow from conclusion types of
statements on pages 10-59 and 10-60. Citations are needed here for proof via
empirical data.
lines 10-13. As described above, these responses should be minimal as
suggested on pages 10-59 and 10-60.
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lines 13-15. Need citations here to demonstrate cause and effect,
especially in changes to insect and disease attack verified associated with N
depositions?
line 18. Seem? Does not belong in Criteria Document.
10.3.6.2 Soil-Mediated Effects on Vegetation
Page 10-71. lines 1-3. Give rates of N deposition.
lines 4-12. Can some of the subjective be deleted, i.e., might include,
may allow?
line 14. The use of the term forest decline is an absolute misnomer.
Whole forests never declined on a regional scale basis. Very site specific tree
declines did occur with many, many possible explanations including severe drought,
over utilization of sites and resultant nutrient deficiencies (Mg and K in, particular)
provenance failures, and disease and insect (normal) attacks. Numerous studies (not
reported within the document; nor could they all be) address these causes. In
addition, several studies (notably by Kenk, et al.) have demonstrated normal to
increase growth of Norway spruce stands in the part two decades, i.e., no unexplained
forest decline exists.
Page 10-72. Since so many topics are being discussed (hypothesis) in this
section why not include that in the high elevation forests of the S. Applachians, 92% of
the stands were Fraser fir and Balsam fir with nearly 100% mortality due to the balsam
wooly adelgid. Hence, 8% (red spruce) of the stand are left open to the harsh
environment of these mountain tops with all of the associated stresses. Also, it would
be appropriate to note that these stands are regenerating to spruce and fir so thick that
walking is nearly impossible and that these trees appear quite healthy (Zedaker, et
al.).
Page 10-72. line 1. ...of well below 200 uM/L has been noted. How much
below and is this below the 70 uM/L peak total Aluminum concentrations (see Line 26,
page 10-71).
10.3.6.3 Ecosystem Levl Responses to N Deposition
Page 10-73. lines 8-26. These studies were all with fertilizer applications and
hence the differences in pulsed versus long term low inputs of N must also be restated
as discussed previously on pages 10-47 to 10-62. For instance, the P and N studies in
slash pine showed a much greater early season flush and succulence of new growth
thus affording a longer time in concert with the rust fungus life cycle and more easily
penetrated tissues. There is no evidence offered that low longer term N deposition
would afford the same advantages to the cycle. Need studies first-conclusions to
follow.
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line 8. Conjecture, see lines 22-24. Suggest deletion of the whole
concept of interactions with N depositions and disease and insect attacks both here
and previously where no citations have been offered. (See previous comments.).
lines 17-21. State rate of fertilization.
lines 24-26. Clearly stated, agreed.
10.3.7 Critical Loads for Atmospheric N Deposition
Page 10-73 to 10-79. Opinion: Until the concepts associated with critical loads
are more fully evaluated with 'in vivo1 data which withstands peer review, and use of
such a concept in deciding issues related to the NAAQS processes should not be
employed. Terms such as 'subjective guesses', 'assumption1, 'in our judgment', all
add little to a solid conclusion on the use of critical loads.
Thus far, there is only little evidence, and quite controversial at that, which
suggests relationships between excess N depositions, soil acidification processes,
and subsequently on forest species health and productivity. To adjust a critical load
on N deposition solely to soil acidification potential on to whole ecosystem level effects
is a gigantic assumption.
Page 10-74. lines 9 and 10. Why the page numbers?
Page 10-76. line 30. Add; these values were quantitatively...
10.3.9 Conclusions
Page 10-79. line 17. Pronounced? Reference to the natural N cycle should
proceed this less readers conclude at the outset that this is N as an anthropogenic
pollutant.
line 20. ...is likely to be... Have any studies been done at ambient N
depositions which clearly demonstrate increased growth has taken place over and
above natural N depositions (N-cycle?).
In line 19, it is stated that "...islikelvto be a growth increase". Now is line 20, the
increase becomes fact and the only question is whether or not the ... "growth increase."
Now in line 20, the increase becomes fact and the only question is whether or not the
"...growth increase is deemed desirable or undesirable..."
line 23. Delete such.
line 31. Reference is 20 years old; is this still true in 1992; if indeed this
is so, the pollutant N depositions must not yet have reached even a balanced N input-
output.
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Page 10-80. line 4. Delete be.; again the use of the word may is subjective.
Agree with statements in this paragraph as referenced in previous comments.
10.4.2 Indirect Effects
Page 10-81. The definition of a direct effect is not consistent with the literature.
The rate of addition of N to a system and its relationship to indirect effects has nothing
to do with succession. What are positive effects in terrestrial ecosystems? Disagree
with the statement that many ecosystems are nitrogen limited. The disagreement is
that others would argue that current systems are CC>2 limited. Which is it? Are indirect
effects only positive or are there negative indirect effects?
Page 10-83. line 17. Kenk and Fisher's article should be checked. Do they
suggest or better yet define an impact of atmospheric N depositions playing a role in
observed growth increases since 1960 or it this a Criteria Document author
interpretive suggestion?
line 19. Delete fee..
line 31. ...forest decline? Norway spruce is a species; and as a species
in Germany it has suffered only from very site specific decline phenomena. "Forest
decline" is a very serious and dangerous misnomer. Not one citation in this entire
document has given evidence of a forest decline. Delete.
10.4.3 N Saturation, Critical Loads, and Current Deposition
Is the repetition on pp 1-72 and 10-84 necessary?
10.4.3.1 Critical N Loads That Have Been Proposed
Page 10-85. lines 30-33. The meaning of the argument is not clear.
Page 10-86. line 23. Based upon what evidence should a critical load be
established for N deposition to high elevation coniferous forests? The document has
not clearly demonstrated any direct or indirect impacts of N on coniferous ecosystems
(to be deleterious to tree health).
WHO is not peer review literature, but is rather review articles with generalities
and all inclusive statements.
lines 26-33. could: would: may not be keeping pace; - all subjective.
10.4.3.2 Current Rate of Total N Deposition
Page 10-87. line 13. How does figure 10-16 fit in here (is it 10-14)?
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line 14. Disagree with the conclusion that North American sites have
typically less deposition than sites in Europe. With the exception of the Netherlands
and its special problem of NH3, the data in Table 10-14 suggest that there is
comparability between the two continents. If the table is right, the conclusions do not
seem consistent.
line 27. The section is confusing on units of deposition. Are the units of
deposition N or NH4 or NC>3?
Page 10-93. lines 3-7. Compare this sentence suggesting minor changes on
some ecosystems as due to N depositions to the lead-in sentence on Page 10-79
where the first conclusion is little doubt that N deposition has a pronounced effect on
many, if not most terrestrial ecosystems.
Which is correct? Can critical loads rally hold up when there are such
conflicting statements and conflicting evidence offered in the document?
line 16. It seems odd that the range of N2O emissions is not 0-4 rather
than 2 - 4kg ha"1 y"1. Systems that are nitrogen deficient are not likely to re-emit
nitrogen to the atmosphere under any conditions and most natural ecosystems are N
deficient.
Table 10-14: Measurements of Various Forms of Annual N Deposition to North
American and European Ecosystems. In the table 10-14, the data on footnote "b"
indicate that through fall data include dry deposition of nitrogen. Most of the dry
deposited nitrogen is retained by the canopy so that through fall is not a surrogate for
dry deposition.
Table 10-15. Mean Annual Wet Nitrate and Ammonium Deposition to Various
States Located Throughout the United States. This data would be easier to digest if
they were plotted on a map with isopleths.
10.5 Ecosystems Effects ~ Wetlands and Bogs
10.5.1 Introduction
Page 10-94. lines 26-30. Stratospheric Ozone - Is this information correct?
Are combustion sources of N2O contributing to strat ozone depletion?
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10.5.2 Atmospheric Nitrogen Inputs
Page 10-96. lines 1-4. (Analogy between North America and Europe in
Wetlands). It is concluded that similar effects can b anticipated in North America with
respect to nitrogen effects on species composition. Is this speculation?
(Atmospheric Inputs to Wetlands) This section is an interesting contrast to the
earlier section on nitrogen inputs from the atmosphere to terrestrial landscapes. The
problem is that the two sections discuss the same topics but with no common
references. Is deposition mechanistically different between the two landscapes?
lines 5-8. This is not consistent with previous discussions in Chapter 9
(solubility in water of NO and NO2 is low and not linear). The reference regarding dry
deposition is different from that used earlier (line 7). The section on interception (lines
15-23) suggests concurrence between the phenomenon at high elevations and in
wetlands. This is difficult to imagine given the differences in wind speed and
architecture of the two canopies.
lines 24-31. This discusses the contribution of NO3 and NH4 to
deposition in wetlands via wet deposition. These conclusions are at odds with Table
10-15 both in terms of relative contribution of the two anions and the total rate of
nitrogen deposition.
Page 10-98. line 19 and 10-99. lines 1-5. Concludes that atmospheric N
deposition is a major source of NC>3 to surface waters in North America. Is this
statement generically accurate? Later on lines 4 and 5 the conclusion is that the
"direct" contribution is not known with certainty. Which statement is correct?
10.5.4.4 Effects on Biotic Diversity and Ecosystem Structure
Page 10-114. lines 23-31. 10-115. lines 1-7. 10-116. lines 1-5 and 10-117. lines
1-17. (Species Changes in Wetlands in Britain). The discussion on changes in
Sphagnum in bogs places some of the blame on nitrogen. The work of Lee and others
is solely descriptive of sulfur not nitrogen. If so, the association needs to be clarified.
On page 10-114, line 31, nitrogen is implicated without a reference.
10-5.4.5
Page 10-117-120. This section is written without any obvious overlap with the
earlier discussion of nitrogen cycling in forests. Any reason? Is the forest sentence
accurate? Are toxic effects solely from excess nitrogen? On lines 21+, the discussion
again focuses on the work of Lee and Ferguson. This study was for sulfur not nitrogen
deposition and its application needs to be made clear in this section.
Table 10-20. Distribution of 2,164 Central European plant species in the
gradient of nitrogen indicator values (from Ellenberg, 1988, p. 379). Rates of nitrogen
deposition are reported as equivalents here and kg elsewhere. Why the discrepancy?
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10.6.2.3 Nitrogen Saturation
Pages 130-134. The process of inhibition of water by a sponge is strictly
physical. Conversely, the process of nitrogen uptake and assimilation in landscapes
is principally one of complex biological reactions that are spatially and temporally
variable. The analogy is unfortunate and misleading. Earlier, the document goes to
great lengths to indicate how the biology of the system affects the application of the
critical loads concept and the sponge overlooks that aspect.
Page 131. lines 14+. The statement is made that the growing season in
forested landscapes coincides with periods of lower nitrogen deposition. The
statement is counter to the discussion in Chapter 9. What happened to the effect of
leaf area index in dry deposition and interception of wind-blown precipitation? See
also page 10-140, lines 25-27.
10.6.3.1 Chronic Acidification
Page 10-42. line 5. Insert "almost" before "as important."
lines 15 and 16. 0.17 is not high. Delete "high" in line 15 and delete
"good" in line 16.
10.6.3.3 Biological Effects
Page 10-167. lines 7-25. Is this section applicable to solely nitrogen deposition
or is the argument more specifically accurate for sulfur deposition?
10.6.4.3 Evidence for Nitrogen Deposition Effects in Estuarine Systems --
Case Studies
Page 1Q-191+. The Chesapeake Bay. The issue of this section being included
is discussed under the general comments. The precedent of inclusion is not a good
one.
In the budgets for N transport, why are the rates of deposition given as
equivalents rather than kg to be consistent? This makes comparison of deposition
rates between the peer-reviewed material and the Chesapeake Bay study difficult.
The section on how nitrogen deposition and transport was calculated for the Bay area
needs to be thoroughly evaluated from the original reports, and the data need to be
consistent with the literature discussed earlier in this volume on what controls nitrogen
deposition, uptake and cycling in terrestrial and aquatic landscapes.
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10.7 Discussion and Summary
10.7.1 Introduction
Page 10-205. lines 27 and 28. Suggest deletion of this sentence since the
statement is not citable to a specific peer review paper. Many "views" emerge over the
course of years and decides but only hard science should be cited here. This is the
type of sentence that can be lifted directly from the Criteria Document and cited
correctly to the credit of the US EPA. Yet, the conflicting evidence as so well detailed
in the document will not be cited, just the quoted sentence. Suggest deletion since
second sentence is factual and citable back to US EPA.
Page 10-206. line 4. Compare this very generalized statement (2) ecosystems
formerly limited by nitrogen have become nitrogen saturated via atmospheric
depositions to page 10-79, lines 23-24 "All current information indicates that such 'N
saturated' forests are relatively rare and limited in extent, especially in managed
forests." Which is correct? It is very important that the summary and conclusions be
representative of the text and not digress into general statements which then become
the 'fact'. Most people read summaries.
lines 7 and 8. Critical loads are again noted here as if they are a solution
to the perceived problem but the section concludes with all types of warnings as to as-
yet inadequacies in their usefulness across forested ecosystems. Again, a simple
sentence but perhaps through its simplicity, it becomes too easily accepted.
lines 27-30. These are subjective conclusions, "...not readily reversed
and will significantly alter the ecosystem." Such phrases are not supported by the
document.
10.7.3 Nitrogen Deposition
Page 10-210. lines 14-23. Statement not supported by the document; see page
10-78.
Page 10-211. Table 10-31. Should clearly state that these are site averages,
not state averages: the deposition patterns do not follow state boundaries.
Page 10-212. Table 10-32. Once again, there are not "ecosystems" especially
for North American sites. See page 10-88. For instance the Georgia data was for 1
site in loblolly pine area. So many questions could be asked of this one site as to its
representativeness of all. sits of loblolly pine (millions of acres?) in Georgia. Indeed is
loblolly pine really an ecosystem type except as a component in natural climax forests
of the south. This site was most likely a managed, heavily "plantationed" area.
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10.7.4 Effect of Deposited Nitrogen on Forest Vegetation and Soils
Page 10-213 and 214. 'N' saturated soils have been clearly stated as very rare
in the US. Why is this not included here as well? N saturation tends to be more
common in older forests...? But on page 10-29, line 23, N saturated soils are declared
rare. Which is it?
Page 214. (check spelling).
Page 10-218. Appears as subjective. There are concerns...? Have these
concerns yet been documented.
line 5. ...the potential exists...? High enough inputs for a sufficiently long
time?
Page 10-219. lines 1 and 2. Weathering rates cited again a significant void in
our knowledge...does not add credence to use of critical loads.
line 15. Ulrich may have hypothesized that Al pulses caused root
damages but nowhere does he demonstrate that pathogens (normally occurring)
were ever investigated as another more likely cause?
line 18. Forest decline is a misnomer.
line 24. There is no forest decline in both countries. There have been
historically known species declines See Kandler, Plant Disease, 1988? and Millers et
al., 1989, USDA-NE For. Exp. Station) for description of species declines on a
regional basis with mostly known causalities.
lines 29-31. Increased N deposition can cause significant changes in
tree physiological function, susceptibility to insect and disease attack and even plant
community structure? No evidence of this has been so clearly and significantly
reported in this Criteria Document to support such a dramatic and all inclusive
statement.
Page 220. lines 3 and 4. Agree. Should precede all of these 'conclusions' so
as to protect the document from misquotes.
lines 5-9. Give rates of deposition.
lines 10-22. Conjecture, suggest deletion; lines 20-22, this is correct, but
only at much higher deposition rates would the potential be significant.
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10.7.5 Effects of Nitrogen on Terrestrial Vegetation
Page 10-221. lines 18-22 and lines 23-27. Appear to be in conflict although it is
clearly stated that the latter are hypothesis and the former are subjective through the
use of phrase "seems unlikely at the current time."
Page 222. lines 1 and 2. Delete forest decline; suggest site specific symptoms
on this species.
lines 20 and 21. Reference to Liljelund and Torstensson (1988) ...have
shown clear signs of vegetation changes in response to N deposition rates of 20 Kg
ha"1 yr"1. However, at least in this one place that I could find in my review, on Page
10-86 citing this same reference, the statement reads "Critical loads less than 30 Ka
ha~1yT1 have been proposed based on criteria to minimize species changes." Which
is it, 20 or 30 Kg. ? Also, no data have been presented from these authors' papers
which actually demonstrate species changes have clearly taken place.
10.7.6 N Saturation, Critical Loads, and Current Deposition
Page 10-223. line 19. Maintenance of N inputs...
lines 33-34. 3 to 48 Kg N ha yr for calcareous based
soils? This is very broad and therefore, until better defined, useless 'Critical load' and
points to the general lack of agreement as to N deposition elicited effects on natural
ecosystems. Regionality of N depositions becomes more and more complex when
such figures (i.e., 3 to 48 Kg) are suggested.
Page 224. lines 1 and 2. Even a further spread of 1 to 100 Kg.
lines 3-32. Repeat of lines 4-33, page 10-86. See previous comments.
Page 10-225. line 1. Typo, pronounced.
lines 1 and 2. This is a previously presented statement but without clear
evidence demonstrated in the document.
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CHAPTER 11 Effects of Nitrogen Oxides on Visibility
11.1 Overview of Light Scattering and Absorption
Page 11-1. lines 23 and 24. Not only does nitrous acid interfere with
chemiluminescent NC>2 measurements, nitric acid and PAN also interfere.
lines 24-29. First of all, the reason is not that NH3 reacts preferentially
with sulfate, it is because acid sulfate reacts with NH4NO3 and re-releases the HNC^.
Secondly, there are other forms of nitrate aerosol that are not affected by the presence
of acidic sulfate (see comment on section 4.2.2, page 4-7). Third, NH4, NO3 can exist
in warm climates (see Wolff et al., Atmospheric Environment, vol. 25A, p 2173-2186,
1991.).
Page 11-3. line 1. "Cattle grazing fields," as opposed to concentrated feedlots,
are not significant ammonia sources. Large areas of the country are covered by
grazing fields, and there are some large NOy sources in the vicinity of some of them,
but ammonium nitrate seems to show up only downwind of feedlots.
Nitrate aerosols are important in urban areas only in the western U.S.
line 8. Just say particles. Saying non-nitrogenous implies that
nitrogenous particles have some special property that makes them brown.
line 21. radiative transfer.
line 27. The detail within the [ ] brackets is not used in any of the
discussion and poses an unnecessary hurdle for the reader. Suggest replacing the
bracketed expression by the symbol J ( , ) for the source function.
Page 11-4. line 1. figure 11-2 Eliminate the arrowhead at the left end of the r
axis so the reader knows the orientation of r.
Page 11-5. lines 14-30. The discussion of equation 11 -2 should probably some
before equation 11-1, so the reader will have some idea of what the terms appearing
there mean.
This is also the natural place for a paragraph to the effect that bsp usually
dominates bext, and that fine-particle bsp usually dominates total bsp. White (1991) is a
recent, comprehensive review supporting this point.
line 15. Should read "light absorption components:".
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Page 11-6. line 4. The reference for Figure 11-3 should be "adapted from
Middleton (1952)." This figure appeared several times (e.g., Figure 2-10 in the 1979
EPA Report to Congress on visibility (EPA-450/5-79-008)) before the 1980 Latimer
and Ireson document.
line 8. Need to point out that it is because of the particle size of the
nitrate aerosol, not some other property.
lines 12-17. This paragraph introduces bext, and should come before the
discussion of equation 11 -2.
Page 11-7. lines 5 and 6. This sentence seems, incorrectly, to identify bap and
bsp as efficiencies.
Page 11-8. lines 3-30. This paragraph seems to be the only discussion of
nitrate particle size distribution in the whole CD. Why is it in the "overview"? Toward
the end, it turns into a very compressed discussion of nitrate particle formation
mechanisms. Both of these topics deserve more thorough coverage, if not in chapter
11, then in chapter 3 (for size distribution) and chapter 5 (for formation mechanisms).
More recent studies on nitrate particle size distributions include Watson, et al.
(1991), Sloane et al. (1991) and Wexler and Seinfeld (1992). As discussed above,
there needs to be a clear and consistent distinction drawn between reliable and
suspect measurements.
11.2 Atmospheric Discoloration Caused By Nitrogen Oxides
Page 11-10. lines. If the -dependence of lr ( ) and I0( ) is to be explicit in
equation 11-3, then the -dependence of ( ) andJ( ) should be similarly explicit.
line 22. The right-hand side of equation 11-4 should be (1 + bag/bscat)'1
rather than (1 + bag/bext)"1.
line 22. The right hand side of equation 11-4 should be (1 + bag/bscat)'1
rather than (1 + bag/bext)"1.
line 25. A more recent determination of NO2 absorption is presented by
Davidson et al. (1988). Copies of two of their figures are attached.
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line 28. The value of 0.33 km"1 ppm"1 derived from Dixon is for 0 degrees
Centigrade, and corresponds to 0.30 km"1 ppm"1 at the more standard 25 degrees
Centigrade. Watson et al. (1991) obtained a value corresponding to 0.21 km"
1ppm"1 at STP when they averaged the measurements of Davidson et al. (1988) over
the spectrum of a narrowband 550 nm filter of the type used in visibility monitoring.
Watson et al. noted that absorption is 70% larger at 545 nm than at 555 nm, because
of the fine-scale oscillations evident in the Davidson figures.
A value of 0.33 km"1 ppm"1 is given for the light absorption coefficient for
NC>2 at = 0.55 um, while Figure 11-5 seems to show a value closer to 0.2 km"1 ppm"1
at 0.55 um.
lines 30 and 31. The sentence should read "When Equation 1 1-4 is
evaluated as a function of wavelength ( ) and the -dependence of b^ is neglected,
the curves shown in Figure 11-6 are obtained...".
Page 11-11. line 1. Figure 11-5. The y-axis legend of Figure 11-5 should be
babs( )/N02(km"1ppm-1).
lines 8-13. The neglect in Figure 11-6 of b^s dependence on
wavelength cannot be justified at large visual ranges, where Rayleight scattering is
dominant. A 200 km visual range corresponds to a b^of about 15 Mm"1 at
aa = 550 nm. About 10 Mm"1 of this total is from Rayleight scattering, with an
Angstrom exponent of -4; if we assume an Angstrom exponent of -1 .5 for the aerosol,
we get a bgcatof 44 zmm"1 at 400 nm. The bNO2 of 0.0015 ppm is 2.6 Mm"1 at 400 nm,
yielding a relative horizon brightness of 44/(44+2.6) = 0.94 at 400 nm. This represents
a darkening of 6% rather than 14%, and would probably not appear "quite noticeably
colored".
Page 11-12. line 1. Figure 11-6. The y-axis legend of Figure 1 1 -6 should be
Bhorizon/Bhorizon ([NO2] = 0).
lines 2-4. All three bext should be b.^.
Page 11-13. line 1. Presumably, Table 11-1's assumed size distributions are
log normal.
line 16. The defining expression for should be reformatted to make
clear that it is an exponent.
line 23.. radiative transfer
line 32. scattering
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11.3 Visual Range Reduction Caused By Nitrogen Oxides
Page 11-14. lines 14-16. The range of contrast thresholds supported by
literature extends to about 20 percent (Gritting, 1980; Dzubay et al., 1982). (Both these
studies are by EPA RTP!).
Page 11-15. line 3. Samuels et al. (1973) was an influential early reference.
11.4 Nitrate Phase Changes and Hygroscopicity
Page 11-15. lines 24 and 25. This sentence should be rewarded. For
example, non-volatile nitrates such as NaNO3 a'so ex'st- A better way to say this
might be "Assessment of the role played by nitrate particles in urban, regional and
layered haze and in plumes is more difficult than for sulfates because certain of the
nitrate aerosols (e.g. Nh^NC^) can volatilize during sample collection."
Page 11-17. line 13. Insert "and any acidic sulfate" after
line 16. Not true; see comment 1.
11.4 Nitrate Phase changes and Hygroscopicity
Page 11-18. lines 7-30. The nitrate sampling artifact is treated much more
thoroughly in Chapter 6.10, and this paragraph should probably just summarize and
reference the earlier discussion.
line 7. Strike extreme, and extremely. Good measurements can be
made if the care is exercised.
Page 11-19. lines 23-26. The Tang calculations for internal mixtures, on which
this discussion is based, were wrong (Tang, 1982).
Page 11 -20. lines 1. Figure 11-8 is for a ug/m^ (dry) of ammonium sulfate
aerosol.
line 3. Should read "having lognormal particle size distributions..."
Page 11-21. line 1. Figure 11-9. This figure shows particle size changes for
(HN4)2SO4 aerosol as a function of relative humidity, not bscat.
Page 11-20. Figure 11-8 and page 11-21. Figure 11-9. The first part of these
captions says that these Figures apply to sulfate o_r nitrate aerosol, while the curves
with their delinquence points at 82% RH look like sulfate curves only. Fix the caption.
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11.5 Role of Nitrogen Oxides in Urban Haze
Page 11-21. line 9. This review of extinction budgets and efficiencies needs a
good deal of work. As noted above, it needs to draw a clear and consistent distinction
between reliable and suspect measurements.
The contribution of particulate nitrate to fine-particle mass should be given for
each study reviewed, since nitrate mass rather than nitrate extinction is what is actually
measured. The picture emerging from modern measurements that minimize sampling
artifacts is that nitrate contributes a significant fraction of particle mass in western
cities, and only in western cities.
Given the directly measured contribution of nitrate to fine particle mass in places
like Los Angeles, Phoenix, and Denver, and the well known importance of fine particle
mass for total particle scattering, it is not necessary to present the individual extinction
estimates. If extinction estimates are presented, then these should be presented
according to a common format: for example, Chapter 11.5.1 on California urban areas
now given efficiencies, while Chapter 11.5.2 on other eastern urban areas given
mostly budgets. If estimated extinction efficiencies based on regression are
presented, then estimates based on size distribution measurements should also be
presented (e.g., Sloane et at., 1991, and references therein).
lines 11 and 12. This sentence is confusing, because Phoenix and
Denver are themselves "western urban areas."
Page 11-22. line 1. Figure 11-10 is for 1 ug/m3 (dry) ammonium nitrate aerosol.
Figure 11-10. Again, the caption begins by referring to sulfate fir nitrate,
while in this case only nitrate is shown.
line 3. Should read "(having lognormal particle size distributions...".
Page 11 -23. line 1. Figure 11-11 is wrong (Tang, 1982).
Page 11-24. line 1. Figure 11-12 is wrong (Tang, 1982).
Page 11-23. Figure 11-11 and Page 11-24. Figure 11-12. I believe that at least
one of these figures was the subject of a correction by the author (Tang) which
appears in a later issue of Atmospheric Environment. Please check. Again, modify
caption to correct for possible confusion caused by reference to "sulfate or nitrate
aerosol.
11.5.1 California Urban Areas
Page 11-25. line 1. The estimates for extinction by particulate nitrate in the
three main studies reviewed here all come from regression analysis. It should be
noted that none of the regressions included a term for organic matter, which is an
important component of the urban California fine aerosol. The Ph.D. thesis of X.
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Zhang (1990), a Peter McMurry student, derives estimates for Los Angeles based on
the size distributions measured in the SCAQS study.
lines 8-1 2. White and Roberts (1977) presented their results in terms of
scattering per ammonium nitrate mass. The conversion to units of scattering per
nitrate ion has been done incorrectly here: the correctly converted values are
2.9 + 6.5u2 m2/g, or 4.5 m2/g at 50% RH. The conversion proceeds as follows:
bscat = (2.2 + 5.0u2) [NH4NO3-] = (2.2 + 5.0U2) (1.3 [NC^-] ) = (2.9 + 6.5U2) [ NO3'].
The nitrate measurements used by White and Roberts were subject to positive
artifacts. The nephelometer used to measure extinction was not at ambient
temperature.
line 16. Cass (1979) used linear and non-linear regression...
lines 21 -24. Like White and Roberts (1977), Cass (1979) presented his
results in terms of scattering per ammonium nitrate mass. Unlike the White and
Roberts results, the Cass results are presented here without conversion to scattering
per nitrate ion, and are thus incompatible with even the corrected values for White and
Roberts.
The nitrate measurements used by Cass were subject to positive artifacts. The
nitrate data were 24h averages, while the extinction data were daytime averages.
Cass, unlike White and Roberts, and Appel et al., derived extinction from visual range
observations rather than nephelometer measurements. He used a Koschmeider
constant of 3.9 rather than the 3.0 recommended in equation 11-7, thereby biasing his
extinction values somewhat high.
Page 11-26. lines 7-10. Appel et al. (1985) presented their results in terms of
scattering per nitrate ion. They are presented here without conversion, and are hence
incompatible with the Cass values.
The denuder and filter pack nitrate measurements of Appel represent the state-
of-the-art.
lines 14-19. The Pratsinis et al. (1984) estimates are irrelevant. They
were based on one day of measurements in Los Angeles, and the extinction estimates
came from a regression relationship (Groblicki et al., 1981) for wintertime Denver, the
particulate nitrate values are from Teflon filters, and almost certainly understate actual
ambient concentrations. NO2 was not measured, only estimated as 1/2 NOX.
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lines 19 and 20. Gray et al. (1984) apportioned mass, not light extinction.
The paper by Gray (1984) is not a visibility study per se. That paper shows that
9.4% of the fine aerosol mass was NO3~ ion from which one would infer that about
13% of the fine mass consisted of nitrate aerosol compounds (considering both anions
and cations). But no calculations were performed to translate fine mass into
contributions to the extinction coefficient. A more complete, version of Gray's data
base is available in Environ. Sci. Technol.. 1986. pp 580-589. A better reference
would be the study by Larson et al (1989) Environ. Sci. Techno!., pp. 281-289, where
from Tables III and IV, one could calculate fine and coarse aerosol nitrate and NO2
contributions to light extinction at midday in Los Angeles in the summer months.
(Note that much higher nitrate levels are observed at other times and places in
Southern California than during these summer midday periods).
11.5.2 Urban Areas in the Western United States
Page 11-26. line 22. Additional studies using modern, artifact-free nitrate
sampling techniques are: Watson et al., 1988 (Denver); Watson et al, 1991 (Phoenix);
Sloane et all, 1991 (Denver).
lines 26 +. The regression analysis discussed here is by Groblicki et al.
(1981); the Lewis et al. (1986) reference presents a different set of measurements from
a different year, and is not discussed anywhere in the paragraph. This is unfortunate,
because the Lewis et al. nitrate measurements were by state-of-the-art denuder and
filter pack, while the earlier Groblicki et al. measurements were subject to negative
artifacts.
Page 11 -27. line 7. Wolff et al. (1981) is based on the same measurement set
as Groblicki et al., subject to the same negative participate nitrate artifact.
lines 14 and 15. The Hasan and Dzubay (1983) efficiency estimates are
for aerosol heated to drive off any water. They are presented here in terms of
scattering per ammonium nitrate mass, a change from the convention adopted (albeit
inconsistently) in the preceding section on urban California.
lines 16 +. The extinction estimates of Solomon and Moyers (1984)
came from a regression relationship (Groblicki et al., 1981) for Denver. Subsequent
work lead than to conclude (Solomon and Moyers, 1986) that their nitrate
measurements incorporated a significant positive artifact.
lines 27 +. Houston is climatologically eastern despite the cowboy boots.
The measurements of Dzubay et al. (1982) were subject to negative artifacts.
11.5.3 Urban Areas in the Eastern United States, Europe, and Mexico
Page 11-28. line 11. The susceptibility to artifacts of measurements in this
section should be noted.
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Page 11-29. lines 1 and 2. Diederen et al. (1985) estimated the contribution of
ammonium nitrate to dry particle scattering, not total extinction.
11.5.4 Modeling Urban Haze Effects
Page 11-29. line 9. This section should note the equilibrium models developed
by a succession of John Seinfeld students for aerosols containing sulfate, nitrate,
ammonium, and water (Saxena et al., 1986, and references therein).
Watson et al. (1991) used one of these models to examine the relative
sensitivity of ammonium nitrate in Phoenix to total nitrate and total ammonia (Figure
attached).
lines 17 and 18. The study by Russell and Cass (1986) states that
"Reduction in NH3 emissions suppresses aerosol nitrate formation, resulting in higher
HNO3 levels. Because of this increase in HNO3 |eve|Si it wouid be a mjstake to
conclude that ammonia suppression is the "most effective," emission control strategy
until more is known about the effects of
If one really wants to look at a thorough study of the effect of emission controls
on nitrate and NO2, the study by Russell et al. 1988 referenced on line 19 of page 11-
29 is accompanied by a second part (Russell et al. 1988b, Environ. Sci. Technol. pp
1336-1347) that goes into considerable detail on the effects of alternative emission
controls.
11.6.1 Nonurban Areas of the Western United States
Page 11-30. line 1. Richards et al. (1991) report state-of-the-art nitrate
measurements at Grand Canyon.
lines 7-9. The potential artifacts in the Macias et al. (1981) data should
be noted.
lines 17-20. Most of the Trijonis et al. (1988) data were subject to
artifacts. The percentage given here is of non-Rayleigh bext, which is significantly
smaller than total bext in the RESOLVE study area.
11.6.2 Nonurban Areas of the Eastern United States
Page 11-31. lines 16-18. The numbers cited do not add to 100%.
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11.6.3 Modeling Regional Haze Effects
More needs to be said about the nitrate formation mechanism used in the
model. It was a pretty crude linear mechanism which had little in common with reality,
and the performance was so poor that we gain little or no information from the results.
11.7 Role of Nitrogen Oxides in Plume Visual Impact
Page 11-34. line 24. The visible plume NC>2 burden should be 90 ppm-m not
ppm-km.
Page 11-35. lines 5. 18. and 31. Why not identify the Navajo Generating
Station?
line 9. Should this be ammonia not ammonium ion?
lines 25 +. The discussion should make clear that the PLUVUE and ERT
models treat only NO2, primary particles, and secondary sulfate. That is, they do not
attempt to model nitrate aerosol. The prediction of nitrate formation in plums is tackled
by Seigneur et al. (1982), Joos et al. (1987), and Hudischewskyj and Seigneur (1989).
11.8 Contributions of Nitrogen Oxides to the Light Extinction Budget
Table 11-2: Nitrogen Dioxide Contributions to Total Light Extinction.
A caption for "RURAL EAST" is missing.
Page 11-36. line 14. Section 11.8 is wholly unintegrated with the extensive
discussion o pages 11-25 through 11-31. Some studies discussed there are not
included here. Some studies are covered in both places. What's the rationale?
line 22. See comment at line 28, page 11-10.
Page 11-37. Table 11-2. Data for RESOLVE are out of alignment.
Page 11-39. Table 11-3. Data for top 3 lines are out of alignment. Two entries
for nitrate concentration in bottom line.
Page 40. 41. Incorrect column headings: should match those on 11-39.
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11.9 Summary of Effects on Visibility
Page 11 -42. line 32 and too of next page. Change sentence as follows "nitrate
aerosol does not appear in high concentration in areas of high concentrations of acid
sulfate..."
(We have had high concentrations of both sulfates and nitrates in Southern
California in the past, but the aerosol here is more or less neutral); may have some
coarse aerosol nitrate even with acid sulfate around.
Page 11-43. lines 16 and 17. Some of these control issues are addressed in
the reference given earlier to the second Russell et al. (1988b) paper, the "non-
linearity" did not turn out to be as extreme in that case as it could be in theory.
11.10.1 Basic Concepts of Economic Valuation
Page 11-44. lines 13-15. Is a 12% effect that is "small" necessarily
insignificant?
11.10.3.2 Economic Valuation Studies for Urban Haze
Page 11-50. lines 10 and 11 and Page 11-51. Table 11-6: Economic Valuation
Studies on Urban Haze. Part I. Uniform Urban Haze.
On what basis was it decided that a 10% chance in visibility was the relevant
illustration? Such a small percentage change elsewhere in the report has been
dismissed as apparently insignificant.
If one were to examine the per capita value of a doubling of visual range, for
example, and to multiply by the number of people affected, the dollar totals would be
staggeringly large. At least then the reader would recognize that visibility degradation
has important costs (even if it is not all attributable to the oxides of nitrogen). As it
stands now, the costs of visibility degradation appear at first glance to be trivial.
11.10.4 Conclusions
The conclusions appear to be detached from the preceding text. Instead of just
presenting a catalog of work that remains to be done, the conclusions should
summarize those things that are known about this issue.
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REFERENCES NOT ALREADY CITED IN CHAPTER 11.
Davidson J.A., Cantrell C.A., McDaniel A.M., Shatter R.E., Madronich S., and Calvert
J.G (1988) Visible-ultraviolet absorption cross sections for NC>2 as a function of
temperature. Journal of Geophysical Research 93, 7105-7112.
Griffing G.W. (198) Relations between the prevailing visibility, nephelometer scattering
coefficient and sunphotometer turbidity coefficient. Atmospheric Environment 14, 577-
584.
Hudischewskyj A.B. and Seigneur C. (1989) Mathematical modeling of the chemistry
and physics of aerosols in plumes. Environmental Science & Technology 23, 413-
421.
Joos E., Mendonca A., and Seigneur C. (1987) Evaluation of a reactive plume model
with power plant plume date -- application to the sensitivity analysis of sulfate and
nitrate formation. Atmospheric Environment 21, 1331-1343.
Pierson W.R., Brachaczek W. W., Gorse R.A., Jr., Japar S.M., Norbeck J.M., and Keeler
G.J. (1989) Atmospheric acidity measurements on Allegheny Mountain and the origins
of ambient acidity in the northeaster United States. Atmospheric Environment 23, 431-
459.
Richards L.W., Blanchard C.L., and Blumenthal D.L. (1991) Navajo Generating Station
Visibility Study, draft #2. Final Report STI-90200-1124-FRD2, Sonoma Technology
Inc., Santa Rosa.
Samuels H.J., Twiss S., and Wong E.W. (1973) Visibility, Light Scattering, and Mass
Concentration of Particulate Matter. California Air Resources Board.
Saxena, P., Hudischewskyj A.B., Seigneur C., and Seinfeld J.H. (1986) A comparative
study of equilibrium approaches to the chemical characterization of secondary
aerosols. Atmospheric Environment 20, 1471-1483.
Seigneur C., Saxena P., and Hudischewskyj A.B. (1982) Formation and evaluation of
sulfate and nitrate aerosols in plumes. The Science of the Total Environment 23, 283-
292.
Sloane C.S., Watson J., Chow J., Pritchett L, and Richards L.W. (1991) Size-
segregated fine particle measurements by chemical species and their impact on
visibility impairment in Denver. Atmospheric Environment 25A, 1013-1024.
Solomon P.A. and Moyers J.L (1986) A chemical characterization of wintertime haze
in Phoenix, Arizona. Atmospheric Environment 20, 207-213.
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Tang, I.N. (1982) Letter to the editors. Atmospheric Environment 16, 2753.
Watson J.G., Chow J.C., Richards L.W., Neff W.D., Andersen S.R., Dietrich D.L, Houck
J.E., and Olmez I. (1988) The 1987-88 Metro Denver Brown Cloud Study. Final Report
#8810.1F2, Desert Research Institute, Reno.
Watson, J.G., Chow J.C., Richards L.W., Haase D.L., McDade C., Dietrich D.L., Moon
D., and Sloane C. (1991) The 1989-90 Phoenix Urban Haze Study, Volume II: The
Apportionment of Light Extinction to Sources. Final Report #8931.5F1, Desert
Research Institute, Reno.
Wexler A.S. and Seinfeld J.H. (1992) Analysis of aerosol ammonium nitrate:
departures from equilibrium during SCAQS.
White W.H. (1991) The components of atmospheric light extinction: a survey of
ground-level budgets. Atmospheric Environment 24A, 2673-2679.
Zhang X. (1990) Measurements of size resolved atmospheric aerosol chemical
composition with impactors: data integrity and applications. Ph.D. Thesis, University
of Minnesota.
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CHAPTER 12 Effects of Nitrogen Oxides on Materials
12.1.3 Deposition Process
Page 12-4. line 10. ...yield a deposition velocity for NO2 to galvanized steel...
lines 16-31 and Table 12-1: Smog Chamber Reactions on NO2 and
and Deposition of Reaction Products on Galvanized Steel
Table 12-2: Smog Chamber Reactions of NO2, ^H^ and SC>2 and
Deposition of Reaction Products on Galvanized Steel
If the text in Table 12-1 is for a NO2 and propylene mixture along, how did 133
nmol/cm2 of sulfate show up on the surface of the steel?
line 25 and Title of Table 12-1 : Smog Chamber Reactions of NC>2 and
C3H3 and Deposition of Reaction Products on Galvanized Steel. What is C^h^?
There is no such compound.
Page 12-5. lines 5-7. This may not be true. It depends on the relative
concentrations of nitrogen and sulfur species in the air.
1 2.1 .4 Chemical Interactions of Nitrogen Oxide Species
Page 12-8. line 30. Replace photochemical with "photochemically-initiated."
Page 12-10. lines 2-4. One would think that the result depends on the ratio of
NH3 to H2S04 as an excess of NH3 jnto the |jquid phase
lines 2-6. this is an incorrect interpretation. Bassett and Seinfeld were
dealing with an aerosol system not a dilute solution of HNO3. HNO3 will not volatilize
from a dilute solution when trace amounts of NH3 and H2SO4 are added. If it did, we
would never find HNO3 in rainwater. It is clear that NOg and 804 can and do coexist
in rain, dew, and dry deposition (see Wolff et al., J. Air & Waste Management Assoc..
vol. 40, p 1638-1648, 1990).
lines 6-8. Also, most nitrate compounds are water-soluable and thus
may be washed off of damaged surfaces by rain.
lines 8-11. This concluding sentence does not necessarily follow from
the preceding discussion says that it may be difficult to find nitrate residues on
damaged surfaces because they can be driven off by strong acids (or may be washed
off). That is distinctly different then concluding that NOX species are not a problem.
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12.2 Effects of Nitrogen Oxides on Dyes and Textiles
12.2.1 Fading of Dyes by Nitrogen Oxides
Page 12-14. lines 4-7. If a reference is available that attests to the fact the few
NOX susceptible dye and fabric combinations are produced? What about the stability
of the rather large amount of dyed textiles (clothing) imported from overseas these
days?
12.2.2 Degradation of Textile Fibers by Nitrogen Oxides
Page 12-14. line 11. fibers (plural).
12.3 Effects of Nitrogen Oxides on Plastics and Elastomers
12.3.1 Chemical Changes Induced by Nitrogen Oxides
Page 12-15. line 14. ...exposed to UV radiation...
Page 12-16. lines 8-1 4. Did they distinguish between the direct effect of
sunlight on the materials vs. the effect of sunlight on the pollutant mixes, which could
produce reactive intermediates that many then attack the materials?
12.4 Effects of Nitrogen Oxides in the Corrosion Process
Page 12-17. last paragraph. This discussion of translation of the findings of the
three chamber studies to outdoor conditions reads like pure conjecture. No new data
are offered, no further references are cited, and the work "may" appears three times.
The paragraph should be deleted if it cannot be written with more authority.
1 2.4.2 Effect of Nitrogen Oxides on Economically Important Metals
Page 12-18. line 15. Check network name. Is it National Air Surveillance
Network?
line 22. ...however, their measurement techniques...
Page 12-19. lines 17 and 18. Why would N©2 decrease the solubility of the
corrosion layer?
Paae12-2Q. lines 27-29. Is there a conflict between the statement that NO2 is
synergistic with SO2 (line 27) but that when N©2 is increased at constant SO2
concentration then "little change" occurs (line 29).
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12.6 Effects of Nitrogen Oxides on Stove and Concrete
Page 12-25. line 12. As I understand it, the study of the Taj Mahal is quite
controversial. It might be better to stick to the Parthenon as an example.
line 17. Is the word "dark" necessary here? Gypsum alone is light-
colored, it becomes dark as soot (for example) accumulates in the crust.
12.8 Costs of Materials Damage from Nitrogen Oxides
Page 12-28. The cost data given here are for such a small subset of the
relevant materials and are so old as to not by very useful, and may even be
misleading. If a thorough job of cost analysis is not to be done, then this section would
be deleted, the citation involving 69, 697 thousand million lira (to 5 significant figures)
on line 7 of p 12-30 adds to the confusion. Preservation and repair budgets are likely
to greatly understate the amount of damages being done as there is no assurance that
full remediation is possible or is even being attempted.
Page 29. lines 2 and 3. It should be pointed out that these 1977 damage
estimates were also based on 1977 (or earlier) pollutant levels which are different from
today's. On page 12-22, line 5, the document reports "rapid" deterioration of aluminum
when exposed to nitric acid, but the summary (lines 22-23, page 12-30 "discounts"
attack on metal across the board. The summary lines 26-27) seems to discount NOX
damage because SO2 and 03 are "more directly damaging." Is that comparative
statement relevant? If abrasion were "more directly damaging" than SO2 would we
ignore all pollutants? As mentioned previously, the cost data should in my opinion be
updated thoroughly or not included at all.
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CHAPTER 13 Studies of the Effects of Nitrogen Compounds on
Animals
13.1 Introduction
The most toxic nitrogen species; respiratory and extrapulmonary effects;
emphasis on exposure concentrations <5ppm.
Page 13-1. line 9. Who, 1987 - reference states 1977
Page 13-3. lines 9-11. Reword to: The amount of a gas acting at a given site in
the lung is dependent on the transport of N0£ from the airway lumen to the cellular
components of the respiratory tract. In the movement from the airway lumen to the
cellular components NO2 first comes into contact with the liquid or fluid...
line 11. Most now believe that a surfactant mono- or bi-layer extends all
the way to the larynx.
line 25. Do you really mean "species specific-chemical reactions"?
13.2.1.2 Principles of Gas Uptake and Dosimetry Models
Page 13-3. line 28. What's the difference between "air phase" and "air
compartment"?
Page 13-4. line 4. Not clear what "physiological processes" vary among
species in this context.
line 30. The model might assume all path widths and lengths are
identical, but we all know this is far from true.
Page 13-5. line 6. The only concentration that matters is that at the interfacing
surface.
lines 20-24. Reword to: For the NO2 dosimetry investigation of Miller et
al. (1982), the uptake at a site was modeled by an instantaneous reaction at the
surface with the tissue dose defined in terms of the flux of NC>2 at the surface.
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13.2.1.3 Dosimetry of Nitrogen Dioxide
This section nicely summarizes factors factors affecting NO2 dosimetry to
different levels of the respiratory tract and the effects of increased ventilation and
exercise on the linear increase of NO£ absorption by deeper levels of the lung.
Page 13-7. lines 1-10. Note discrepancies in NC>2 mass transfer coefficient.
Page 13-8. NC>2 fractional uptake fairly comparable across species, including
humans, at 75-90% at rest increasing to 95-100% at exercise or rapid ventilation;
increase with exercise is attributable to pulmonary uptake which increases
disproportionately and penetrates more deeply with exercise.
line 19. Can you call Wagner and find out what the exposure periods
were?
Page 13-9. line 20-24. This sentence doesn't make sense as written.
line 20. Not clear what is meant by "adequately." Have they been
evaluated at all?
Page 13-10. NC>2 absorbed and distributed systemically as NO}?.
Page 13-11. line 7. Green and Hiatt, 1954 - reference states Greene..,
13.2.2 Mortality
Mortality occurs only at prolonged exposures >10-30 ppm; there is some
species differences in sensitivity (e.g., monkey, guinea pig).
Tables 13-1 and 13-2. Present a nice summary of literature findings.
This section isn't useful for the purpose of the document.
13.2.3 Respiratory Effects
13.2.3.1 Host Defense Mechanisms
Page 13-17. The emphasis on particle deposition and clearance may be
misplaced since NO2 is not inhaled as a particle; the reasoning behind the discussion
of particle processing by the defense mechanisms in relation to NO2 as a non
paniculate exposure is not stated or clearly implied.
line 6. In the phrase "proximal upper and lower airways" proximal should
be removed.
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Page 13-18. line 31. Statement "There is little replacement of T cells in the
adult human" is either unclear or in error.
Page 13-19. line 24. Burleson, 1987 - missing from references.
Page 13-20. lines 15 and 16. "Continual loss of these dialated ells with
eventually result in the replacement of the normal ciliated eipthelium with squamous
metaplasia of other nonciliated cell types." Is this referring to what happens hen there
is an "unwanted accumulation of inhaled carcinogens (Schlesinger et al., 1987)"?
References supporting this process are needed.
line 19. Name the species in the text.
line 24.. Table 13-3 is a useful summary of NO2 effects on ciliated
epithelial cells in vitro and mucociliary velocity and clearance in vivo; however, despite
the morphologic and functional effects the only two studies to report on clearance as
such showed no effects of NC>2 at 1.0 or 10.0ppm (Schlesinger); thus the functional
significance of mucociliary effects is unclear.
Page 13-21-59. A fairly thorough discussion on the interaction of infectious
agents and NC>2 in animals. Exposure concentrations were 10-1000x the ambient
standard and tended to show enhanced lethality or decreased pulmonary bactericidal
activity above 0.5-5.0ppm. Important suggestive leads are that heightened sensitivity
to the effects of NO2 are found where multiple combined exposures take place, as with
corticoids, or virus infection, plus infectious bacteria and NC^. One is struck by the
absence of studies of susceptibility to infection in animals nutritionally prepared to be
biochemically susceptible to oxidants, such as defined in the next section.
Table 13-3. Give strains and ages. Also, Mauderly et al. '89 & '90 have
clearance data after long-term NC>2 exposure. Mauderly et al. '87 has clearance data
as well.
Schiff, 1977 - exposure was 1-4 wk, not 14 wk.
Page 13-23. lines 1 to 3. Need to make certain the reader knows if you are
talking about cilia per se, or ciliated cells.
lines 11-14. This sentence needs rewriting.
lines 21-25. This paragraph seems disconnected from the flow of the
text.
Page 13-24. lines 15 and 16. The threshold NC>2 exposure for morphologica
effects on RAM in mice appears to be between 0.5-2.0ppm.
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Page 13-25. line 19. "...failed to find any changes in the number..." should
read "...did not find any statistically significant changes in the number." the normalized
volume density of the nitrogen dioxide group was elevated by 25% above controls,
and the number of AM was elevated by 34%. The results were not statistically
significant as only 4 controls and 4 exposed animals were studied.
lines 19-28. This write-up is confusing - line 20 states no changes in the
number of AMs, yet Table 13-4, p. 13-30, states that "increase in number of AMs"
(Crapo, 1984 reference), then Change et al., 1986 (lines 22-23) are referenced - yet
table says Crapo et al., 1986. It must be Change because there is no 1986 Crapo
reference. This paragraph needs reviewing and rewriting for clarification. The table
probably needs correction for this reference.
Page 13-25-28. Numerous in vivo studies show effects on numbers or other
parameters of RAM but at exposure concentration 1-3 order of magnitude above
current standard.
Page 13-27. line 2. Why not call the author and ask?
lines 26-29. It's not clear that "protection" is the correct term. It didn't get
worse, but it didn't get better either - maybe adaptation or tolerance or some other term
might be better.
Page 13-28. line 6. In vitro exposures are too unphysiologic to be meaningful.
line 17. What "high" levels?
Page 13-29 through 33. Nice summary table; however, the first entry - the
Frampton studies in humans at .OSppm with three 15 min peaks to 2.0 ppm appears to
show an effect on RAM ability to inactivate influenza virus, when in fact there was no
effect stated in text at 13-26,1. 23; the positive effect was found at higher
concentration of 0.6 ppm (same citation 1. 20).
Table 13-4. Add strain & age.
Vollmuth et. al., 1986 - table shows "...effects from repeated exposures to two
highest...." However on line 27, p. 13-27, it is stated "1 or 10 ppm" -- needs correction.
Page 13-34 through 40 and Table 13-5. The effects of NO2 on components of
the immune system in animals show sensitivity to NO2 exposure at concentrations 5-
500x the ambient standard, but the results are variable in terms of inhibition or
stimulation, and the studies are on systemic, rather than local pulmonary immunity.
the studies are useful in raising questions regarding further studies needed for the
lungs, but are not directly applicable to standard setting or to shedding much light on
the issue of NC>2-induced susceptibility to pulmonary infection.
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Page 13-35. line 2. "...impact on NO2..." - change to "...impact of NO2..."
starting with line 11. Correct this statement to read "...difference in the
animal species used for the adaption of the A/PR/8/34 virus used for immunization..."
The reason for this change is that the critical difference is that the virus was adapted n
two different host systems-not that two different influenza A strains were used.
Page 13-37. line 1. This 1990 Richters and Damji is missing-only 1988 is
shown.
line 22. This should accurately read: "Fenters et al. (1971) findings in
monkeys given mouse-adapted A/PR/8/34 influenza virus and exposed to 9,400 ug/m^
(5.0 ppm) for one year.
Page 13-38. Table 13-5. Add strain and age.
Page 13-39. Table 13-5. Renter et al. (1971) reference should read: "no effect
on hemagglutin inhibition titer." Delete "on secondary response."
Page 13-42. lines 26-30. This is very confusing the way it is written. This
should be reviewed again. Think that the Jakab reference on line 30 is really 1987-
not 1988-not sure, to help clarify this, a rewrite would help. For example-the 1987
reference should be in one paragraph and line 26 would continue as one paragraph,
ending with Jakab, 1988 (which probably is Jakab, 1987) on line 30. Then start new
paragraph with "The combination of corticosteriods, etc." on line 30~which really is
Jakab, 1988 reference and is properly so cited on p. 13-49, lines 1 and 2. Back to
page 13-42: it is stated on lines 23 and 24 that 4 ppm NO2 significantly depressed
normal bactericidal defenses using S. aureus, but lines 28 and 29 state that "4.0 ppm
produced no significant response in mice using staphylococcus organisms."
[While on the subject-could the final draft show consistency in how
concentrations are expressed? For example, p. 13-42, line 23, is 4 ppm-yet line 29 is
4.0. In many cases when converting ug to ppm, the rounding is very different, e.g., 750
ug/m^-same line 12].
Page 13-43. Table 13-6. Add strain and age.
Page 13-44. Table 13-6. Erlich & Henry reference: The infective agent is K.
pneumoniae_-also, line 9, p. 13-49.
Page 13-46. Table 13-6. There is no Gardner et al., 1981 reference-but there
is a Gardner, 1981 reference.
Page 13-49. line 15. Erlich M975. 1980) found that hamsters exhibited
enhanced mortality at...
line 17. ...25.0 ppm NO2). In addition, the mouse model, etc.
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line 19. reference (Erlich, 1975& 1980).
Page 13-52. lines 26-28. The fact that the study of McGrath and Oyervides had
a 95% mortality in the control group makes this a flawed study and, as stated in line
28, makes it impossible to detect any enhancement in mortality. Frankly, because it is
flawed, it shouldn't be referenced nor used.
Page 13-53. line 9. They (not he) reported that...
13.2.3.2 Lung Biochemistry
For the most part, studies have explored the oxidant hypothesis of NOX injury to
lipids and proteins of the epithelial lining of the lungs and have found dose related, but
modest, effects in several animal species at exposure concentrations 10-100 or more
times the short term ambient standard. Results are difficult to interpret in terms of
pulmonary health effects; perhaps the most persuasive arguments in favor of the
theory are the heightened effects in anti-oxidant depleted (Vitamins A, C, & E) animals.
Probably the most significant gap in knowledge is the lack of correlation of the
biochemical and functional findings. Tables 13-7, 8, & 9 contain helpful summaries of
relevant studies.
Page 13-59. line 25. No references listed for Patel & Block, 1987,1988. Also
shown in Table 13-7, p. 13-61.
Page 13-60. Table 13-7. Add strain and age.
Page 13-61 and Page 13-68. line 3 . Table 13-7. Sekharam et al. (1991)--not
shown in reference.
Page 13-62. Table 13-8. Sherwin and Layfield (1976) - reference says 1974.
Page 13-70. line 11. Should read 24 ug/m3.
Page 13-71. line 28. Prutz et al. (1985)--missing in references.
13.2.3.3 Pulmonary Function
Page 13-76. Most studies performed at exposure concentrations 10-1000x
ambient standards and show dose related effects on lung distensibility, gas exchange,
and flow resistance consistent with inflammatory parenchyma! effects. Effects were
greater in newborn than adult animals. Again, the most significant deficiency in these
studies is the lack of correlation with related effects on lung biochemistry, pulmonary
infection, and dietary modification.
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lines 13 and 14. "Compared with humans, rats and hamsters used in
experimental studies of NC>2 have very immature lungs at birth." While this is true, it is
also true that by day 21 the rat and hamster have nearly adult lungs; the same process
requires 8 years in the human. Suggest that this sentence is amended to add: "...at
birth; however lungs in these species develop more rapidly than human lungs."
Table 13-10. Add strain and age.
Page 13-78. Table 13-10. Is it Yoshida et al., (1980 a &b)?
Page 13-79 - last reference. There were only 2 groups - those conceived in the
exposure atmosphere and those entered at 6 mo. of age. The present description
suggests 3 groups.
Page 13-85. line 17. 7 wk. old rates are hardly "mature."
13.2.3.4 Morphologic Studies
There is an abundance of literature on morphologic findings which are clearly
summarized in Tables 13-11, 12 & 13 for acute, subchronic, and chronic respectively.
There are clearly pathologic effects caused by NO2 exposure, but the critical variables
are exposure concentrations, dose rate, duration of exposure, and species sensitivity.
Since, for a given CxT, concentration seems to be more determinative of effect, dose
rate may be the critical exposure parameter, thus accounting for the importance of brief
exposure spikes in influencing the effects. That conclusion is relevant since human
exposures at excessive levels are commonly intermittent, especially under indoor
conditions.
Page 13-98 through 106. The biologic effects are found mainly at exposure
levels >1ppm although some minimal changes are reported at 0.5 ppm in the long-
term chronic studies. These changes are characterized as morphologic changes in
cilia in peripheral airways, inflammatory bronchiolitis and alveolitis, and proliferative
changes in the alveolar epithelium with a shift in predominance of Type 1 to Type 2
cells. Hamster, guinea pig, dog and monkey are more sensitive than rat, but even
these species show no pathology at O.Sppm in acute studies, and only mild changes
with chronic exposure, the data are well described in the discussion on pp. 13-106 -
120. Extrapolation of these studies to humans would bring them within a 10-100 fold
margin of safety, although it is not certain that these morphologic findings would be
manifest as health effects. For example, emphysema is found only after chronic
exposure at high concentration (.5ppm, Table 13-15, except in Beagle dogs where it
was found at 0.6ppm). Furthermore, extrapolation is confounded by apparent
differences of emphysema in animal studies and in humans relating to the presence of
alveolar wall destruction without fibrosis in addition to dilation of the airspaces.
Although this distinction in classification and its evolution over 25 years is important, it
may receive too much space in this document (pp. 13-105 through 108). Of grater
importance may be the issue of differences in species sensitivity (e.g., beagle vs. rat).
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Page 13-86. Table 13-11. Add strain and age.
Table 13-11. Stavert & Lehnert (1990)-Reference says 1988 (p. 13-213,
line 28).
Page 13-89. Table 13-12. Add strain and age.
Page 13-91. First Reference. Before reporting nasal findings, check the
manuscript and/or call the author and find out whether or not the transitional epithelial
zone was examined. We now know that effects might show up there even if other
epithelia are unaffected.
Page 13-93 (Blair et al. reference). Does the paper allow judgement as to
whether the "pneumonitis" might have been microbial in origin, rather than from NO2?
Page 13-94. (Fenter's reference), the listing of "no pathology" would seem to
be incorrect, the manuscript shows a photomicrograph of "pneumonitis" in an "NO2
only" exposed monkey. What's the correct interpretation?
Pages 102. lines 6-9 and Page 13-103. lines 2 and 3. In both cases, it is not
clear how the facts related to exposure pattern, the topic of the section.
Page 102. line 6. Define "morphologic examination (light microscopy)". Is this a
pathology scoring system of paraffin sections or a quantitative evaluation of lung
structure at the level of resolution provided by the light microscope?
Page 103. line 24. 60 days of age is hardly "adult."
Page 105. lines 2-4. Are these established hypotheses or pure conjectures?
line 13. If a study was done that would seem to directly examine the
issue of developmental effects and none were found, how can the conclusion be that
"the available data base does not provide an answer?" Rats were exposed from
conception to "maturity" and no functional, structural, or biochemical differences were
found from controls. Although not all possible types and levels of evaluations were
applied, the ones that were applied would pick up changes at a level that would have
created problems had they occurred in humans.
lines 14-17. Were the neonates in the Lam study compared to adults?
This isn't clear from the text.
lines 18 through Page 13-106. line 5. The dose of elastase used in the
studies of compromised animals has generally been so high that potentiation by
pollutant exposure may be reduced.
Page 106. line 5. This section is missing inclusion of the Mauderly et a. 1989 &
1990 study which is the most comprehensive evaluation to date of NO2 - elastase
emphysema interactions in rats.
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Page 13-110. lines 11 and 12. It's not clear why "rupture" is not equated to
"destruction." Isn't rupture damage?
Page 13-111. line 17. The term "statistically larger" isn't very good - presumably
the meaning is "statistically significantly larger."
Page 13-113. line 13. Why not call the authors and find out how the tissues
were fixed?
Page 13-114. line 13. Capitalize "Beagle".
Page 13-115. lines 27 and 28. The sentence beginning "Exposed rats..." is
awkward and needs rewriting.
Page 13-116. line 22. Again, this paragraph is missing reference to the
Mauderly et al. 1989-1990 study. If this study is deemed irrelevant, this needs to be
explained.
Page 118. Table 13-14. Add strain and age.
13.2.4 Extrapulmonary Effects
Page 13-120 through 153. There is an excellent, critical, discussion and
summary cataloging of experiments (Tables 13-15 - 24) that show variable production
of extrapulmonary biologic effects (not health effects, as stated in the summary, pp. 13-
151, line 28) of generally high concentrations of N02 on weight gain, hematological
system, liver, spleen, kidney, neurobehavior, and reproduction. While a variety of
effects are reported, they are neither marked nor consistent. Taken together, they
support a conclusion that continuous exposure to NO2 at levels >10-1 OOx the
ambient standard might incur a risk of biochemical, metabolic, and behavioral effects
that are reversible on removal from exposure.
13.2.4.1 Body Weight
Page 13-120. line 27. Does the writer really mean that there was na difference,
or that there was no statistically significant difference?
Page 13-121. Table 13-15. Add strain & age.
Page 13-125. Table 13-16. and Page 13-127. line 24. The reference by Oda et
al. (1981) in the text is opposite of the same reference in the table.
Page 13-126. Table 13-17. Add strain and age.
Page 13-129. Table 13-18. Add strain and age.
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13.2.4.3 Cardiovascular Effects
Page 13-132. Table 13-19. and Page 13-131. line 8. Text says decreased
serum cholesterol while table (Kosmider, 1975) shows slightly elevated serum
cholesterol.
13.2.4.4 Hepatic Function
Page 13-134. Table 13-20. Add strain and age.
Page 13-134. Table 13-20 and Page 13-136. line 10. Takahashi et al. (1986) in
table says first 8 weeks of exposure while text says first 12 weeks of exposure.
13.2.4.5 Effects on the Kidney and on Urine Content
Page 13-138. Table 13-21. Add strain and age.
13.2.4.6 Effects on the Central Nervous System and Behavioral Effects
Page 13-140. Table 13-22. Add strain and age.
Page 13-141. line 8. 94 ug/m3 (0.05 ppm), not 0.1 ua/m3.
line 9. Trusl et al., 1975--in table, but 1973 in text.
line 30. Again that lack of consistency-this should read 1880 ua/m3. not
1800.
13.2.4.8 Potential Carcinogens or Co-Carcinogenic Effects
Page 13-144 through 151. The discussion of potential carcinogenic or co-
carcinogenic effects centers on the possible action of NO£ as a direct carcinogen (no
evidence), a tumor promoter through its epithelial proliferative and inflammatory effect
(the effects are produced, but no excess tumors appear, even with the joint use of a
known carcinogen), and the metabolic production of carcinogens (nitrosamines) by
absorbed NC>2- and NO3_. Additional research is facilitator of neoplastic disease can
be drawn.
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13.3 Effects of Mixtures Containing NO2
Page 13-153 through 168. The discussion on these pages including the
summarized results in Table 13-25, are well-presented, but rather inconclusive
regarding the role of NO2 in the observed additive, synergistic, or no-effect results. In
the NO2/O3 combinations, 63 seemed to be the determinative agent at low
concentrations while additive or synergistic effects seemed to require high
concentrations of NO2- However, in the NO2/SO2 or H2SO4 combinations, there
seemed to be a greater tendency to additive or synergistic effects especially in regard
to the susceptibility to infection endpoint. Particles have been shown to increase NC>2
effects presumably by offering adsorptive surfaces for transport into the deep lung.
The real deficiency in the study of mixtures is an effective strategy of study design that
will permit the attribution of effect to specific components. Some pretty complex
protocols have been presented, but the results remain inconclusive.
Page 13-154. Table 13-25. Add strain and age.
13.4 Nitric Oxide
Page 13-168. NO exposure has been tested for isolated biologic effects (e.g.
on GSH transferase) ad in integrated systems (e.g., the mortality from infection model)
and found to be similar to N02 (with the exception of methb formation), but
considerably less potent. The presentation is inconclusive.
line 12. Don't overlook the possibility of citing the filtered diesel exhaust
studies as a source of information on NO-NO2 exposures as an "upper bound of
effects." There were other agents in the exposure atmosphere, but to the extent that
there were negative findings, the data set a type of benchmark.
Page 13-169. line 17. The Stavert and Lehnert, 1990 reference is not given in
the reference section. Is this the 1988 reference?
Page 13-170. Table 13-26. Add strain and age.
More attention needs to be given to the first reference listed (Azoulay et at.).
Didn't find the "emphysema11 described in the text. What were the criteria used for the
"emphysema-like" lesions, and how do they related to the present authors' criteria for
emphysema?
Page 173. line 5. The sentence is worded awkwardly. It's not clear that "any
reduction of 02 transport" would not be lethal.
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lines 6-9. There is an apparent discrepancy between the findings in the
Oda et al. 1980b and the Oda et al. 1976 references, but the author makes no attempt
to reconcile the differences. 2.4 ppm NO2 gave 0.3% MetHb in mice, but 10.0 ppm
NO2 gave 0.2% MetHb. Was this a methodological difference, such as difference in
the time after exposure? The difference needs some comment.
Page 13-174. lines 23-25. This reference is not inhalation study, as the
paragraph implies. Are these cells of respiratory tract origin? The significance of the
finding is not clear, and is not placed in context.
13.5 Nitric Acid and Nitrates
Page 13-175. Except for one study showing increased bronchoreactivity in
sheep, these studies are either unphysiologic (intra-tracheal instillation of HNC^) or
negative.
13.6 Summary
Page 13-177 through 188. This section accurately reflects the text discussion
and the tabular material. NO2 and, to a lesser extent, NO cause morphologic lesions,
physiologic impairment in respiratory function and host defenses, biochemical, and
metabolic changes that are consistent with observed pathologies theorized to be
related to NO2 exposures in humans at 10 to 100 times lower concentrations. The
qualitative comparisons are supportive of a causal relationship in humans, but the
quantitative extrapolations are problematic. Remaining unknowns include: (1) the
relevant exposure pattern for humans, which may reflect the intermittent peak pattern
such as that measured for indoor pollution by gas stoves rather than steady low-level
exposures experienced in the community; (2) the importance of concentration over
time in determining the effective pulmonary dose of NO2 to lung tissue; (3) the biologic
mechanisms and characteristics determining host susceptibility to the different effects
(e.g., host defenses vs. broncho reactivity; and (4) the relationship between the evident
oxidant mechanisms of injury and antioxidant defenses, including nutritional status,
with integrated effects on defense mechanisms, cytotoxicity, and cell proliferation.
13.6.3 Summary Effects on Host Defenses
Page 13-180. A review of the literature reveals no consistent pattern of
immunological alterations following inhalation exposure to NO2- Whereas limited
alterations in systemic immune parameters have been noted, these generally occur at
very high concentrations. A possible explanation for this variability is that respiratory
exposure to NO2 may result in the production of elevated levels of immuno modulatory
cytokines to be examined may include interleukin-1 (IL-1), IL-6, IL-8 (human samples
only), IL-10, tumo necrosis factor (TNF), and transforming growth factor-beta (TGF-B).
All of these cytokines exhibit both suppressive and stimulatory effects; a detailed
profile of their production in response to various NO2 concentrations and exposure
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regimes may reveal cellular mechanisms leading to altered immune function.
Especially important in this regard may be TGF-B and TNF, which appear to have the
widest range of effects on both immune and non-immune cells. It is conceivable that
these factors may be produced in the lungs during exposure, then released
systemically; thus, elevated levels of either or both of these factors may be responsible
for the limited systemic effects noted with NO2 exposure. Potential sources of these
cytokines include the alveolar macrophages, which have been demonstrated to
elucidate a wide variety of immuno modulatory and inflammatory cytokines, and T-
lumphpcytes trafficking through the lungs and the thoracic lymphatics (Kelly, 1990). A
potential profile in both alveolar macrophages and T-lumphocytes from the lung, as
well as lymphocytes isolated from the thoracic lymph previously reported in the
literature, would be of lesser priority as an experimental model, as this system does
not address indirect effects of test agent exposure. It has been demonstrated that
interaction of immune cells with their cellular environment is important for function
(Newman and Tucci, 1990). Thus, tissue damage directly mediated by NO£ may play
a major role in any immune alterations noted following exposure.
Finally, there have been limited studies examining the potential effect of NO2
exposure on natural killer (NK) cell activity. NK cells are responsible for resistance to
certain infectious organisms (e.g., viruses) as well as neoplastically-transformed cells.
As the lung represents an intimate interface between the organism and the
environment, the surveillance role in NK cells is of vital important, and future studies
should include evaluation of NK function in both the lungs and associated lymphatics.
Page 13-180. line 21. "Insure" should be "ensure."
References: Kelley, J. (1990). Cytokines of the lung. Am Rev Respir Dis
141:765-788. Newman, SI and Tucci, MA (1990). Newman, SL and Tucci, MA.
(1990). Regulation of human monocyte/macrophage function by extracellular matrix.
JClin Invest 86703-714.
13.6.4 Effects of Chronic Exposure on the Development of Chronic Lung
Disease
Page 13-183. lines 8-21. This paragraph suggests a greater degree of
uniformity in the respiratory function effects among studies than actually exists.
Perhaps the problem is one of too great a degree of generalization across species,
concentrations, exposure pattern, and time. For example, long-term exposure of
rodents to relatively high concentrations of NO2 have shown no. decrease in gas
exchange efficiency. As a summary, these selective generalizations aren't quite on
target.
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13.6.7 Susceptibility of Subpopulations
Another subpopulation that must be considered is that of the immune
suppressed population. When earlier studies of the effects of NO2 on host resistance
were initiated, the AIDS epidemic was not a factor in the medical community. Today,
millions of people are HIV-positive or have AIDS in various stages. It should be
important to work with immune suppressed animal models (suppressed wither
chemically or genetically, e.g., the SCID mouse r the nude mouse) to determine the
effects of NO2 alone or in mixture with other pollutants when challenged with very low
doses of viruses, parasites, bacteria, etc. Also, it would be important to evaluate the
immunologic system in conjunction with vaccinations, etc. Certainly this population is
as critical for our assessment of health effects as the young, those with heart disease,
lung disease, etc. This applies to aJi immunosuppressed populations-transplant
populations, cancer chemotherapy, etc.
(This also applies to Chapter 16.3.5).
Overall Comment: Need additional work with more viruses and mixed
pollutants.
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CHAPTER 14 Epidemiology Studies of Oxides of Nitrogen
14.1 Introduction
Pages 14-2 to 14-5. Suggest some demarcation be included to indicate each of
the seven points being discussed, e.g., use bold for the key phrase such as
Publication Bias.
line 17. Even personal monitoring, because of the integrated multi-day
sampling, does not adequately measure short term peaks nor long term chronic
exposures.
Suggest that it is explicitly stated "exposure measurement error" rather than
"measurement error" throughout these paragraphs.
Page 14-3. line 1. Do you mean close to the null, i.e., relative risks of 1 or
incremental risks of 0?
lines 11-12. Neas et al. (Abstract; Amer Rev Resp Disease, Part 2, April
1992) have recently reanalyzed the Six Cities data showing no substantial differences
in effect estimates when kitchen, bedroom, or living room NO2 concentrations were
used to estimate individual exposure.
lines 23-24. Responses to symptom questions will be correlated and will
depend on the interpretation of the respondent. As noted later in the chapter, a
specific respiratory disease is likely to be reported by a constellation of symptoms.
Therefore it is appropriate to consider aggregate rather than single specific symptoms
reports.
Page 14-4. lines 7-15. This paragraph is weak compared to the other
discussions. I think this should be expanded somewhat.
Page 14-5. lines 11-14. It appears you are laying down some specific criteria
for causality. The previous seven points are similar to criteria proposed by Bradford-
Hill and others. You also add consistency which is frequently included in such
discussions. Do you wish to be a little more formal about your criteria?
14.2 Studies of Respiratory Illness
Page 14-7. line 26. Some transition is needed at this point to change from the
discussion of LRI in genera to the specific studies.
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14.2.1 United Kingdom Studies
Page 14-10. line 3. Do not see any evidence for the statement that the effect of
gas stoves was limited to children under 8 years of age.
line 25. The p-value of ,.0001 does not match with the value in Table 14-
4 of .0012.
lines 29-31. The argument for reduced effect with aging is very weak,
and it should be eliminated.
Page 14-12. line 7. Spelling of triethanolamine????
Page 14-14. line 2. Please include more significant figures for the effect
estimate and standard error, e.g., the estimated relative odds and 95% Confidence
interval as opposed to the 11% increase reported in line 4.
14.2.2 United States Six Cities Studies
Page 14-15. line 5. There are two separate cohorts of children considered in
the Six Cities study, the first cohort, considered by Speizer et al. (1980) and Ware et
al. (1984) was enrolled between 1974 and 1979 as first and second graders.
Approximately 14,000 children were included. The second cohort, considered by
Dockery et al. (1989) and Neas et al. (1991), were enrolled as second through fifth
graders in the mid-1980's. Approximately 8,000 children were included. A subset of
approximately 2,000 children were selected by random stratified sampling to
participate in an indoor monitoring program between 21/2 and 3 years after initial
enrollment.
lines 14 and 15. Suggest deleting description of study as very careful
with excellent quality control. I think those types of adjectives suggest other studies
were inferior.
Page 14-16. lines 24-31. Should also report associations with current
symptoms, even though a composite LRI indicator was not included.
Page 14-17. lines 1-3. Suggest changing to: Neas et al. (1990, 1991) studied
this same cohort of children from the Six Cities Study enrolled between 1983 and
1986 (?), restricting to white children 7 to 11 years of age..."
lines 9 and 10. Suggest "...study was based on a symptom questionnaire
(third annual) which was completed by parents..."
Page 14-18. line 9. No mention was made of the internal consistency of these
associations across cities or source of NC^. Also by analysis by categorical
breakdown of NO2 exposure is important regarding linearity of response.
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14.2.4 Iowa Study
Page 14-19. line 18-21. Move discussion of lung function to page 14-33.
14.2.5 Dutch Studies
Page 14-19. line 31. Move discussion of lung function to page 14-33.
14.2.6 Ohio Study
Page 14-23. line 4. Change reference from personal communication to ScD
Dissertation.
14.2.8 Connecticut Study
Page 14-26. line 19. Change reference from personal communication to ScD
Dissertation.
14.2.11 Maryland Study
Page 14-28. lines 1-14. Can the results of the Helsing study be quantified?
14.2.12 Glendora, California Study
Page 14-29. lines 4-9. Move to lung function section 14.3
14.3.3 New York Study
Page 14-33. Ijnes 18-20. Can the description of the results of Goldstein study
be made more specific?
Not included are the NHANES II study of lung function by Schwartz (1989) and
the Dockery et al. (1989) analysis of lung function across six cities, both compared to
ambient NO2 concentrations. The first shows an association and the second does not.
Include pulmonary function results from Iowa study (pg 14-19) and Dutch
Study (pg 14-19). Also Six Cities study on outdoor NO2 concentrations (Dockery et
al., 1989) and NHANES II results (Schwartz, 1989).
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14.5.3 Quantitative Analysis
Page 14-48. lines 23-24. NC>2 concentrations indoors were measured in a
selection of homes in all Six Cities, and are reported in Spengler et al. (1979).
Page 14-49. lines 21-26. Since the Schwartz analysis has now been
published, it might be included. For the Berwick study, an odds ratio over all ages can
be produced for the published data, and suggest including.
14.7 Summary
Page 14-56. A list of items is presented related to the meta-analysis. Item five,
publication bias, is the fundamental concern. This is so important that this item should
be elevated in importance even to the point of presenting the list as publication bias
and a set of other technical issues. The NC>2 studies have been so large in scope and
their results so sought after that, fortunately, statistical significance appears not to be a
criterion upon which publication was based. This is a major point supporting the meta-
analysis for NO2-
Page 14-57. line 19. Delete "on" such that end of lie reads "Melia et al. (1980)
described the results..."
Page 14-60. line 1. The idea of the magnitude of the common effect being
underestimated is a solid one. But the document falls short in not attempting to
provide adjusted estimates, within each study, due to the well documented error in
exposure measurements. (And, with reasonable quality assurance in the conduct of a
study, the magnitude of error in exposure is not likely to depend upon the illness
category of a child participant), the adjustment involved in the "errors in variables"
problem is an inflation of the estimated effect based upon a scaling of the
measurement error magnitude.
line 10. The impression given on the "consistency demonstrated" should
be clarified. On page 14-53, line 9, a P-value of just under 10% suggests that the fixed
effects model is marginal at best. And conceptually, the idea of one common value for
NC>2 effect without extensive control of design and concomitant variables, like in a set
of identical study designs with all relevant concomitant variables measured, is just not
attractive. Fortunately, the random effects model allows for a distribution of estimates
about a common value. Specifically, if there were no error of estimate within each
study, the random effects model would still require variance commensurate with the
variation in effects across studies. And, the fixed effects model can be viewed as a
special case of the random effects model where the between study component of
variance is zero.
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Tables 14A-1 and 14A-2. There is a discrepancy in the reporting of the NO2
levels in the Glendora, California study - The text on page 14-28 lists NO2 levels
3.2ug/m3 for Lancaster and 11.4ug/m3 for Glendora (0.002-0.006 ppm); on page 14A-
3 and 14A-10 the NC>2 levels are listed in the Tables as 2.3 to 3.9 ppm for Lancaster
and 9.5 to 12.0 ppm for Glendora. The error needs correction.
Page 14A-5. Furthermore, the listing of NC>2 levels for the Los Angeles Nurses
Study shows outdoor NO2 exposure ranging from 1 to 45 ppm over a 3-year period;
can even L.A. be this bad?
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CHAPTER 15 Controlled Human Exposure Studies of Oxides
of Nitrogen
15.1 Introduction
Page 15.6. lines 24-25. The statement: "In contrast to many animal models,
humans have a wide range of response to a variety of physiological and pathological
stimuli" is confusing. It needs clarification.
Page 15-7. line 19. This line should read as follows: "...the applicability of
these data is limited..."
15.2 Effects of NOX in Healthy Normal Subjects
15.2.1 Lung Function Effects of NO2
Page 15-9. line 15. All studies are not in Table 15.1--Johnson (1990) should be
in Table.
Page 15-10. Table 1. Relative to the listing of studies of the Effects of Healthy
Normal subjects by alphabetical order, rather than a list by the relative dose of
exposure~i.e., not just by ppm level, but by the total inhaled dose, is OK as long as
some significant mention of the latter is provided.
Page 15-15. Table 15-1. Legend. Healthy Normal seems redundant unless we
are presuming behavioral effects. -Same comment regarding Table 15-2.
Table 15-1. Morrow and Utell, FEV-,/FVC = 76-95%.
15.2.1.1 Concentrations Above 1.0 ppm
Page 15-19. line 18. Should be "placebo pretreatment."
Page 15-20. line 24. Changes were significant for "FEV^ as well as FVC.
15.2.3
Page 15-26. Subject characteristics in Table 15-2 are incomplete in some
respects, e.g., Adams et al. Ss were health (normal) vouna adults.
Page 15-31. A "real world" finding of no apparent influence of NO2 level
between the responses of asthmatics and normal subjects is suggested on lines 14-
16. The important qualifier on lines 21-24 should be more effectively blended.
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15.2.4 Summary
Page 15-32. See above general comment re use of total inhaled dose
concerning airway resistance-though isolated von Nieding 5 minute exposure results
appear to make this unnecessary. OR, perhaps you are suggesting a specific early
evidenced effect which is missed otherwise.
15.3.1 The Effects of NO2 on Asthmatics
Good to identify potential confounding effect of exercise on asthmatic response
to NO2 exposure.
Page 15-33 continuing on oaae 41. Agree that variability in asthmatics'
response to specific NC>2 exposure could be due to their "asthma severity," but don't
believe an appendix section of 12 pages is necessary. Consider synthesizing the
essence of this further in this section and expanding, as appropriate, on p. 84 of the
Conclusions and Discussion section.
Page 15-34. 35. 36. Table 15.3. FE^/FVC in title needs to be corrected. What
is "allergy" -- actual skin testing or verbal report?
Page 15-44. paragraph 2. This description of the study by Orehek et al. (1976)
might be somewhat confusing to a reader unfamiliar with the study. Specifically, it is
important to indicate that changes in S Row across NO2 exposure was a primary
endpoint of the study. For example, the sentence starting with "Following NO2
exposure" on lines 17-18 might be better placed before the previous sentence on lines
16 and 17. It is also important to better explain the issue of the post hoc comparison of
"NC>2-responders" vs. "NO2-nonresponders."
Page 15-45. line 18. What makes Hazucha subjects "well characterized" vs.
other studies? Table 15.3 does not suggest any difference in characterization. Koenig
subjects are much better characterized. This should be deleted.
Page 15-46. lines. "Forced expiratory spirometry" should be "spirometry";
"effect" should be "response".
lines 8-10. The reference to the paper of O'Connor et al. (1987) Is
somewhat misleading in the context of this sentence. The current wording suggests
that the use of the dose which would cause a 10% decrease in FENA, is recommended
by the authors of the paper, which is not the case.
Page 15-4. line 9. Strongly disagree with use of "minimal asthma"; conveys
incorrect message when extrapolating to general population - use "mild" asthma or
indicate that "minimal" refers only to study populations.
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lines 13-15. The suggestion that exposure to outdoor aeroallergens is
minimal during March in southern California is misleading. Spring is a high-exposure
period in terms of outdoor aeroallergens in California.
Page 15-50. line 24. The exposure level in Jorres and Magnussen (1990)
should be 0.25 ppm rather than 0.30 ppm (Table correct).
15.3.1.1 Effects of HNO3 Vapor on Asthmatics
Page 15-51. line 29. the papers by Koenig et al. do not report the results of just
one single study, but in fact, refer to at least two separate studies of asthmatic
adolescents, both of which had 9 subjects (but not the same 9 subjects).
lines 29 and 30. For clarity, the sentence which starts with "Subjects
were exposed" should be revised to read as follows: "In the first study (Koenig et al.,
1988), subjects were exposed..."
lines 30 and 31. While it is true that mean FEV-j was reported to have
decreased following exposure under all 3 study conditions, it should also be pointed
out that no dose-response relationship was found (i.e., the decrease in mean FEV-,
was not grater after 100 ppb than after 50 ppb HNO3).
Page 15-52. line 1. For clarity, this line should read as follows: "Koenig et a.
(1989a, 1989b)..."
lines 1 and 7. Koenig (1989b).
line 3. Again, for clarity, the sentence which starts with "In the initial
study," should read as follows: "In the initial study (Koenig et al, 1989a)..."
line 4. The second percentage in this line should actually be 1.8% rather
than 1.7%.
line 6. The percentage in this line should actually be 7.5%.
line 7. The "second study" to which this line refers is actually Koenig et
al., 1989b rather Koenig et a., 1989a.
lines 11-14. These lines are misleading since Koenig et al. actually
measured FEVt and Vsa%vc & 2 points with each exposure (immediately post-
exposure and 10 min post-exposure). These lines only report the values from the first
of these points. In fact, if data from the later point are considered, the sentences in
question are actually incorrect as currently worded. The authors of the study
summarized their results as follows: "FEV! decrease after HNOg exposure was 0%;
after HNC^-lemonade 2%. V^ decrease after HNC^ exposure was 9%; after HNC^-
lemonade 6%." The authors' summary is inconsistent because they use the data from
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the second post-exposure measurement point for FEVi and the data from the first P°st'
exposure measurement for VSQ. Suggested wording for lines 11-14 is as follows: "The
authors measured pulmonary function at 2 time points after each exposure,
immediately (PE^ and 10 min post-exposure (PE2). There were small, but not
statistically significant, changes in FEN/! after most exposures, -3.3% (PE^ and -2.3%
(PE2) after HMC^ alone, -1.7% and +0.3% after HNO3 P|us 'emonade, and -1.7% and
0% after air. Similar trends (-9.4% and -9.7%, HN03; -5.5% and +0.4%, HNO3 plus
lemonade; -5.1% and -7.2%, air) were observed for Vg^^." Presentation of the data
for both post-exposure measurement time points is important because the data in their
entirety suggest a general lack of effect of
Page 15-52. lines 11-16. Lemonade should remove NH3 and enhance
response. This section is confusing. HNC>3 and Lemonade should cause greatest
decrements in lung function. Not the case here ~ why suggest "HNO3 vapor likely to
have been neutralized"? Also, what is the evidence for preferential neutralization with
gaseous HNOs (lines 16-18)?
15.3.2 Effects of NO2 on Patients with Chronic Obstructive Lung Disease
Page 15-52. line 22. "some" not many. COPD usually characterized by lack of
bronchodilator response unless asthmatic bronchitis.
Good rationale given for treating COPD patients as an important potentially
sensitive group.
Page 15-56. line 11. Section 15.3 does not contain a discussion regarding
differences in ambient concentration due to place of residence. However, Section
15.3.1 does contain such a discussion.
15.3.3 Summary
Page 15-56. lines 23-25. These results indicate that there is no concentration
response relationship, not that such a relationship is problematic. In fact, the results at
lower concentrations appear inconsistent enough that they might not really suggest
possible small changes (lines 22-23). The data given in Figures 1 and 2 (pp 59 and
60) underline this point.
lines 27 and 28. Some qualifier should be added here (as is discussed
in the previous section on this page) since Linn et al. Ss were exposed to a higher
total dose at 1 ppm.
15.4.2 Asthmatic Subjects
Page 15-67. line 9. Should be "increase" in airway responsiveness.
Page 15-68. lines 16 and 17. Confusing and not correctly written.
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Page 15-69. lines 3-17. Referring to data presented in Table 15-9 (p. 70), add
reference to statistically significant observations in the text of this section.
line 11. "required" is misspelled.
line 12. The use of the wording "(i.e., no effect)" at the end of this
sentence is not clear. The correct wording suggests that an increase in airway
responsiveness is evidence for no effect of NO2 exposure.
Page 15-71. lines 4 and 5. NO2 exposure doses. Do you mean concentration?
It would be interesting to calculate the total inhaled NO2 dose from the data given for
normals in Table 15.8 on p. 64 (perhaps eliminating the one study using exercise) and
compare to the change in airway responsiveness.
15.6 Effects of NO2 or HNC>3 Vapor Exposure on Human Pulmonary
Host Defense Responses
Page 15-76. line 15. Sentence is incorrect. Exposure to 1.5 ppm NO2 resulted
in a small but significant increase in airway reactivity (Frampton, 1991).
Page 15-77. lines 28 and 29. Frampton et al. (Am. Rev. Respir. Dis. 143:A89,
1991) with 2.0 ppm NO2 x 6 hrs with exercise found a small increase in neutrophils but
no change in lymphocytes or mast cells.
line 30. This sentence would read better if the wording "an unspecific
inflammatory response" was changed to "a nonspecific inflammatory response."
Page 15-77. line 30 and Page 15-85. line 10. "unspecific" should be non-
specific.
Page 15-79. paragraph 2. This paragraph needs to be completely rewritten.
Becker et al. have updated the results of this study, which are about to be published in
the-Amefican Review-of Respiratory Disease-as an abstract in the-April supplement for
the 1992 International Conference. The new abstract presents the following results:
"Airway resistance (SRAW) and spirometric FEV, and FVC were measured before and
after exposure, but none of these airway functions changed in response to HMC^.
Bronchoalveolar lavage (BAL) was performed 18 h after exposure and the fluid was
analyzed for indicators of inflammation. The alveolar macrophages (AM) were tested
in assays for phagocytosis of Candida albicans and susceptibility to infection with
respiratory syncytial virus (RSV). Compared to air, there was no significant increase in
BAL protein concentration, LDH, fibronectin, PGE2, LTB4 C3a, a-1-antitrypsin, or PMN,
in HNO3 exP°sed BAL. This indicates that inhalation of HNO3 does not cause tne
permeability changes, cell damage, or inflammatory events in the lung previously
found after ozone exposure. On the other hand, a significant increase in phagocytic
activity of AM was found with unopsonized (85%) and serum opsonized (24%) C.
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albicans after HMC^ exposure. Furthermore HNO^-exposed AM showed increased
resistance to infection RSV and released 70% less RSVthan AM exposed to filtered
air." In light of these updated results, the current summary of this study is incorrect.
paragraph 3. This summary of the study by Aris et al. (1991) is somewhat
incomplete. In addition to lavage fluids, Ans et al. obtained bronchial biopsies for
histologic evaluation of inflammation. Further, in addition to no change in lavage fluid
LDH levels, these investigators found no change in lavage fluid total protein
concentrations after HNO3 exposure
Another study by Aris et al. which should be included in this review of the health
effects of HNO3 exposure was recently published in the American Review of
Respiratory Disease (1991; 143:85-91). In this study, the investigators found no effect
on various parameters of pulmonary function of a 2-h exposure during moderate
exercise to a fog containing HNO^ at a concentration of 500 ug/m3. In addition, there
was no enhancement by this HNC>3 *°9 exposure of the physiologic effects of a
subsequent 3-h exposure to 0.2 ppm ozone.
15.8 Conclusions and Discussion
Page 82. line 13. Don't believ6 any statistical significant observation of
increased airway resistance in healthy Ss was seen below 2.5 ppm.
line 17. Believe 1.0 should be 2.0 or 2.5 ppm.
lines 19-23. Very important point effectively made.
Page 83. line 2. 1.0 should be 1.5 ppm.
Page 84. lines 3-7. Very important qualifying point re inconsistent results.
lines 10-11. Very important qualifying point made effectively.
lines 17-19. Important point effectively made.
line 27-31. Important point effectively made.
Page 15-86. lines 15-16. The sentence that begins with the words "In addition
to other pollutants" is somewhat unclear as currently worded. This sentence would
read better with the following wording: "In addition to interactions with other
pollutants..."
lines 27-29. These lines are somewhat misleading as currently written.
Responses to HNO3 vapor have been studied in adolescent asthmatics (Koenig et al.
1989a,b) and in healthy adults (Aris et al., 1991; Becker et al., 1992). Further, as
pointed out above (see comments re: p. 15-52), the results of Koenig et al. (1989b) are
not really suggestive of even small changes in lung function.
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Page 15-87. line 3. 1.0 should be changed to 2.5 ppm; also, some idea of
length of NO2 exposure should be given.
NC>2 levels above 1.5 ppm may result in inflammatory response. Suggest:
"NO2 exposure at levels above 1.5 ppm may alter inflammatory cell population in the
distal airways or alveoli, but these changes depend on exposure level, duration, and
frequency. NO£ exposure may alter cellular function and mediators that are important
in host defense and in protection against proteolytic enzymes."
line 6. 0.1 should be 1.5 ppm.
lines 20 and 21. Asthmatics do not consistently show these responses at
these NO2 levels; length of exposure for COPD patients should be given.
lines 23 and 24. These lines should be changed to the following: "Nitric
acid exposure may cause some pulmonary function responses in adolescent
asthmatics but not in healthy adults. Other commonly occurring nitrogen oxide
species..."
Page 15-88. lines 20-22. The Aris et al. reference should be updated. It was
published in abstract form in the American Review of Respiratory Disease 1991; 142,
No. 4 (Part 2):A97.
Page 15-89. lines 16-17. As noted above (see comments re: p. 15-79), the
Becker et al. reference should be updated, the new reference should read as follows:
"Becker, S.; Roger, L.J.; Devlin, R.B.; Koren, H.S. (1992) increased phagocytosis and
antiviral activity of alveolar macrophages from humans exposed to nitric acid. Am.
Rev. Respir. Dis. (in press)."
Appendix 15A. While the intent of trying to standardize the characterization of
subjects with asthma for comparison of the results of various controlled human
exposure studies should be applauded, do not believe that this goal is achieved when
the effort is done in isolation and is buried in the EPA Air Quality Criteria for NOX
document. There is no longer consensus regarding the Scadding categorization of
asthma presented on p. 15A-2 and the severity of disease classification scheme
presented on pp. 15A2-5 is different from that recently promulgated by the National
Asthma Education Program (NAEP) Expert Panel from the National Heart, Lung, and
Blood Institute. It would be preferable for the EPA to use the NAEP Expert Panel
scheme than to invent one of its own. the NAEP Expert Panel report, which was
extensively peer-reviewed, was recently mailed to a large number of physicians
across the country.
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Appendix 15A is an interesting effort, but has a number of problems.
o Page 15A-1, 2nd paragraph: Asthma is now most often characterized as
an inflammatory disease rather than strictly a disease of smooth muscle
(NHLBI, 1991).
o Page 15A-2: The Scadding classification has little to offer. We rarely talk
about cryptogenic asthma. What is the difference between "cryptogenic
intrinsic" and "cryptogenic unspecified". Table 15A-1 is a useless addition
which only confuses rather than clarifies.
In addition, disagree with the statement that moderate asthmatics require
steroids -- some do and some don't.
o Finally, asthmatics with near normal function should not be an a priori
be classified as "minimal" asthmatics. Some asthmatics may have normal lung
function one day and be in the intensive care unit the next, this is an
inappropriate classification. Table 15A-2 is far too simple to be useful.
o The sentence about the nonspecific airway reactivity of allergic subjects is
technically correct as written, but somewhat misleading. While the airway
responsiveness of allergic persons may be within the normal range,
frequently these persons have increased airway responsiveness.
o Table 15A-4, is a reasonable questionnaire for asthmatic college students. But
for others, it should ask about concomitant disease, smoking, etc.
o In summary, this Appendix has many weaknesses and some inaccuracies
which greatly limit its usefulness. This simplification conveys the wrong
message and the Appendix should be deleted.
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CHAPTER 16 Health Effects Associated with Exposure to Nitrogen
Dioxide
16.2 Ambient and Indoor Nitrogen Dioxide Levels
The summary adequately reflects the text and presents a balanced view of the
data reported.
Page 16-2. lines 7-30 an Page 16-3. lines 16-31. What are they doing indoors?
PPM level is one important factor distinguishing between indoor and outdoor
exposure, but time and ventilation rate are also important. For example, one hour of
jogging outdoors raises ventilation 8 to 10 times that at rest and is roughly equivalent
to 8 to 10 hours of NO2 inhalation at the same concentration while at rest.
16.3.1 Airway Reactivity in Asthmatics and Short-Term (1-3h) Exposure to
NO2
This is an excellent summary of the most sensitive effect of short term exposure
to NO2- The effects seems to be reversible in terms of the bronchospasm of asthma,
so the health effect is significant for morbidity rather than mortality. However, the role
of NC>2 in the longer term association of decreased airflow rate and mortality is an
unresolved issue.
Page 16.4. lines 8-16. Definition of "Asthma" should be revised to include
recommendations of National Asthma Education Program, NHLBI, 1991. this is,
incorporation of inflammation in the definition.
lines 24-29. Prevalence of airway hyperactivity should be discussed in
this paragraph as well. Some data are available from East Boston studies.
Page 16-5. line 4. Is the analysis on airway reactivity a true "meta-analysis"?
This should be examined regarding wording in Chapter 15 as well.
line 5. What is a "slight excess increase of airway
hyperresponsiveness"? The wording here needs clarification.
16.3.1 Airway Reactivity in Asthmatics and Short-Term (1-3h) Exposure
toNO2
Page 16-4. lines 8-11. These lines summarize the 1987 American Thoracic
Society definition of asthma. A better definition of asthma to use here would be that of
the National Asthma Education Program Expert Panel Report.
lines 16 and 17. Chapter 15 conclusions do no include this assertion.
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lines 24-29. This paragraph would benefit from inclusion of information
on the prevalence of non-specific airway hyperresponsiveness in the general
population as well as that of asthma (the clinical tip of the airway hyperresponsiveness
iceberg).
line 30. 1.0 should be 2.0 or 2.5 ppm.
Page 16-5. lines 4-8. This sentence regarding the "meta-analysis of data on
more than 300 asthmatics" is somewhat misleading as it currently stands. The
statement that the meta-analysis "indicates a slight excess increase of airway
responsiveness following NO2 exposure" gives the impression that a formal statistical
analysis of the combined data from multiple controlled human exposure studies was
performed and that a "slight excess increase of airway responsiveness" was the result.
A better way to present the information gained from the review of the combined data
described in Chapter 15 would be to state that it is clear that some, but not all,
asthmatics develop increased airway responsiveness after exposure to concentrations
of NO2 in the range of 0.2 to 0.3 ppm.
lines 8-13. It is unclear how NO2 might cause increased airway
epithelial permeability without causing airway inflammation.
16.3.2 Respiratory Morbidity in Children Associated with Exposure to
NO2
An excellent and balanced summary of a complex epidemiologic and
biostatistical issue; Figure 16.1 and the accompanying discussion is very illuminating.
The relative risk levels of 1.1 to 1.4, while statistically significant in the combined data,
is surely a weak association and not confirmed as causative for NO2 alone.
Page 16-6. line 12. This line should read as follows "...supportive of an adverse
effect of exposure to NO2 on respiratory disease..."
Page 16-8. line 5. This line should read as follows: "meta-analysis carried out
by EPA..."
line 9. The sentence which starts with the phrase, "For purposes of
discussion," should be revised. The sentence should be improved if this phase was
eliminated.
Page 16-10. line 8. "Combining the eleven studies giving qualitative extent of
effects tends..."
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16.3.3 Biological Bases Relating NO2 Exposure to Respiratory Morbidity:
Effects of NC>2 on the Respiratory Host Defense System
This section is a problem as it appears biased toward the direct relevance of the
animal data for the human epidemiologic findings.
Page 16-12. lines 15-17. This sentence is a misstatement, is unnecessary, and
should be deleted, the epidemiologic data contain no information that can attribute the
increase in symptoms to "infectious origin".
Page 16-13. line 3-5. "The biologic bases...are presented..."
line 8. It would be fair here to assert that there have been no observed
impairment of mucociliary clearance, despite the effects on cilia and mucus velocity.
line 12. Start a new paragraph with "As a foreign agent" as the subject
turns to alveolar macrophages.
Pages 16-13 through 14. The repeated use of the phrase "as low as" in
presenting the NO2 concentrations used in experimental studies biases the message
of the relative resistance of the animals' lungs to NO2 in comparison with the human
epidemiologic studies. Ranges of exposure concentrations used in these studies
should be provided rather than just the low end. Also in this presentation, the author
relies heavily on the mortality model of susceptibility, when the concern of the human
condition is not with increases in mortality rates of a lethal infection, but with morbidity
from non-lethal respiratory symptoms. The defense mechanisms under the two
different conditions are quite different, and this summary blurs those distinctions.
Thus, the summary argument on pp. 16-16, lines 11-24 seems very overstated, and
may even be irrelevant.
o The referenced literature throughout this Section needs a careful review and
some revisions. For example:
Page 16-13. line 21. Goldstein et al., 1974 - reference missing. Suzuki et al.,
1986- listed twice.
Pages 16-13. line 28 through Page 16-14. line 6. This paragraph seems a bit
out of place. The idea of NOX enhancing susceptibility to pulmonary carcinogens was
not well developed in Chapter 13. Indeed, the entire issue of the direct or indirect
relationship of NOX influence on experimental colonization of lungs with tumor cells in
a summary chapter, when it hadn't previously been an issue of focus. There have
been several long-term rodent bioassays of NO2 in which cancer might have occurred
if NO2 was a significant carcinogen. The current literature does not support NO2 as
either a direct carcinogen or a co-carcinogen.
lines 28-31 and 1-6. This paragraph is out of context in a discussion of
host defense against infection and should be deleted.
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Page 16-14. lines 13 and 14. There is no listed Fujimaki et a., 1982 but there is
a Fujimaki & Shimizu, 1981. (p. 16-23, lines 1 & 2).
line 31. Goldstein et al., 1973 - reference missing.
Page 16-15. line 4. Jacob, 1987 - reference missing.
Page 16-17. line 7. Freeman et al., 1977 - reference on p. 16-22, line 51 says
1972 - which is correct?
16.3.4 Emphysema and Exposure to NC>2
Page 16-17. lines 11-23. Evaluation of the available morphometric
measurements in terms of alveolar wall destruction is difficult. For instance, the Hyde
et. al. (1978) study of beagle dogs found a statistically significant decrease
(approximately 18%) in the density of alveolar surface area per unit volume of lung
parenchyma in the high NC>2 group while total lung surface area of the high NC^
group did not differ significantly from controls. Thus, with statistically significant
quantitative measurements, the authors of this study concluded that there was
enlargement of the alveolar air spaces. The authors noted that the enlargement of
airspaces occurred with and without an increase in the number and size f interalveolar
pores. With the exception of the ventral region of the lungs, the frequency of
interalveolar pores in the high NO2 group was not different from controls. In he high
NO and sulfur oxide groups there were statistically significant increases in the
frequency of interalveolar pores. As the only evidence which has direct bearing on
alveolar wall destruction is the presence and potential coalescence of interalveolar
pores it is difficult to conclude from this study that NO2 results in emphysema if
evidence of alveolar wall destruction is the basis.
Page 16-18. lines 5 through 8. The quantitative morphometric methods which
have been applied to the study of nitrogen dioxide have been limited to measurement
of gas exchange surface area and are not likely to detect a small loss of alveolar
surface area. These methods, therefore, can not resolve the early stages of an
emphysematous lesion. The sensitivity of qualitative morphological evaluations to
detect such lesions is unknown but typical pictures illustrating emphysematous
lesions suggest that a significant proportion of alveoli are involved before the lesion is
detectable. A small loss of alveolar surface area (e.g., less than 5%) over a one or two
year exposure is not detectable by the morphometric methods applied to date;
however, this rate of surface area destruction, if irreversible, would result in a
functionally significant loss of gas exchange capacity from continuous exposure for 5
or 10 years. While the destruction of alveolar walls is an important criteria to evaluate
the toxicity o oxides of nitrogen, the available data base is not adequate to detect this
injury in low levels of exposure.
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16.3.5 Subpopulations Potentially Susceptible to NO2 Exposure
A good summary, but it does not include the studies (e.g., Utell) that fail to show
increased susceptibility of COPD patients t NC>2.
Page 16-18. line 18. This sentence would read better as follows:
"Subpopulations that already have reduced ventilatory reserve (e.g., the elderly and
persons with asthma, emphysema, and chronic bronchitis) will be more impacted that
other groups by decrements in pulmonary function."
lines 26-29. This statement is essentially refuted by the essence of what
is said on page 5, lines 19-29.
line 31. Some patients with COPD have airway hyperresponsiveness --
not many.
Page 16-18. lines 30 and 31 and Page 16-19. lines 1-5. The discussion of
COPD should not focus exclusively in inadequate pulmonary reserve. It may well be
that NO2 exposure alters already impaired defense mechanisms making this
population susceptible to respiratory infections. This concept should be incorporated
into the Discussion.
Page 16-19. line 2. I would use the term ventilatory reserve rather than
pulmonary reserve.
lines 3-5. Good observation; important point well made.
line 19. At present, the evidence is non-existent between 1 and 6 years
of age.
line 22. "Data...provide..."
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