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DOMINANT SUBORDERS
J Argids Oyids J OO~INANT
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Histels
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11in Dominant Soil Orders

Al.fl Al.fl:iOl.S (High N ulrien1 Soil e.)

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D ARIOOOL:i (De,,;er1 Sail"-)

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• GEUSOI.S (P1i1m1111rost Soils)

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HISTOSOLS
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MOLLISOLS .,. INCEPTISOLS

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DOMINANT SUBORDERS
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Aquolls Udolls CJ Aq uepts Ustepts

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 Brie ~ontents

The Soils Around Us 1 Soil Acidity, Alkalinity, Salinity,

and Sodicity 312

Formation of Soils from Parent

Materials 29 Organisms and Ecology of the
Soil 369

Soil Classification 72
Soil Organic Matter 419

Soil Architecture and Physical

Properties 117 Nutrient Cycles and Soil
Fertility 466

Soil Water: Characteristics and

Behavior 164 Practical Nutrient Management 548

Soil and the Hydrologic Cycle 197 Soil Erosion and Its Control 606

Soil Aeration and Temperature 239 Soils and Chemical Pollution 652

The Colloidal Fraction: Seat of Soil

Chemical and Physical Activity 275

•• •
V 111
"'"""""ontents
Preface xxi
.
About the Authors XXIV
The Soils Around Us 1
1.1 What Ecosystem Services Do Soils Perform? 2
1.2 How Do Soils Support Plant Growth? 3
1.3 How Do Soils Regulate Water Supplies? 6
1.4 How Do Soils Recycle Raw Materials? 7
1.5 How Do Soils Modify the Atmosphere? 7
1.6 What Lives in the Soil Habitat? 7
1. 7 How are Soils Used in Building and
Engineering? 9
1.8 The Pedosphere and the Critical Zone? 10
1.9 Soils as Natural Bodies 11
1.10 The Soil Profile and Its Layers (Horizons) 13
1.11 How Does Topsoil Differ from Subsoil? 15
1.12 Soil-Interface of Air, Minerals, Water, and
Life 17
1.13 What Are the Mineral (Inorganic) Constituents
of Soils? 17
Soil Texture 18
Soil Minerals 18
Soil Structure 19
1.14 What Is Soil Organic Matter Like? 19
1.15 Why Is Soil Water So Dynamic and
Complex? 21
Soil Solution 21
1.16 Soil Air: A Changing Mixture of Gases 21
1.17 How Do Soil Components Interact to Supply
Nutrients to Plants? 22
Essential Element Availability 22
1.18 How Do Plant Roots Obtain Nutrients? 24
1.19 Soil Health, Degradation, and Resilience 25
Soil Quality and Health 26
Soil Degradation and Resilience 26
1.20 Conclusion 27
Study Questions 27
Re fe rences 28
Formation of Soils from Parent
Materials 29
2.1 Weathering of Rocks and Minerals 29
Characteristics of Rocks and Minerals 30
Weathering: A General Case 32
Physical Weathering (Disintegration) 33
Biogeochemical Weathering 34
2.2 What Environmental Factors Influence Soil
Formation? 36
2.3 Parent Materials 36
Classification of Parent Materials 37
Residual Parent Material 37
Colluvial Debris 38
Alluvial Stream Deposits 39
Coastal Sediments 41
Parent Materials Transported by Glacial Ice and
Meltwaters 42
Parent Materials Transported by Wind 43
Organic Deposits 44
2.4 How Does Climate Affect Soil Formation? 47
Effective Precipitation 48
Temperature 48
2.5 How Do Living Organisms (Including People)
Affect Soil Formation? 49
Role of Natural Vegetation 50
Role of Animals 51
2.6 How Does Topography Affect Soil Formation? 53
2. 7 How Does Time Affect Soil Formation 55
2.8 Four Basic Processes of Soil Formation 58
Soil-Forming Processes in Action: A Simplified
Example 60
2. 9 The Soil Profile 62
The Master Horizons and Layers 62
Subdivisions Within Master Horizons 64
Transition Horizons 65
•
IX
X CO NTE NTS

Subhorizon Distinctions 65 3.12 Mollisols (Dark, Soft Soils of Grasslands) 96

Horizons in a Given Profile 66 Distribution and Use 97
Soil Genesis in Nature 67 3.13 Alfisols (Argillic or Natric Horizon, Moderately
2.10 Urban Soils 67 Leached) 98

Pedological Properties Unique to Urban Soils 67 Distribution and Use 99

Physical Properties Unique to Urban Soils 68 3.14 Ultisols (Argillic Horizon, Highly Leached) 99

Chemical Properties Unique to Urban Soils 68 Distribution and Use 100

Biological Properties Unique to Urban Soils 69 3.15 Spodosols (Acid, Sandy, Forest Soils, Highly
Leached) 101
2.11 Conclusion 70
Distribution and Use 102
Study Questions 70
References 71 3.16 Oxisols (Oxic Horizon, Highly Weathered) 102
Distribution and Use 102
3.17 Lower-Level Categories in Soil Taxonomy 104
Suborders 104
Soil Moisture Regimes (SM Rs) 104
Soil Classification 72 Great Groups 104
3.1 Concept of Individual Soils 72 Subgroups 105
Pedon and Polypedon 73 Families 108
Groupings of Soil Individuals 74 Soil Temperature Regimes 108
3.2 Soil Taxonomy: A Comprehensive Classification Series 108
System 75 3.18 Mapping the Different Soils in a Landscape 111
Bases of Soil Classification 75 Soil Description 111
Diagnostic Surface Horizons of Mineral Soils 75 Delineating Soil Boundaries 112
Diagnostic Subsurface Horizons 75 Online Interactive Soil Survey 113
3.3 Categories and Nomenclature of Soil How to Use Web Soil Survey 113
Taxonomy 79
''There's an App for That'' 114
Nomenclature of Soil Taxonomy 79
3.19 Conclusion 115
3.4 Soil Orders 81
Study Questions 115
3.5 Entisols (Recent: Little If Any Profile References 116
Development) 83
Distribution and Use 83
3.6 lnceptisols (Few Diagnostic Features: Inception
of B Horizon) 85
Distribution and Use 86
Soil Architecture and Physical
3.7 Andisols (Volcanic Ash Soils) 86
Properties 117
Distribution and Use 87
4.1 Soil Color 117
3.8 Gelisols (Permafrost and Frost Churning) 87
Causes and Interpretation of Soil Colors 118
Distribution and Use 88
4.2 Soil Texture (Size Distribution of Soil
3.9 Histosols (Organic Soils Without Permafrost) 89 Particles) 120
Distribution and Use 91 Nature of Soil Separates 120
3.10 Aridisols (Dry Soils) 92 Influence of Surface Area on Other Soil
Distribution and Use 93 Properties 122
3.11 Vertisols (Dark, Swelling, and Cracking Clays) 94 4.3 Soil Textural Classes 123
Distribution and Use 95 Alteration of Soil Textural Class 124

Determination of Textural Class by the "Feel"
Method 124
Laboratory Particle-Size Analyses 125
4.4 Structure of Mineral Soils 127
Types of Soil Structure 128
Description of Soil Structure in the Field 131
4.5 Formation and Stabilization of Soil
Aggregates 131
Hierarchical Organization of Soil
Aggregates 131
Factors Influencing Aggregate Formation and
Stability in Soils 132
Physical-Chemical Processes 132
Biological Processes 134
4.6 Tillage and Structural Management of
Soils 137
Tillage and Soil Tilth 137
Conventional Tillage and Crop Production 138
Conservation Tillage and Soil Tilth 139
Soil Crusting 139
Soil Conditioners 140
General Guidelines for Managing Soil Tilth 140
4. 7 Soil Density 141
Particle Density 141
Bulk Density 141
Factors Affecting Bulk Density 141
Useful Density Figures 144
Management Practices Affecting Bulk
Density 145
Influence of Bulk Density on Soil Strength and
Root Growth 149
4.8 Pore Space of Mineral Soils 150
Factors Influencing Total Pore Space 150
Size of Pores 150
Cultivation and Pore Size 152
4.9 Soil Properties Relevant to Engineering
Uses 153
Field Rating of Soil Consistence and
Consistency 153
Soil Strength and Sudden Failure 154
Settlement-Gradual Compression 156
Expansive Soils 157
Atterberg Limits 157
Unified Classification System for Soil
Materials 158
•
CONT E N T S XI
4.10 Conclusion 161
Study Questions 161
References 162
Soil Water: Characteristics
and Behavior 164
5.1 Structure and Related Properties of
Water 165
Cohesion Versus Adhesion 166
Surface Tension 166
5.2 Capillary Fundamentals and Soil Water 166
Capillary Mechanism 166
Height of Rise in Soils 166
5.3 Soil Water Energy Concepts 168
Forces Affecting Potential Energy 168
Soil Water Potential 168
Gravitational Potential 169
Pressure Potential (Including Hydrostatic and
Matric Potentials) 169
Osmotic Potential 170
Units Used to Quantify Water Potentials 171
Combined Potentials 171
5.4 Soil Water Content and Soil Water
Potential 171
Soil Water Versus Energy Curves 171
Measurement of Soil Water Status 172
Volumetric Water Content 173
Measuring Soil Water Status 174
5.5 How Does Water Move in Soil? 177
Saturated Flow Through Soils 177
Factors Influencing the Hydraulic Conductivity
of Saturated Soils 179
Unsaturated Flow in Soils 180
5.6 Infiltration and Percolation 181
Infiltration 182
Percolation 182
Water Movement in Stratified Soils 183
Water Movement in Stratified Soils 185
5.7 Qualitative Description of Soil Wetness 185
Maximum Retentive Capacity 186
Field Capacity 186
 • •
X 11 CONTENTS

Permanent Wilting Percentage or Wilting 6.7 Enhancing Soil Drainage 220

Coefficient 187 Reasons for Enhancing Soil Drainage 220
Hygroscopic Coefficient 188 Surface Drainage Systems 222
5.8 Factors Affecting Amount of Plant-Available Subsurface (Internal) Drainage 222
Soil Water 189
6.8 Septic Tank Drain Fields 226
Water Content-Potential Relationship 189
Operation of a Septic System 227
Compaction Effects on Matric Potential,
Aeration, and Root Growth 190 Soil Properties Influencing Suitability for a
Septic Drain Field 228
Osmotic Potential 190
6. 9 Irrigation Principles and Practices 229
Soil Depth and Layering 190
Importance of Irrigation Today 230
5. 9 Mechanisms by Which Plants Are Supplied with
Water 193 Water-Use Efficiency 231

Rate of Capillary Movement 193 Surface Irrigation 232

Rate of Root Extension 193 Sprinkler Systems 233

Root Distribution 193 Microirrigation 235

Root-Soil Contact 194 6.10 Conclusion 236

Study Questions 237
5.10 Conclusion 194
References 238
Study Questions 195
References 196

Soil Aeration and Temperature 239

7 .1 Soil Aeration-The Process 239
Soil and the Hydrologic Cycle 197
Soil Aeration in the Field 240
6.1 The Global Hydrologic Cycle 198
Excess Moisture 240
Global Stocks of Water 198
Gaseous Interchange 240
The Hydrologic Cycle 198
7 .2 Means of Characterizing Soil Aeration 241
Water Balance Equation 199
Gaseous Composition of the Soil Air 241
6.2 Fate of Incoming Water 200
Air-Filled Porosity 242
Effects of Vegetation and Soils on Infiltration 200
7 .3 Oxidation-Reduction (Redox) Potential 242
6.3 The Soil-Plant-Atmosphere Continuum
(SPAC) 205 Redox Reactions 242

Evapotranspiration 205 Role of Oxygen Gas 243

6.4 Control of ET 209 Other Electron Acceptors 243

Control of Transpiration 209 7 .4 Factors Affecting Soil Aeration and EH 245

Control of Surface Evaporation 211 Rates of Respiration in the Soil 245

6.5 Liquid Losses of Water from the Soil 213 Depth in the Soil Profile 245

Percolation and Leaching 213 Drainage of Excess Water 246

Percolation-Evaporation Balance 214 Small-Scale Soil Heterogeneity 246

6.6 Percolation and Groundwater 216 Seasonal Differences 247

Groundwater Resources 216 Effects of Vegetation 247

Shallow Groundwater 217 7 .5 Ecological Effects of Soil Aeration 247

Movement of Chemicals in the Drainage Effects on Organic Residue Degradation 247

Water 218 Oxidation-Reduction of Elements 248
Chemical Movement Through Macropores 218 Effects on Activities of Higher Plants 249

7.6 Soil Aeration in Urban Landscapes 251
Container-Grown Plants 251
Tree and Lawn Management 252
7.7 Wetlands and Their Poorly Aerated Soils 253
Defining a Wetland 253
Wetland Hydrology 254
Hydric Soils 255
Hydrophytic Vegetation 255
Wetland Chemistry 257
Constructed Wetlands 257
7 .8 Processes Affected by Soil Temperature 259
Plant Processes 259
Microbial Processes 261
Freezing and Thawing 262
Permafrost 262
Soil Heating by Fire 263
Contaminant Removal 263
7.9 Absorption and Loss of Solar Energy 264
Slope Angle and Aspect 265
7 .10 Thermal Properties of Soils 266
Specific Heat of Soils 266
Heat of Vaporization 267
Thermal Conductivity of Soils 268
Variation with Time and Depth 269
7 .11 Soil Temperature Control 270
Organic Mulches and Plant-Residue
Management 270
Plastic Mulches 271
Moisture Control 272
7 .12 Conclusion 273
Study Questions 273
References 273
The Colloidal Fraction: Seat of Soil
Chemical and Physical Activity 275
8.1 General Properties and Types of Soil
Colloids 276
Size 276
Surface Area 276
Surface Charges 276
Adsorption of Cations and Anions 276
• • •
CONTENTS X 111
Adsorption of Water 277
Types of Soil Colloids 278
8.2 Fundamentals of Layer Silicate Clay
Structure 279
Tetrahedral and Octahedral Sheets 279
Source of Charges 281
8.3 Mineralogical Organization of Silicate Clays 281
1 :1-Type Silicate Clays 281
Expanding 2:1-Type Silicate Clays 283
Nonexpanding 2:1 Silicate Minerals 285
8.4 Structural Characteristics of Nonsilicate
Colloids 286
Iron and Aluminum Oxides 286
Humus 287
8.5 Genesis and Geographic Distribution of Soil
Colloids 288
Genesis of Colloids 288
Distribution of Clays by Geography and Soil
Order 289
8.6 Sources of Charges on Soil Colloids 290
Constant Charges on Silicate Clays 290
pH-Dependent Charges 291
8. 7 Adsorption of Cations and Anions 293
Outer- and Inner-Sphere Complexes 294
8.8 Cation Exchange Reactions 295
Principles Governing Cation Exchange
Reactions 296
8. 9 Cation Exchange Capacity (CEC) 298
Methods of Determining CEC 298
Cation Exchange Capacities of Soils 300
pH and Cation Exchange Capacity 301
8.10 Exchangeable Cations in Field Soils 302
Cation Saturation and Nutrient Availability 303
Influence of Complementary Cations 303
Effect of Type of Colloid 304
8.11 Anion Exchange 304
Inner-Sphere Complexes 304
Weathering and CEC/AEC Levels 305
8.12 Sorption of Organic Molecules to Soil
Colloids 306
Distribution Coefficients 307
Binding of Biomolecules to Clay and Humus 308
8.13 Conclusion 309
Study Questions 310
References 311
 •
XIV CONTENTS
Soil Acidity, Alkalinity, Salinity,
and Sodicity 312
9 .1 What Processes Cause Soil Acidity and
Alkalinity? 313
Acidifying Processes That Produce Hydrogen
Ions 314
Alkalizing Processes That Consume Hydrogen
Ions or Produce Hydroxyl Ions 315
9.2 What Role Does Aluminum Play in Soil
Acidity? 317
9.3 Pools of Soil Acidity 318
Principal Pools of Soil Acidity 318
Cation Saturation Percentages 320
Acid (or Nonacid) Cation Saturation and pH 320
9 .4 Buffering of pH in Soils 321
Why Is Soil pH Buffering Important? 322
9.5 How Can We Measure Soil pH? 323
Potentiometric Methods 323
Variability in the Field 324
9.6 How Do Humans Acidify Soils? 325
Nitrogen Fertilization 325
Acid Deposition from the Atmosphere 326
Exposure of Potential Acid Sulfate
Materials 328
9.7 How Does Soil pH Affect Living Things? 330
Aluminum Toxicity 330
Manganese, Hydrogen, and Iron Toxicity to
Plants 331
Nutrient Availability to Plants 332
Microbial Effects 333
Optimal pH Conditions for Plant Growth 333
Soil pH and Organic Molecules 335
9 .8 Raising Soil pH by Liming 336
Agricultural Liming Materials 336
How Do Liming Materials React to Raise Soil
pH? 337
Lime Requirement: How Much Lime Is Needed
to Do the Job? 338
How Lime Is Applied 340
Special Liming Situations 340
9. 9 Ameliorating Acidity Without Lime 341
Using Gypsum 341
Using Organic Matter 341
9.10 Lowering Soil pH 343
Acid Organic Matter 343
Inorganic Chemicals 343
9 .11 Development of Salt-Affected Soils 346
Accumulation of Salts in Nonirrigated Soils 346
Irrigation-Induced Salinity and Alkalinity 347
9.12 Measuring Salinity and Sodicity 348
Salinity 348
Sodium Status (Sodicity) 350
9.13 Classes of Salt-Affected Soils 350
Saline Soils 350
Saline-Sodic Soils 352
Sodic Soils 352
9.14 Physical Degradation in Soil-Sodic Soils 352
Slaking, Swelling, and Dispersion 353
Two Causes of Soil Dispersion 353
9.15 Biological Impacts of Salt-Affected Soils 354
How Salts Affect Plants 354
Selective Tolerance of Higher Plants to Saline
and Sodic Soils 355
Salt Problems Not Related to Arid Climates 355
9.16 Water-Quality Considerations for Irrigation 356
9 .17 Reclamation of Saline Soils 358
Leaching Requirement (LR) 358
Management of Soil Salinity 359
Some Limitations of the Leaching Requirement
Approach 361
9 .18 Reclamation of Saline-Sodic and Sodic Soils 362
Gypsum 362
Sulfur and Sulfuric Acid 362
Physical Condition 363
Management of Reclaimed Soils 363
9 .19 Conclusion 364
Study Questions 366
References 367
Organisms and Ecology of the Soil 369
10.1 The Diversity of Organisms in the Soil 370
10.2 Organisms in Action 373
Trophic Levels and the Soil Food Web 373
Sources of Energy and Carbon 373
 CONTENTS XV

Primary Producers 375 10.12 Beneficial Effects of Soil Organisms on Plant

Primary Consumers 375 Communities 406

Secondary Consumers 375 Soil Organic Matter Formation and Nutrient

Cycling 406
Tertiary Consumers 376
Breakdown of Toxic Compounds 406
Ecosystem Engineers 377
Inorganic Transformations 406
10.3 Abundance, Biomass, and Metabolic
Activity 378 Nitrogen Fixation 406

Comparative Organism Activity 378 Rhizobacteria 407

10.4 Earthworms 379 Plant Protection 407

Influence on Soil Fertility, Productivity,
and Environmental Quality 380
Deleterious Effects of Earthworms 381
Factors Affecting Earthworm Activity 382
10.5 Ants and Termites 384
Ants 384
10.13 Soil Organisms and Plant Damage 407
Plant Pests and Parasites 408
Plant Disease Control by Soil Management 408
Disease-Suppressive Soils 409
10.14 Ecological Relationships Among Soil
Organisms 412

Termites 384 Mutualistic Associations 412

10.6 Soil Microanimals 386 Biocrusts 412

Nematodes 386 Effects of Agricultural Practices on Soil

Organisms 413
Protozoa 388
10.15 Conclusion 415
Other Fascinating Soil Microcreatures 389
Study Questions 415
10.7 Plant Roots 390 References 416
Root Morphology 390
How Roots Alter Soil Conditions 391
Rhizosphere 391
Rhizodeposition 391
10.8 Soil Algae 393 Soil Organic Matter 419
10.9 Soil Fungi 393 11.1 The Global Carbon Cycle 419
Molds 394 Basic Processes 420
Mushroom Fungi 395 Carbon Sources 421
Activities of Fungi 395 11.2 Organic Decomposition in Soils 423
Mycorrhizae 397 Composition of Plant Residues 423
10.10 Soil Prokaryotes: Bacteria and Archaea 400 Decomposition of Organic Compounds
in Aerobic Soils 424
Characteristics 400
Example of Organic Decay 425
Prokaryote Diversity in Soils 400
Production of Simple Inorganic Products 426
Sources of Energy 402
Decomposition in Anaerobic Soils 426
Importance of Prokaryotes 402
11.3 Factors Controlling Rates of Residue
Soil Actinomycetes 403
Decomposition and Mineralization 427
10.11 Conditions Affecting the Growth and Activity
Physical Factors Influencing Residue
of Soil Microorganisms 405
Quality 427
Organic Resources 405
Carbon/Nitrogen Ratio of Organic Materials
Oxygen Requirements 405 and Soils 428
Moisture and Temperature 405 Influence of Carbon/Nitrogen Ratio on Residue
Exchangeable Calcium and pH 405 Decomposition 429
 •
XV I CONTENTS

Examples of Inorganic Nitrogen Release 11.11 Composts and Composting 461

During Decay 430 11.12 Conclusion 463
Influence of Soil Ecology 431 Study Questions 464
Influence of Lignin and Polyphenol Content 431 References 464
11.4 Genesis and Nature of Soil Organic Matter
and Humus 432
Microbial Transformations 434
Examples of Biomolecules in Soil Organic
Matter 436
Colloid Characteristics of Humus 436
Nutrient Cycles and Soil Fertility 466
12.1 Nitrogen in the Soil System 467
Stability of Humus 438
Nitrogen and Plant Growth and
11.5 Influences of Organic Matter on Plant Growth
Development 46 7
and Soil Function 438
Distribution and Cycling of Nitrogen 468
Direct Influence of Humus on Plant Growth 438
Nitrogen Immobilization and
Allelochemical Effects 439
Mineralization 470
Influence of Organic Matter on Soil Properties
Ammonium Fixation by Clay Minerals 471
and Indirectly on Plants 440
Dissolved Organic Nitrogen 471
11.6 Amounts and Quality of Organic Matter in
Soils 442 Ammonia Volatilization 472
Labile Organic Matter 442 Nitrification 473
Protected or Stable Organic Matter Soil Conditions Affecting Nitrification 474
(Humus) 442 Gaseous Losses by Denitrification 475
Changes in Labile and Humus Pools with Soil Anammox 476
Management 443
Atmospheric Pollution and Greenhouse Gas
11.7 Carbon Balance in the Soil-Plant-Atmosphere Emissions 476
System 444
Symbiotic Nitrogen Fixation with Legumes 479
Agroecosystems 444
N Fixation in Nodule-Forming Nonlegumes 482
Natural Ecosystems 447
Symbiotic Nitrogen Fixation Without
11.8 Environmental Factors Influencing Soil Nodules 483
Organic Carbon Levels 447
Nonsymbiotic Fixation by Heterotrophs 484
Differences Among Soil Orders 448
Fixation by Autotrophs 484
Influence of Climate 449
Nitrogen Deposition from the Atmosphere 484
Influence of Natural Vegetation 450
12.2 Sulfur in the Soil System 487
Effects of Texture and Drainage 450
Roles of Sulfur in Plants and Animals 487
11.9 Soil Organic Matter Management 451
Natural Sources of Sulfur in Soils 488
Influence of Agricultural Management and
Cycling of Sulfur in Soils 491
Tillage 451
Sulfur Retention and Exchange 494
Influence of Rotations, Residues, and Plant
Nutrients 452 Sulfur Fertility Maintenance 495
The Conundrum of Soil Organic Matter 12.3 Phosphorus in Plant Nutrition and Soil
Management 453 Fertility 496
General Guidelines for Managing Soil Organic Phosphorus and Plant Growth 496
Matter 453 The Phosphorus Problem in Soil Fertility and
11.10 Soils and Climate Change 454 Environmental Quality 497
Global Climate Change 454 The Phosphorus Cycle 498
Carbon Dioxide 455 Organic Phosphorus in Soils 501

Inorganic Phosphorus in Soils 503
Phosphorus-Fixation Capacity of Soils 507
How Do Plants Obtain Adequate
Phosphorus? 509
Management Strategies for Meeting Plant
Phosphorus Needs in low· P Soils 510
Management Strategies for Controlling Over-
Enrichment of Soils and Water Pollution 512
12.4 Potassium: Nature and Ecological Rol•s 514
Potassium in Plant and Animal Nutrition 514
The Potassium Cycle in Soil-Plant Systems 516
The Potassium Problem in Soil Fertility 518
Forms and Availability of Potassium in
Soils 518
Factors Affect.Ing Potassium Fixation in
Soils 520
Some Practical Aspects of Potassium
Management 521
12.5 Calcium as an Esuntial Nutrient 522
Calcium in Plants 522
Soil Forms and Processes 523
12.6 Magnesium as a Plant Nutrient 524
Magn•sium in Plants 524
Magne-sium in Soil 524
Ratio of Calcium to Magnesium 525
12.7 Silicon in Soil-Plant Ecology 526
Silicon in Plants 526
Silicon in Soils 527
12.8 Micronutrients in the SoU-Plant System 528
Deficiency Versus Toxicity 528
Micronutrient Cycles, Forms., and Reactions in
the Soil 532
Organic 534
Influence of Soil pH 534
Oxidation State 535
O rganic Matter and Clay 536
Role of Mycorrhizae 537
Organic Chelating Agents 538
Soil Management and Trace El•ment Needs 539
Fertilizer Applications 540
Fighting Micronutrient Hunger 540
12.9 Conclusion 542
Study Questions 543
Refetences 545
CON1' ENTS XVII
13
Practical Nutrient Management 548
13.1 Goals of Nutrient Management 548
Plant Production 549
Soil Health and Productivity 549
CoMervation of Nutrient Resources 549
Environmental Impa ct: Nutrient Budgets and
Balances 550
13.2 Nutri•nts as Pollutants 551
Nutrient Damage to Aquatic Ecosystems 551
Nutrient Management Plans 552
Best Management Practices (BMPs) 554
Buffer Strips 554
Cover Crops for Nutrient Management 556
Conservation Tillage 559
Combining Practices on the landscape 560
13.3 Ecosystem Nutrient Cycl•s 560
Nutrient Cycling in Grasslands 562
13.4 Recycling Nutrients Through Animal
Manures 564
Nutrient Composition of Animal Manures 564
Concentrated Animal-Feeding Operations
(CAFOs) 564
Storage, T,..atment, and Manag &ment of Animal
Manur•s 567
Methods of Manure Application 569
13.5 Industrial and Municipal By-Products 570
Garbage and Yard Wastes 570
Food-Processing Wast•s 570
Wood Wastes 570
Wastewater Treatment By.Products 571
Sewage Effluent 571
Sewage Sludge or Biosollds 572
Integrated Recycling of Wastes 572
13.6 Practical Utilization of Organic Nutrient
Sourcff 573
13.7 Inorganic Commercial Fertilizers 576
Origin and Proc•ssing of Inorganic
Fertilizers 577
Properties and Use of Inorganic Fertilizers 577
Fertilizer Grade 578
Fate of FertiUzer Nutrients 578
The Concept of the Limiting Factor 581
 •• •
XVI 11 CONTENTS
13.8 Fertilizer Application Methods 581
Broadcasting 581
Localized Placement 584
Foliar Application 585
13.9 Timing of Nutrient Application 585
Availability When the Plants Need It 585
Environmentally Sensitive Periods 586
Physiologically Appropriate Timing 586
Practical Field Limitations 586
13.10 Diagnostic Tools and Methods 586
Plant Symptoms and Field Observations 587
Plant Analysis 587
13.11 Soil Analysis 591
Sampling the Soil 591
Chemical Analysis of the Sample 593
Interpreting the Results to Make a
Recommendation 594
Merits of Soil Testing 595
13.12 Site-Index Approach to Phosphorus
Management 596
Overenrichment of Soils 596
Transport of Phosphorus from Land to
Water 597
Phosphorus Soil Test Level as Indicator of
Potential Losses 597
Phosphorus Site Index 599
13.13 Some Advances and Challenges in Nitrogen
Management 599
13.14 Conclusion 602
Study Questions 603
References 603
Soil Erosion and Its Control 606
14.1 Significance of Soil Erosion and Land
Degradation 607
Land Degradation 607
Soil-Vegetation Interdependency 607
Geological Versus Accelerated Erosion 608
14.2 On-Site and Off-Site Impacts of Accelerated
Soil Erosion 610
Types of On-Site Damages 610
Types of Off-Site Damages 610
14.3 Mechanics of Water Erosion 612
Influence of Raindrops 612
Transportation of Soil 613
Types of Water Erosion 613
Deposition of Eroded Soil 613
14.4 Models to Predict Water-Induced
Erosion 614
The Universal Soil-Loss Equation (USLE) 615
The Revised Universal Soil-Loss Equation
(RUSLE) 616
14.5 Factors Affecting lnterrill and Rill
Erosion 616
Rainfall Erosivity Factor, R 616
Soil Erodibility Factor, K 616
Topographic Factor, LS 616
Cover and Management Factor, C 618
Support Practice Factor, P 619
14.6 Conservation Tillage 622
Conservation Tillage Systems 624
Adaptation by Farmers 625
Erosion Control by Conservation Tillage 626
Effect on Soil Properties 627
14.7 Vegetative Barriers 628
14.8 Control of Gully Erosion and Mass
Wasting 629
Remedial Treatment of Gullies 629
Mass Wasting on Unstable Slopes 630
14.9 Control of Accelerated Erosion on Range and
Forestland 631
Rangeland Problems 631
Erosion on Forestlands 631
Practices to Reduce Soil Loss Caused
by Timber Production 632
14.10 Erosion and Sediment Control on Construction
Sites 634
Principles of Erosion Control on Construction
Sites 634
Keeping the Disturbed Soil Covered 634
Controlling the Runoff 636
Trapping the Sediment 637
14.11 Wind Erosion: Importance and Factors
Affecting It 638
Mechanics of Wind Erosion 640
Factors Affecting Wind Erosion 641

14.12 Predicting and Controlling Wind
Erosion 641
Control of Wind Erosion 642
14.13 Tillage Erosion 644
Movement of Soil by Tillage 644
Quantification of Tillage Erosion 645
14.14 Land Capability Classification and Progress in
Soil Conservation 647
Conservation Management to Enhance Soil
Health 648
Finding Soil Conservation Win-Win
Systems 648
14.15 Summary and Conclusion 649
Study Questions 650
References 650
Soils and Chemical Pollution 652
15.1 Toxic Organic Chemicals 652
Environmental Damage from Organic
Chemicals 653
The Nature of the Pesticide Problem 653
15.2 Kinds of Organic Contaminants 657
Industrial Organics 657
Pesticides 657
15.3 Behavior of Organic Chemicals in Soil 659
Contamination of Groundwater 662
Chemical Reactions 662
Microbial Metabolism 662
Plant Absorption and Breakdown 664
Persistence in Soils 664
15.4 Effects of Pesticides on Soil Organisms 665
Fumigants 665
Effects on Soil Fauna 665
Effects on Soil Microorganisms 666
15.5 Remediation of Soils Contaminated with
Organic Chemicals 667
Physical and Chemical Methods 667
Bioremediation 669
Phytoremediation 6 72
•
CONTENTS XIX
15.6 Soil Contamination with Toxic Inorganic
Substances 674
Sources of the Contaminants 674
Accumulation in Soils 675
Concentration in Living Tissues 675
Some Inorganic Contaminants and Their
Reactions in Soils 6 78
15.7 Potential Hazards of Chemicals in Sewage
Sludge 678
Heavy Metals in Sewage Sludge 6 79
15.8 Prevention and Remediation of Inorganic Soil
Contamination 681
Reducing Soil Application 681
Immobilizing the Toxins 681
Bioremediation by Metal Hyperaccumulating
Plants 683
Management to Enhance Phytoremediation 684
15.9 Landfills 685
The Municipal Solid Waste Problem 685
Two Basic Types of Landfill Design 686
Natural Attenuation Landfills 686
Containment or Secured Landfills 688
Environmental Impacts of Landfills 688
Land Use After Completion 690
15.10 Radionuclides in Soil 690
Radioactivity from Nuclear Fission 690
Nuclear Accident at Chernobyl 691
Nuclear Accident at Fukushima 692
Radioactive Wastes 692
15.11 Radon Gas from Soils 693
The Health Hazard 693
How Radon Accumulates in Buildings 693
Radon Testing and Remediation 694
15.12 Conclusion 695
Study Q uestions 695
References 696
APPENDIX A . World Reference Base, Canadian, and
Australian Soil Classification Systems 698
APPENDIX B. SI Units, Conversion Factors, Periodic
Table of the Elements, and Plant Names 703
Glossary of Soil Science Terms 709
INDEX 728
 e

On November 24, 2015, soil science lost one of its giants. Nyle C. Brady passed
away at t he age of 95 . Dr. Brady was a global leader in soil science, in agriculture,
and in humanity. He was born in 1920 in the tiny rural town of Manassa, Colorado,
USA. He earned a BS degree in chemistry from Brigham Young University in 1941
and went on to complete his PhD in soil science at North Carolina State University
in 1947. Dr. Brady then served as a member of the faculty at Cornell University in
Ithaca, NY, USA, for 26 years, rising from assistant professor to professor and chair of
the agronomy department and finally to assistant dean of the College of Agriculture.
During this period, he was elected president of both the American Society of Agron-
omy and the Soil Science Society of America.
Soon after arriving at Cornell University, he was recruited by Professor
Harry 0. Buckman to assist in co-authoring the then already classic soil science
textbook, The Nature and Properties of Soils. The first edition of this textbook to
bear Nyle Brady's name as co-author was published in 1952. Under Nyle's hand,
this book rose to prominence throughout the world and several generations of soil
scientists got their introduction to the field through its pages. He was the sole
author of editions published between 1974 and 1990. He continued to work on
revised editions of this book with co-author Ray Weil until 2004.
Dr. Brady was of that generation of American soil scientists that contributed so
much to the original green revolution. He conducted research into the chemistry of
phosphorus and the management of fertilizers, and he was an early researcher on min-
imum tillage. Known for his active interest in international development and for his
administrative skills, he was recruited in 1973 to be the third Director General of the
International Rice Research Institute (IRRI) in the Philippines. Dr. Brady pioneered
new cooperative relationships between IRRI and the national agricultural research in-
stitutions in many Asian countries, including a breakthrough visit to China at a time
when that country was still quite closed to the outside world. He oversaw the transi-
tion to a second-generation of green revolution soil management and plant breeding
designed to overcome some of the shortcomings of the first generation.
After leaving IRRI, he served as senior assistant administrator for Science and
Technology at the U.S. Agency for International Development from 1981 to 1989.
He was a fierce champion of international scientific cooperation to promote sustain-
able resource use and agricultural development. During the 1990s Dr. Brady, then in
his 70s, served as senior international development consultant for the United Nations
Development Programme (UNDP) and for the World Bank, in which capacity he
continued to promote scientific collaboration in advances in environmental steward-
ship and agricultural development.
Dr. Brady was always open-minded and ready to accept new truths supported
by scientific evidence, as can be seen by the evolution of the discussion of such top-
ics as pesticide use, fertilizer management, manure utilization, tillage, soil organic
matter, and soil acidity management in The Nature and Properties of Soils under his
guidance. Nyle Brady had a larger-than-life personality, a deep sense of empathy, and
an incredible understanding of how to work with people to get positive results. He
was the kind of person that friends, associates, and even strangers would go to for ad-
vice when they found themselves in a perplexing position as a scientist, administrator,
or even in their personal life. He will be very much missed for a long time to come by
his family and by all who knew him or were touched by his work.
xx
By opening this fourth edition of The Elements of the Nature and Properties of Soils, you
are tapping into a narrative that has been at the forefront of soil science for more than a
century. The first version of the parent book from which this book has been abridged,
was published in 1909. It was largely a guide to good soil management for farmers in
the glaciated regions of New York State in the northeastern United States. Since then,
the books have evolved to provide a globally relevant framework for an integrated un-
derstanding of the diversity of soils, the soil system, and its role in the ecology of
planet Earth.
If you are a student reading this, you have chosen a truly auspicious time to take
up the study of soil science. Scientists and managers well versed in soil science are in
short supply and becoming increasingly sought after. Much of what you learn from
these pages will be of enormous practical value in equipping you to meet the many
natural-resource challenges of the twenty-first century. You will soon find that the soil
system provides many opportunities to see practical applications for principles from
such sciences as biology, chemistry, physics, and geology.
The importance of soils and soil science is increasingly recognized by business
and political leaders, by the scientific community, and by those who work with the
land. Soils are now widely recognized as the underpinning of terrestrial ecosystems and
the source of a wide range of essential ecosystem services. An understanding of the soil
system is therefore critical for the success and environmental harmony of almost any
human endeavor on the land.
This latest edition of Elements of the Nature and Properties of Soils is the first to fea-
ture full color illustrations throughout. As is the case for its parent book, The Nature and
Properties of Soils, 15th edition, this newest edition of Elements of the Nature and Properties
of Soils strives to explain the fundamental principles of soil science in a manner that you
will find relevant to your interests. The text emphasizes the soil as a natural resource
and soils as ecosystems. It highlights the many interactions between soils and other
components of the larger forest, range, agricultural, wetland, and constructed ecosys-
tems. This book is designed to serve you well, whether you expect this to be your only
formal exposure to soil science or you are embarking on a comprehensive soil science ed-
ucation. It is meant to provide both an exciting, accessible introduction to the world of
soils and a reliable reference that you will want to keep for your professional bookshelf.
Every chapter has been thoroughly updated with the latest advances, concepts,
and applications. This edition includes new or updated discussions on soils and human
health, organic farming, engineering properties of soils, colloids and CEC, humus and
organic matter, the proton-balance approach to soil acidity, soil salinity and alkalinity,
irrigation techniques, soil food-web ecology, disease suppressive soils, soil archaea, soil
contamination and bioremediation, nutrient management, soil health, soil ecosystem
services, soil interactions with global climate change, and many other topics of current
interest in soil science. At the same time, this abridgement of the original book omits
or simplifies some of the more technical details, presents fewer chemical equations and
calculations, and focuses the text more clearly on the basics of soil science such that a
survey of the field is be accomplished in 15 instead of 20 chapters, comprising about
700 instead of nearly 1,100 pages.
If you are an instructor or a soil scientist, you will benefit from changes in this latest
edition. Most noticeable is the use of full-color throughout, which improves the new
and refined figures and illustrations to help make the study of soils more efficient,
engaging, and intellectually satisfying. Every topic, from soil classification to soil
•
XXI
 ••
XXI I PREFACE

carbon, has been updated to reflect current thinking in the discipline. Hundreds of
new key references have been added. This edition includes in-depth discussions on
such topics of cutting edge soil science as carbon sequestration, subaqueous soils, urban
and human engineered soils, cycling and plant use of silicon, inner- and outer-sphere
complexes, radioactive soil contamination, new understandings of the nitrogen cycle,
cation saturation and ratios, acid sulfate soils, water-saving irrigation techniques, hy-
draulic redistribution, cover crop effects on soil health, soil invertebrate ecology, dis-
ease suppressive soils, soil microbial genomics, soil ecosystem services, biochar, soil
interactions with global climate change, digital soil maps, and many others.
In response to their popularity in recent editions, I have also added or improved
"boxes" that present either fascinating examples and applications or technical details
and calculations. These boxes both highlight material of special interest and allow the
logical thread of the regular text to flow smoothly without digression or interruption.
Examples of applications boxes or case study vignettes include the following:
• "Dirt for Dinner"
• "Subaqueous Soils Underwater Pedogenesis"
• "Practical Applications of Unsaturated Water Flow in Contrasting Layers"
• "Char: Is Black the New Gold? "
• "Where have All the Humics Gone?"
• "Tragedy in the Big Easy A Levee Doomed to Fail"
• "Costly and Embarrassing Soil pH Mystery"
• "Gardeners' Friend Not Always So Friendly
• "Soil Microbiology in the Molecular Age"
• "The Law of Return Made Easy: Using Human Urine"
Boxes also are provided to explain detailed calculations and practical numerical
problems. Examples include the following:
• "Estimating CEC and Clay Mineralogy"
• "Calculating Lime Needs Based on pH Buffering"
• "Leaching Requirement for Saline Soils"
• "Calculation of Percent Pore Space in Soils"
• "Calculating Soil CEC from Lab Data"
• "Concentrations and Toxicity of Contaminants"
• "Calculation of Nitrogen Mineralization"
As the global economy expands, exponentially societies face new challenges with
managing their natural resources. Soil as a fundamental natural resource is critical to
sustained economic growth and the prosperity of people in all parts of the world. To
achieve balanced growth with a sustainable economy while improving environmen-
tal quality, it will be necessary to have a deep understanding of soils, including their
properties, functions, ecological roles, and management. I have written this textbook
in a way designed to engage inquisitive minds and challenge them to understand soils
and actively do their part as environmental and agricultural scientists, in the interest of
ensuring a prosperous and healthy future for humanity on planet Earth.
In this textbook, I have tried to take a broad view of soils in the environment and
in relation to human society. In so doing, the book focuses on six major ecological roles
of soil. Soils provide for the growth of plants, which, in turn, provide wildlife habitat,
food for people and animals, bio-energy, clothing, pharmaceuticals, and building ma-
terials. In addition to plant production, soils also dramatically influence the Earth's
atmosphere and therefore the direction of future climate change. Soils serve a recycling
function that, if taken advantage of, can help societies to conserve and reuse valuable and
finite resources. Soils harbor a large proportion of the Earth's biodiversity a resource
 • • •
PREFACE XX I 11

which modern technology has allowed us to harness for any number of purposes.
Water, like soil, will be a critical resource for the future generations. Soils functions
largely determine both the amount of water that is supplied for various uses and also
the quality and purification of that water. Finally, knowledge of soil physical properties
and behavior, as well as an understanding of how different soils relate to each other in
the landscape, will be critical for successful and sustainable engineering projects aimed
at effective and safe land development.
For all these reasons it will be essential for the next generation of scientists, busi-
ness people, teachers, and other professionals to learn enough about soils to appreciate
their importance and to take them into full consideration for development projects and
all activities on the land. It is my sincere hope that this book, early editions of which
have served so many generations of soil students and scientists, will allow new genera-
tions of future soil scientists to benefit from the global ecological view of soils that this
textbook expounds.
Dr. Nyle Brady, although long in retirement and recently deceased, remains as
co-author in recognition of the fact that his vision, wisdom, and inspiration continue
to permeate the book. Although the responsibility for writing this edition was solely
mine, I certainly could not have made all of the many improvements without innumer-
able suggestions, ideas, and corrections contributed by soil scientists, instructors, and
students from around the world. This 4th edition of Elements of the Nature and Properties
of Soils, like preceding editions, has greatly benefited from the high level of profes-
sional devotion and camaraderie that characterizes the global soil science community.
Special thanks go to Dr. Rachel Gilker for her invaluable editorial and research
assistance. I also thank the following colleagues (listed alphabetically by institution)
for their especially, valuable suggestions, contributions, reviews, and inspiration:
Alan Bayless (Mineral Area College); Doug Malo (South Dakota State University);
Gobena Huluka (Auburn University); James Crum (Michigan State University); Ka-
malesh Panthi (East Carolina University); Vivek Tandon (University of Texas at El
Paso); William Moore (Abraham Baldwin Agricultural College); Pichu Rengasamy
(The University of Adelaide); Pedro Sanchez and Cheryl Palm (University of Florida);
Johannes Lehmann (Cornell University); Eric Brevik (Dickinson State University);
Dan Richter (Duke University); Robert Darmody, Laura Flint Gentry, Colin Thorn,
and Michelle Wander (University of Illinois); Lee Burras (Iowa State University); Au-
rore Kaisermann (Laboratoire Bioemco); Daniel Hillel (University of Massachusetts,
Emeritus); Rafiq Islam and Rattan Lal (The Ohio State University); Darrell Schultze
(Purdue University); Joel Gruver (Western Illinois University); Ivan Fernandez (Uni-
versity of Maine); David Lobb (University of Manitoba); Mark Carroll, Glade Dlott,
Delvin Fanning, Nicole Fiorellino, Robert Hill, Bruce James, Natalie Lounsbury,
Brian Needelman, Martin Rabenhorst, Patricia Steinhilber, Barret Wessel, and
Stephane Yarwood (University of Maryland); Martha Mamo (University of Nebraska);
Jose Amador (University of Rhode Island); Allen Franzluebbers, Jeff Herrick, Scott
Lesch, and Jim Rhoades (USDA/Agricultural Research Service); Bob Ahrens, Bob
Engel, Maxine Levine, Paul Reich, Kenneth Scheffe, and Sharon Waltman (USDA/
Natural Resources Conservation Service); Markus Kleber (Oregon State University);
Henry Lin and Charlie White (The Pennsylvania State University); Joseph Heck-
man (Rutgers, The State University of New Jersey); Fred Magdoff (University of
Vermont); W. Lee Daniels and John Galbraith (Virginia Tech); and Peter Abrahams
(University of Wales).
Last, but not least, I deeply appreciate the good humor, forbearance, and patience
of my wife, Trish, and those students and colleagues who may have felt some degree
of neglect as I focused so much of my energy, time, and attention on this labor of love.
 OU ors
Ray R. Weil is Professor of Soil Science. He has earned degrees at Michigan State
University, Purdue University, and Virginia Tech. Before coming to Maryland, he
served in the Peace Corps in Ethiopia, managed a 500 acre organic farm in North
Carolina, and was a lecturer at the University of Malawi. He has become an interna-
tional leader in sustainable agricultural systems in both developed and developing
countries. Published in over 95 scientific journal articles and 8 books, his research
focuses on cover crops and organic matter management for enhanced soil quality and
nutrient cycling for water quality and sustainability. His research lab developed an-
alytical methods for soil microbial biomass and active soil C that have been adopted
by the USDA/NRCS and are used in ecosystem studies worldwide. His contributions
to improved cropping systems and soil management have been put into practice on
farms large and small.
As a University of Maryland professor, Dr. Weil teaches undergraduate and
graduate classes in soil science and sustainable agriculture. He has taught over 7 ,000
students, addressed over 5 ,000 farmers and farm advisors at meetings and field days,
and helped train hundreds of researchers and managers in various companies and
organizations. He has been the major advisor for 42 MS and PhD students. Weil
is a fellow of both the Soil Science Society of America and the American Society of
Agronomy. He has twice been awarded a Fulbright Fellowship to support his work in
developing countries. The synergism between Dr. Weil 's teaching and research, and
his ecological approach to soil science have found expression in various editions of this
textbook since 1995.

Nyle C. Brady (late), a native of Colorado, graduated from Brigham Young University
in 1941 with a bachelor's degree in Chemistry. In 1947 he received his PhD degree in
soil science from the University of North Carolina. He served on the Cornell faculty
from 1947 to 197 3, and in 195 2 became co-author of the world's most widely used
college textbook on Soil Science. He was head of the Department of Agronomy from
July 1955 to December 1963 and served as the director of the Cornell University Agri-
cultural Experiment Station from September 1965 to July 1973. He was associate dean
of the New York State College of Agriculture and Life Sciences from October 1970 to
July 1973.
Dr. Brady served as the director of Science and Education for the U.S. Depart-
ment of Agriculture in Washington, D.C., from December 1963 to September 1965.
From July 1973 to July 1981, he was director general of the International Rice Re-
search Institute in the Philippines. From 1981 to 1989, he served as senior assistant
administrator for Science and Technology of the United States Agency for Interna-
tional Development in Washington, D.C. From 1990 to 1994 he was a full-time senior
consultant for collaborative research and development programs of the World Bank
in Washington, D.C., and the United Nations Development Program in New York.
Dr. Brady passed away in 2015 at the age of 95 .

•
XXIV
Another random document with
no related content on Scribd:
 In November of 1918 an editorial note in the China Medical
Journal reads as follows:
“From nearly all parts of China reports are being sent to the
newspapers of the occurrence of a severe epidemic of disease which
seems to manifest itself in various forms. In Wusuch, where the
disease is called ‘the five days’ plague’ the symptoms are said to be
not unlike those of cholera, death in some cases ensuing in less than
a day. In other cases it is complicated by severe and often fatal
pneumonia. At Anking many cases have all the symptoms of typhoid
fever, but the mortality is great and sudden. In one house four people
died within a few hours of each other, and in another house eight
persons out of eleven died. At Wuhu and other of the lower Yangtze
ports it is said to resemble dengue fever and the mortality is so great
that undertakers are finding it difficult to meet the demand for
coffins. In Shansi, where the victims literally number thousands, the
disease is regarded as influenza. In Peking fully fifty per cent. of the
Chinese have been affected and the mortality has been heavy.
Accurate reports from medical men in these cities would be very
instructive.”
The author has the following personal communication from
Doctor Arthur Stanley of the Health Department of the Shanghai
Municipal Council. “Influenza fever appeared during the recent
epidemic in Shanghai towards the end of May 1918. It swept over the
whole country like a tidal wave. You may take it that it spread like
most rapid extant means of transit. A primary source of origin was
not made known.”
It is to be hoped that more definite and concurrent information
will be forthcoming in the case of China. A thorough search of the
literature as reviewed for China and Japan in the China Medical
Journal reveals no description of the disease previous to April or
May of 1918. Nevertheless we must assume that, until contradictory
reports are made, the disease was present in those countries in
March as stated by Carnwath.
 Autumn Spread in the United States.
By the first of July, 1918, convalescent cases of influenza began to
appear among members of the crews of transports and other vessels
arriving in Boston from European ports. The number of such cases
on each ship was usually not more than four or five, but Woodward
records that in one or two instances between twenty and twenty-five
individuals were sick on incoming vessels. None of these were
seriously ill, none were sent to the hospital, and none died. The
disease in this class of persons did not become severe until late
August. Woodward has found on inquiry among practising
physicians that typical cases of influenza were seen with notable
frequency in private practice in the vicinity of Boston during the
month of August, and that they had developed no serious
complications, the only after effect being the marked prostration.
These mild preliminary cases failed to attract attention; first,
because of their relative scarcity, and second because of their benign
character. Public attention was first directed to the influenza in
Boston by the apparently sudden appearance during the week ending
August 28th of about fifty cases at the Naval Station at
Commonwealth Pier. Within the next two weeks over 2,000 cases
had occurred in the Naval forces of the First Naval District. One week
later there was a similar sudden outbreak in the Aviation School and
among the Naval Radio men at the Massachusetts Institute of
Technology. The first death in Boston was reported on September
8th.
The peak of daily incidence in Boston occurred around the first of
October. In the week ending October 5th a total of 1,214 deaths from
influenza and pneumonia was reported, while by the third week of
October this total had fallen to less than 600, and for the week
ending November 9th was down to 47. Around November 15th the
number of cases rather suddenly increased and this recurrent wave
lasted for about ten days. By the 25th the rate was back to what it had
been around the first of the same month. On or about December 1st
the incidence again rose and continued increasing daily, to reach its
peak in a severe recrudescence around December 31st.
There are conflicting reports concerning the date of first
appearance of the epidemic at Camp Devens, Massachusetts.
Woodward says that a sudden and very significant increase was
reported during the third week in August in the number of cases of
pneumonia occurring in the army cantonment at Camp Devens,
seeming to justify the statement that an influenza epidemic may have
started among the soldiers there even before it appeared in the naval
forces. Soper, on the other hand, as well as Howard and Love in their
official report, place the date of the first case at Devens as September
7th. Soper remarks: “The Devens epidemic is supposed to have
commenced on September 7, 1918, in D Company, 42d Infantry. On
that date a case of supposed meningitis was sent to the hospital from
this company; on the following day twelve cases were sent for
observation. These proved to be influenza. By the 16th thirty-seven
cases had gone from the same company.” Howard and Love state,
“The first authentic cases of virulent influenza of the great autumn
pandemic among troops in the United States appeared on September
7, 1918, at Camp Devens, Mass.” These statements by Howard and
Love do not eliminate the possibility of earlier and less virulent
unrecognized cases. Wooley, who was camp epidemiologist, reports
that influenza began at Camp Devens on the 8th of September, 1918.
It reached its acme on the 16th, 17th and 18th of the month and then
rapidly declined, almost completely vanishing about the middle of
November. He makes no observation as to whether a mild form of
the disease was or was not present in the camp in March and April
preceding.
Influenza entered Massachusetts at Boston. Reeks reports that it
entered Connecticut at New London, the cases coming primarily
from the experimental station and from Fort Trumbull, where
vessels from foreign ports had discharged patients. He believes that
the disease was first introduced by ships arriving in New London
from abroad and by men from the Boston Navy Yard, but numerous
foci developed in a short period of time in various parts of the state.
Many of these had appeared by the middle of September, and the
source, according to Winslow and Rogers, was traced to military
establishments, chiefly Camp Devens. In Wallingford, Willimantic,
Hartland, Rockville and Danbury, all of which towns were attacked
early in the epidemic, investigation showed that the disease
developed in each case two or three days after visits of soldiers from
Camp Devens. In Connecticut the epidemic spread, beginning at New
London, chiefly from east to west, reaching its peak in the Eastern
section around October 4th, in the central section October 15th, and
in the Western part of the state around October 24th. Towns which
had been infected early by visitors from military establishments
reached the climax sooner than other towns nearby. In spreading
from New London north and west the large cities of Connecticut
were successively invaded, New Haven and Hartford reaching their
crest about ten days later than New London, while Fairfield County
did not reach its acme until later than New Haven.
In the cities along the New England coast we see then that the
disease reached epidemic proportions early in September. By
September 21st it had become epidemic in a wide area along the
Atlantic coast extending from the Southern part of Maine to Virginia,
as well as in a number of localities scattered over the entire country.
By September 28th, areas adjacent to the centers in which the
epidemic had already appeared were affected, suggesting radial
movement from these centers. By that time the greater part of the
New England States, the North Atlantic and Central States, and some
of the Gulf and Pacific Coast States had become involved. By October
5th the pandemic had apparently reached all parts of the country
with the exception of the more isolated rural districts and some areas
in the Central States and Mountain States. Within an additional ten
days even these areas, with the exception of the very remote rural
districts, had been reached by the epidemic. Within four weeks the
disease had become distributed to all sections of the country, and
within six weeks from its first epidemic prevalence in Boston
practically the entire country had been invaded.
Sydenstricker in a preliminary report remarks on the fact that the
disease reached an epidemic stage in a number of localities in the
central, northern, southern and western sections at about the same
time as it did in the area along the northeastern coast. “The
possibility is suggested, therefore, that sources of infection existed in
at least some of the larger population centers, well distributed
through the country, some time before the disease appeared as a
nation-wide epidemic. The apparent radial spread of the epidemic
from certain centers would seem to strengthen this hypothesis. It
may also be noted that there is evidence, the collection of which has
not yet been completed, pointing to the existence of cases of the
disease in various centers, probably widely distributed, weeks before
they were definitely recognized as influenza. The possibility that
these foci themselves had a common focus is by no means excluded,
of course, but there is as yet no conclusive evidence that would
warrant the statement that the starting point of the epidemic was
Boston or any specific locality.”
Dublin, from a study of the statistics of the Metropolitan Life
Insurance Company, finds that the virulence of the influenza, as
indicated by the mortality rate, was greatest along the Atlantic Coast
and became progressively less as it progressed westward. There was
one exception. The mortality was high in San Francisco, higher than
in other western communities. Dublin believes that quite possibly
there was a double infection in San Francisco in the fall of 1918, one
coming from the East and of small caliber, while the other came
either by way of the Panama Canal or perhaps from Asia. The
evidence in favor of two ways is that Dublin finds that the peak of
incidence in San Francisco and in some other places on the Pacific
Coast occurred sometime in advance of the similar peak at points
inland from the coast. This is not brought out in Pearl’s chart, and
the latter finds when considering the peak of deaths that the peak for
San Francisco was late. The peak in that city, in Oakland, California,
and in Los Angeles, was reached on the week ending November 2d.
Few cities had as late death peaks. Cleveland and Pittsburgh reached
their peak in the same week, St. Paul, Minnesota in the week ending
November 16th, and St. Louis, Milwaukee and Grand Rapids not
until the week ending December 14th. In the case of Milwaukee and
St. Louis these were the high peak dates but they were second peaks.
In the former the first peak occurred October 26th and in the latter
November 2d. In Grand Rapids the increase in mortality was clearcut
by the middle of October, although the peak was not reached until
the week ending December 14th. These statistics would indicate that
San Francisco was attacked, as evidenced by increase in death
reports, relatively late, and at about the time that would be necessary
for the disease to be carried across the continent.
 In an article by Ely, Lloyd, Hitchcock and Nickson it is said that
influenza first appeared in the Puget Sound Navy Yard, near Seattle,
on September 17, 1918, and that it was introduced by a draft of 987
sailors received from Philadelphia, a number of whom arrived ill, or
came down within a few hours after reaching their destination. As a
result, Seattle and the State of Washington were infected somewhat
ahead of the other West Coast States. According to the record,
influenza did not assume epidemic proportions in the State of
Oregon for nearly a month after this Navy Yard epidemic.
With army camps and cantonments situated in nearly every
section of the country it is difficult to follow the general direction of
spread from camp to camp. During the period of the epidemic, troop
movements were in general from West to East toward points of
embarkation rather than in the reverse direction. This was in the
opposite direction to that taken by the pandemic. Away from the
coast there were, however, many movements of troops from camp to
camp, in the redistribution of forces. That these troop movements
were not discontinued during the epidemic is indicated by the report
of Howard and Love: “The virulent type of influenza had spread
rapidly from camp to camp, from the Atlantic seaboard to the South
and West, due to the continual interchange of personnel from
infected to non-infected camps. Such movements of troops at this
time were recognized as dangerous and inadvisable, and prompt
recommendations were made by the Medical Department that such
movements be discontinued or greatly restricted, if compatible with
military interests, which, of course, were at the time paramount. The
War Department was unable to approve any marked restriction of
movement of men from camp to camp at this time. One result of the
free inter-communication of military personnel was that practically
all military stations in the United States were in the throes of the
epidemic at the same time.”
In addition to this means of inter-communication we had the
possibility of spread to the various camps by the ordinary course of
civilian and commercial travel as in spread to different communities,
and also the possibility of importing large amounts of virus at one
time on the incoming trains with new draft troops.
Soper gives the following order for camps attacked:
Order. Camp. Location. Date.
1 Devens Massachusetts Sept. 12
2 Upton New York Sept. 13
3 Lee Virginia Sept. 17
4 Dix New Jersey Sept. 18
4 Jackson South Carolina Sept. 18

5 Hoboken New Jersey Sept. 19

5 Syracuse New York Sept. 19
5 Gordon Georgia Sept. 19
5 Humphreys Virginia Sept. 19
6 Logan Texas Sept. 20

6 Funston Kansas Sept. 20

6 Meade Maryland Sept. 20
7 Grant Illinois Sept. 22
7 Taylor Kentucky Sept. 22
8 Sevier South Carolina Sept. 23

8 Lewis Washington Sept. 23

8 Newport News Virginia Sept. 23
9 Pike Arkansas Sept. 24
10 Beauregard Louisiana Sept. 25
10 Eustis Virginia Sept. 25

11 Greene North Carolina Sept. 26

11 McClellan Alabama Sept. 26
12 Kearney California Sept. 27
12 Bowie Texas Sept. 27
13 Johnston Florida Sept. 28

13 Sheridan Alabama Sept. 28

14 Sherman Ohio Sept. 29
14 Dodge Iowa Sept. 29
14 Shelby Mississippi Sept. 29
15 Custer Michigan Sept. 30

16 Travis Texas Oct. 1

17 Cody New Mexico Oct. 3
18 Forrest Georgia Oct. 6
19 MacArthur Texas Oct. 7
 20 Wadsworth South Carolina Oct. 11

20 Wheeler Georgia Oct. 11

20 Greenleaf Georgia Oct. 11
Howard and Love have established definitely that the extension of
the virulent influenza from Camp Devens to other camps south and
west in September, 1918, can be traced in many instances directly to
the interchange of military personnel from infected to non-infected
camps. The height of the September outbreak in the United States
Army extended over a period of about nine weeks, from Sept. 13th to
November 15th, and during this period over 20,000 deaths occurred
among troops in the United States alone in excess of the number that
would have occurred, if the disease death rate for the corresponding
period of the preceding year had prevailed.
It is interesting to note with respect to Camp Humphreys, Virginia,
that there were possibly some sporadic cases previous to the autumn
outbreak. Brewer in reporting on the epidemic in September and
October records the first case as having occurred shortly after July
1st. He makes no mention of there having been any outbreak
whatever prior to that date. Between July 1st and September 12th
there were only sporadic cases diagnosed as influenza. The autumn
outbreak began at Camp Humphreys September 13th and ended
October 18th.
 Recrudescences.
We have already seen from the work of Pearl that recrudescences
following the original spread in any one locality were the rule rather
than the exception in this country. He found that in sixty-five per
cent. of the forty cities studied there were two distinct peaks in the
mortality curve and in twenty per cent. there were three, while only
fifteen per cent. had but one peak. The first peak was as a rule the
highest. Although there was no absolute regularity in the time of
occurrence of the recrudescences, Pearl established that the high
peak cities had the second peaks on an average 7.1 weeks after the
first, and the third peak on an average 13.1 weeks after the second.
The two-peak cities are divided into two classes, the first comprising
about a third of the total number, had the second mortality peak
around eight weeks after the first, while the remaining two-thirds
had the second peak about thirteen weeks after the first. The cycle in
the epidemic wave appears to be nearly a multiple of seven weeks.
He suggests that the smaller group of two-peak cities with early
second peak may have been cities which at the time were presumably
destined to show a third distinct wave and peak of mortality, but in
which for some reason not now apparent the third wave did not
eventuate. In contradistinction the larger group of two-peak cities
with the second peak occurring around thirteen weeks after the first
are presumably cities in which the complex of factors determining
the form of the mortality curve was such as to lead definitely to a two
and only two-peak curve. In three-peak cities the first interval was
around seven weeks, the second around thirteen weeks. The two-
peak cities with an interval around thirteen were probably not
destined, according to Pearl, to have another repetition, but those
with an interval of seven were presumably destined to have a second
interval, the thirteen-week interval, which for some reason did not
occur.
This raises the question of periodicity, a subject which we will
discuss at a more appropriate place.
 This experience of recrudescences was similar in the American
Expeditionary Forces. The first outbreak lasted through April and
May and into June. The second came in September and October. The
spring epidemic had been characterized by mildness and was known
as three-day fever, but in the autumn, complications of the
respiratory tract predominated in the symptom complex. By August
18th a severe epidemic had occurred in an artillery camp at La
Valdahon in the Jura Mountains, near Bezançon. Early in September
a larger epidemic occurred in an artillery camp near Bordeaux. The
epidemic in our troops in France, as well as in the French civil and
military population, reached its height during October. The Service
of Supply was more heavily affected than were the troops situated on
the battle front. The morbidity rate appeared to have been almost the
same as that in the United States. That it was not quite as high has
been shown by Howard and Love. Longcope states that it prevailed
particularly among the troops at the base ports where during a part
of the epidemic transports laden with infected troops were being
landed; in those organizations which contained the largest number of
replacement troops; and in organizations being moved on troop
trains, where the men were necessarily closely crowded.
The second outbreak subsided during the early part of November.
A third occurred in January and February, very much as it had done
in the United States. In the interval between the second and third
recurrences there was no time at which the entire Expeditionary
Forces were free from the disease. The author had occasion to study
an outbreak occurring early in December in the 26th Division
stationed in rest area at Montigny-le-Roi. In this outbreak the
respiratory complications predominated, as in October, and the
mortality was comparatively high. We had had occasion to study the
same disease at Camp Sevier, South Carolina in September and early
October, 1918, and in two different localities in France in December,
1918, and February, 1919, and found that the clinical characteristics
were identical on both continents.
The more severe recurrence in England, in October, has been
carefully studied. In fact this recurrence was almost universal in all
countries. The autumn epidemic has been reported as being at its
height in October, 1918, in such widely separated localities as the
United States, England, France, Greece, Brazil, India, Japan and
Korea.
In Europe at any rate the third wave occurring in the winter of
1919 was quite generally distributed. At about the same time the
disease broke out in England, making a third wave in less than a
year. Once again the third attack began less suddenly and less
violently and resulted in a lower number of fatalities. During
February there was reported to have been a great increase in the
number of cases in Paris. It had terminated by March 27, 1919. In
March the disease broke out anew, this time assuming grave
proportions, not only in that city but in several of the Departments.
The second recrudescence has also been reported as being present
in Spain.
On May 5, 1919, report was received from Buenos Ayres that in one
of the concentration zones for naval troops located in the harbor
there had been an epidemic of short duration, but with high
morbidity, with two hundred cases being frequently reported each
day.
Just as Pearl has observed a certain periodic recrudescence in the
United States, there has been described a similar periodicity in
England. The interval, however, is described as twelve weeks. The
first wave began in July and died down about the end of August,
running a two months course. Twelve weeks after the
commencement of the first wave, at the beginning of October, the
second appeared. It had disappeared around the middle of
December. Again, twelve weeks from the beginning of the second
wave, that is, in January, the third appeared.
 Recurrences in Winter of 1919–1920.
We distinguish between the flareups following the autumn spread
of 1918, and which lasted until the spring of 1919, and yet another
widely distributed recurrence in the winter of 1920. We have called
the former recrudescences to distinguish them in point of time from
the latter, but do not imply thereby any difference in the character or
origin of the secondary waves. Between them all there occurred
almost continuously isolated or solitary cases of influenza which
served to keep the fires smouldering. In our own work in the city of
Boston we found record of scattered infrequent cases of clinical
influenza of apparently low infectivity in every month from March,
1919, until the recurrence in January, 1920.
Moreover, in some localities there were during this interval small
epidemic outbreaks. Thus a report from Lisbon, Portugal, on June 1,
1919, states that the deaths from influenza in that city during the
preceding two weeks had been more than the total deaths from all
causes during the preceding four months. A report from London,
October 30, 1919, states that during the preceding few weeks there
had been in the ninety-six great towns of England and Wales a slight
but gradual increase in the number of deaths attributed to the
disease, and a coincident rise in the number of notifications of acute
primary and acute influenzal pneumonia. The feeling at that time
was that the increase was associated with prevailing meteorological
conditions, and did not apparently signify more than the usual
variation in respiratory diseases which was to be expected at that
season of the year. On November 3, 1919, the disease was reported
prevailing at Chile and it was spreading throughout Bolivia. At the
same time influenza had spread over the entire country surrounding
Buenos Ayres and had even reached the neighboring city of
Montevideo. In the latter part of November more than 2,000 cases
had been reported at Lemaies, about fifteen miles northeast of
Granada, Spain.
The winter of 1920.—In the United States the death rates from
influenza and pneumonia in the large cities over the entire country
were below the usual average from May, 1919, until January 1, 1920.
In the week ending January 17th there was a sharp increase in the
influenza-pneumonia rate, which occurred simultaneously in Kansas
City and Chicago. In the latter city an excess over the average was not
reached until some days later, but the maximum mortality occurred
in the week ending January 31st, while in Kansas City the mortality
did not reach its height until one week later. New York, Washington,
San Francisco, Milwaukee and St. Paul soon followed with an
increase in the week ending January 24th, and in the subsequent two
weeks many other cities were added to the list. By February 14th
thirty-two out of the thirty-six large cities reporting had an increase
in the death rate from influenza and pneumonia as compared with
the same period in 1917. The maximum was reached at this time, and
according to the Bureau of the Census reports there were 7,059
deaths from influenza and pneumonia during the week ending
February 14th. In the next week the number of deaths from these
causes in the cities reporting had dropped to 5,088. The February
weekly average for 1917 was 1,489. In the week ending February 14th,
267,643 cases of influenza were reported from forty-one states; the
excess annual death rate as compared with the average for the period
from 1910 to 1916 was 1,319.
In general the 1920 recurrence was decidedly milder than the
autumn outbreak of 1918. Certain cities, however, suffered severely,
particularly Detroit, Milwaukee, Kansas City, Minneapolis and St.
Louis. In these the death rate, while the epidemic lasted, was higher
than that of 1918. The duration of the epidemic was generally,
however, shorter in these cities. Columbus, Ohio, and Indianapolis
suffered severely, but to a less extent than the cities just mentioned.
In Chicago the death rate was not as high as in the fall of 1918, but it
did rise far above the point reached during the 1889–90 outbreak,
and the influenza in the last two weeks of January brought the total
mortality for that month up to 5,149, the highest mortality in the
history of the city with the exception of October, 1918.
We have already discussed the recurrent epidemic as it was
studied in Detroit. The salient characteristics were a rapid and fairly
symmetrical evolution, a shorter duration than in 1918, a lower
morbidity with a higher mortality rate, and finally, a smaller total
number of deaths than in 1918.
 The 1920 recurrence was widespread. It was not confined entirely
to the large cities. Semi-official reports from small towns and villages
show very much the same conditions as were observed in the larger
cities. On the whole, however, most communities, both large and
small, suffered less severely than in the first spread. The few
exceptions to this were distributed over the continent without
uniformity.
The first among the large cities to show an increase in death rate
from the epidemic was Kansas City, in which the mortality first
climbed in the week ending January 17th. The following week there
was an increased rate in Chicago, New York and Milwaukee, and one
week later, Boston, Detroit, San Francisco and Philadelphia were
affected. New Orleans was one of the last large cities affected, not
showing a definite increase until the week ending February 14th. In
contrast to the 1918 pandemic, the influenza of 1920 showed no
clearcut direction of spread, and was as in the years following 1889
due, without doubt, to firing up of the pandemic virus as it had been
left scattered in many endemic foci throughout the earth. There
probably were instances of spread from the larger centers to outlying
districts, but there was no continuous spread over large areas. The
accompanying table shows clearly that the disease this year
commenced in the center of the continent, a fact which would seem
to disconnect it entirely from the late epidemics of 1919, occurring in
Europe:
Annual death rates from all causes by week in certain large cities of
the United States from week ending January 3d to week ending
February 21st.
Week Ending
City. January. February.
3 10 17 24 31 7 14 21
Kansas City 16.3 15.8 19.3 32.7 39.5 61.5 44.0 29.1
Chicago 14.4 13.8 15.1 23.5 41.3 39.1 24.6 17.7
New York 14.0 15.3 14.6 19.5 28.0 35.0 35.1 24.8
Milwaukee 11.6 12.5 9.0 15.6 29.4 34.5 27.1 16.9
Detroit 13.7 13.0 14.2 15.5 33.9 60.9 42.9 21.6
Boston 16.8 16.9 14.1 16.8 20.3 27.1 33.7 32.1
San Francisco 16.5 15.4 19.6 19.2 22.9 25.2 31.8 28.8
Philadelphia 15.6 16.7 16.2 16.8 18.3 22.1 34.3 37.2
New Orleans 18.8 19.6 22.6 18.8 20.9 20.1 25.0 32.3
 The relative severity of the two epidemics in certain of the large
cities has been compared by H. F. Vaughan, and he has found as is
seen by the table that Kansas City and Detroit, two of the early cities
affected, had the highest mortality in 1920. Philadelphia in 1918 lost
nearly three times as many people as Detroit did in 1920. Detroit was
higher than Chicago in 1920, but lower in 1918.
Per cent. of population killed by influenza.
1920. 1918–1919.
First seven First seven Twenty-one
weeks. weeks. weeks.
Detroit 0.20 0.17 0.28
Chicago 0.12 0.34 0.41
Kansas City 0.24 0.30 0.63
Philadelphia 0.10 0.76 0.82
New Orleans 0.05 0.55 0.77
The following table taken from the “Final Influenza Bulletin,” by E.
R. Kelley, Commissioner of Health in Massachusetts, shows
distinctly the difference that must be always borne in mind between
curves of influenza incidence and death curves. In his table the
mortality climbed first on the week ending January 13th, as in the
table above, but the increase in influenza cases began at least one
week earlier. It is characteristic of influenza epidemics that the rise
of mortality curves follows that of morbidity by about a week:
 Influenza and pneumonia cases in Massachusetts in the first three
months of 1920.
Lobar
Influenza.
pneumonia.
Cases. Deaths. Cases. Deaths.
Week ending January 3d 41 0 109 9
Week ending January 10th 46 2 142 50
Week ending January 17th 58 0 145 52
Week ending January 24th 489 4 201 56
Week ending January 31st 4,495 48 313 96
Week ending February 7th 9,627 272 382 212
Week ending February 14th 10,747 133 583 140
Week ending February 21st 5,601 181 510 147
Week ending February 28th 2,375 147 313 114
Week ending March 6th 1,144 54 206 34
Week ending March 13th 490 31 130 54
Week ending March 20th 254 20 105 44
Week ending March 27th 147 14 102 94
Week ending April 3d 218 6 97 12
In Massachusetts in the first three months of 1920 there were
reported 35,633 cases of influenza and 3,158 of lobar pneumonia,
with 906 deaths from the former disease and 1102 from the latter.
The case rate per 100,000 from influenza was 883.4; from lobar
pneumonia, 78.3; the death rate from influenza, 22.4; from lobar
pneumonia, 27.4; and the fatality per cent. from the former disease
was 2.5, and from the latter, 34.9.
The epidemics in Detroit and Boston both showed a symmetrical
evolution and a single wave. This appears to have been the more
frequent type of recurrence in this country. There are examples of
the secondary curve. At the Great Lakes Naval Training Station the
epidemic began during the week ending January 17th. On January
12th there were fifty-one cases. The peak was reached on the third
day with the admission of 182 new cases during twenty-four hours.
Although the peak came early the decline was less rapid and there
were four secondary peaks, but the outbreak terminated on the
twenty-fourth day. On the whole the epidemic was less severe than in
1918. Pneumonia was a complication in about ten per cent. of the
reported cases of influenza at the training station.
 On the European continent there were similar recurrences in the
first three months of 1920. In the large towns of England the
recorded deaths from influenza made an increase in a steady curve
from sixty-six in the last week of January until the week ending
March 27th. After that date there was a gradual falling off. That the
situation was in no way as serious as it was at the same time in the
American cities and in certain other parts of Europe is indicated by
an annotation in the Lancet of March 6th. According to this
annotation, the weekly totals of deaths attributed to influenza in
London and the 96 great towns had on the whole tended to increase
in the early part of 1920, but the absolute increment was so small
and the necessary uncertainty of classification so great that no
unfavorable inferences could be drawn from these fluctuations alone.
On the other hand, the notifications of cases of pneumonia increased
appreciably, too much to be set down as a mere chance fluctuation.
But notification for this disease had not been in force long enough to
enable accurate comparison. There were no indications of epidemic
influenza in any of the large factories situated throughout the
country. But on the other hand there was proof of the existence of
epidemic influenza of an infectious, but relatively non-fatal type in
certain large schools situated in the South and Southwest of England.
The annotation concludes that influenza was epidemic in a few
localized English and Welsh communities, and that the type was
similar to, but less severe than that of 1918–19.
In the city of Paris between the 11th and 31st of January there was
a very definite increase in the death rate from inflammation of the
respiratory tract above the average for other years.
Renon and Mignot studied 141 cases of influenza (71 men and 70
women) during January and February, 1920, at L’Hopital Necker.
Fifteen of the 141 died. According to these observers the grip of 1920
attacked all ages in contradistinction to the 1918 epidemic which
affected especially the young and vigorous. One-third of their group
were over forty years of age, while some were seventy and eighty
years old. In spite of this the disease remained relatively mild. Sixty-
four were cases of simple grip. Forty-three had associated bronchitis
and pulmonary congestion and edema. Twenty-seven had
pneumonia. One had acute pulmonary edema. There were cases of
influenza in tuberculosis individuals. One developed an acute
serofibrinous pleurisy. One had purulent pleurisy, and one
meningitis.
In Copenhagen there occurred between the 18th and 24th of
January, 1920, 1,204 cases of influenza with four deaths; in the
following week, from the 25th to the 31st of January, 7,445 cases
with forty-two deaths; from the 1st to the 7th of February, 11,038
cases with 207 deaths; from the 8th to the 14th of February, 8,308
cases and 327 deaths. This is to be contrasted with the month of
December, 1919, in which there were 1,845 cases of influenza in
Denmark, of which only 272 were at Copenhagen. In Christiania,
Norway, during the week of January 25th to 31st, there occurred
eleven deaths from influenza, whereas during the preceding two
weeks there had not been a single death from this disease.
In December, 1919, there were reported in Switzerland only 511
cases of influenza. During the month of January, 1920, this increased
to 13,162, and in February to 83,008, the estimated population being
4,000,000. From February the disease decreased in prevalence. In
Zurich, with a population of 210,000, the epidemic resulted in
14,534 cases. The first increase began around January 4th. The total
number of cases for January was 1,071. In February the records of
the four weeks showed 2,721, 4,140, 3,341 and 1,899 cases,
respectively; in March the decrease was rapid, 886, 442 and 45 cases
being reported in the first three weeks. The total number of deaths,
mostly due to pneumonia, was 229, a mortality of 1.5 per cent.
During 1920 epidemics were also observed in Valencia, Santander
and other towns in Spain, and in Mexico City. In the latter city the
number of deaths was reported as 1,649, as contrasted with 3,000 in
1918.
 Incubation Period.
An accurate determination of the period of incubation in influenza
presents great difficulties. The large number of cases with the
consequent multiple opportunities for infection in the case of every
individual add to the difficulty. Under any circumstances the period
is very short. Parkes, many years before the 1889 epidemic, believed
that an incubative period sometimes exists; that it was sometimes
very short and sometimes of many days duration.
“In the Transactions of the College of Physicians it is stated that in
the epidemic of 1782, seventeen persons came to London to an hotel,
and on the following day three were attacked with influenza.
Haygarth says that a gentleman came to Chester from London, on
the 24th of May, 1782, ill of influenza; a lady, into whose family he
came, was seized on the 26th, and was the first case in the town.
Haygarth states, evidently with the view to point out the possibility
of a direct contagion, that the gentleman was engaged to be, and was
afterwards, married to this lady. In this case the longest possible
incubative period was two days. In 1782 a family landed at Harwich,
from Portugal, and came to London directly; the day after their
arrival the lady, two servants and two children were all seized. Two
men-of-war arrived at Gravesend from the West Indies; three
Custom-house officers went on board; a few hours afterwards the
crews of both vessels were attacked. Some other cases are on record
where the incubative period, if it existed, could not have been more
than a single day. On the other hand, some cases are on record in
which the incubative period must have been two or three weeks.”
Leichtenstern believed that the usual incubation period is from
one to three days although some cases have been reported in which it
is without doubt no longer than twelve hours. Parsons in reporting
for England also gives the incubation period as from one to three
days as a rule.
It is reported in France in 1918 that in one institution thirty-one
cases out of thirty-three individuals occurred within three days, all of
them infected by one nurse.
 MacDonald and Lyth report in the British Medical Journal for
November, 1918, an interesting observation concerning the
incubation period in influenza. These two individuals were traveling
from London to York in the same compartment with an individual
who was just convalescing from influenza. Exactly forty-one hours
after being on the train with this individual, they both came down
with the disease. One suffered lightly while the other was severely ill.
The wife and two children of the latter contracted the disease in turn,
and with them also the first symptoms appeared suddenly after a
delay of about forty-eight hours.
Stanley, in studying the epidemics of influenza in San Quentin
Prison, found that as a rule there was an increase in incidence
following the Sunday picture shows. This usually occurred on
Tuesdays and Wednesdays, giving an apparent incubation period of
from thirty-six to sixty hours. He tabulated the records of twenty-
nine individuals who had presumably become exposed at the show
and found that the incubation period averaged about forty-eight
hours.
The majority of observers give the incubation period as from
twenty-four hours to four or five days, most often two or three days.