Document 4jYqzVbGgbo1k7bY28B7R8wa

DUP 0813681 DU 009659 MM DU 009660 DUP 0813682 INDUSTRIAL HYGIENE AND TOXICOLOGY Jn Two Volumes VOLUME I DU 009661 DUP 0813683 INDUSTRIAL HYGIENE AND TOXICOLOGY FRANK A. PATTY, Editor Contributors: J. BROZEK F. F. HEYROTH F. A. PATTV L. F. CURTISS F. R. HOLDEN L. SCHWARTZ E. E. DART G. W. JONES H. SPECHT W. B. DEICHMANN R. A. KEHOE J. H. STERNER D. O. HAMBLIN J. B. LITTLEFIELD J. F. TREON I. HARTMANN C. P. MC CORD W. N. WITHERIDGE VOLUME I I DUP 0813684 INTERSCIENCE PUBLISHERS, INC., NEW YORK INTERSCIENCE PUBLISHERS LTD., LONDON J DU 009662 Copyright, 1948 by Interscience Publishers, Inc. All Rights Reserved This book oh any part thereof must not BE REPRODUCED WITHOUT PERMISSION OF THE PUBLISHER IN WRITING. THIS APPLIES SPECIFICALLY TO PHOTOSTATIC AND MICRO FILM REPRODUCTIONS. INTERSCIENCE PUBLISHERS, INC. 215 Fourth Avenue, New York 3, N. Y. For Great Britain and Northern Ireland: INTERSCIENCE PUBLISHERS LTD. 2a Southampton Road, London f*zmtbd of nx Dim*) mm or ucmai it KCStsm. AMS COMTAXT, QIC., UNCiSm, FA. ! 4t I * 1 f DUP 0813685 DU 009663 fcsaaa Jaitiatf<;. liaJiflaMi j,i-3a..aHjfc^ CONTENTS Volume I Preface........................... ...... ............................. ................................. ....................................... ......... v List of Contributors.............................................,. r^r...........i.............. .&............................... xi Table of Atomic Weights................................ ......... .. i............................................................, xiii Conversion Table for Gases and Vapors.................. .... -.............................................................. xiv Table of Useful Equivalents and Conversion Factors................................ .................................... xvi I. Industrial Hygiem Retrospect and Prospect. By FRANK A. PATTY............ - 3 I Historical Rfeum4............................ .. ............... ................... ............................... 3 A. Medical and Industrial Hygiene Literature...................................................... 3 B. Labor Legislation....................... .............................. ........................................... 5 C. Significant Events in the Progress of Industrial Hygiene in the United States 7 II. World War II and Industrial Hygiene Service.................. .................................... 10 A. Official Agencies....................... .......................... ................................................. 10 B. Insurance and Industrial Groups........................................................................ 10 C. Educational Institutions.................................................... .................................. 11 D. Research Organizations........... ............................................................................. 12 III. Industrial Hygiene in Foreign Countries.................................................................. 12 A. England................................................................................................................... 12 B. Russia........................... 13 C. Germany.................................... 14 D. Other Countries................................................................................................... 14 IV. Industrial Hygiene in the United States.................................................................. 15 V. Prospective Roles of Industrial Hygiene................ . .,.. k. ................................ 15 II. Industrial Hygiene Records and Reports. By JOHN B. LITTLEFIELD......... I. Introduction.............................................. II. Records of the Environment................. III. Records of Biological Specimens.......... .................................................................... IV. Interdependence of Medical ancLIndustrial Hygiene Records.............................. V. The Nurse's Records.................................................................................................... VI. Safety Records.............................................................................................................. VII. Personnel Records....................................... ................................................................ VIII. Compensation Claim Records.................................................. ................................. IX. Industrial Hygiene Reports.................................... ............................................... ... 19 19 19 22 23 26 26 26 27 27 III. The Industrial Hygiene Survey and Personnel. By FRANK A. PATTY......... I. Introduction.................................................................................................................. II. Types of Surveys......................................................................................................... A. The Inspection Survey......................................................... ............................... B. The Preliminary Industrial Hygiene Survey.................................................... C. The Investigational Industrial Hygiene Survey............................................... 1. Surveying the Plant..................... ................................................................. 2. Developing Control of Harmful Situations.................. ............................. 3. Records and Reports....................................................... *.......................... D. The Combined Industrial Hygiene and Medieal Survey................................ 29 2 3 3 31 32 32 36 38 39 DUP 0813686 DU 009664 xviii CONTENTS III. The Industrial Hygiene Unit,: ............ IV. Qualifications and Training of Personnel A. Administrative Industrial Hygienist. B. Industrial Hygienist........TT............ . C. Other Personnel ................................ IV. Personal Factors in Competence and Fatigue. Bv JOSEF BROZEK.............. 45 I. General Principles................. _.................................................................................. 45 II. Problems of Selection............................................................................................ . 48 A. Physical Factors................ ........... -,..... .-................................ . -- 49 B. Psychological Factors............................................................................................ 52 1. Interview........................................................................................-- 54 2. Tests................... .. -.................................................................................---? 55 C. Limitations--Physical Handicaps................ ....................................... 62 D. Limitations--Old Age.................................................................................. -- - 65 III. Problems of Fatigue..................................... ...................................................... 69 A. Approach to the Study of Fatigue..................................................................... 69 1. Subjective Reports___U.................................................................. -- 69 2. Measured Functional Changes....................................................... .-- 70 3. Industrial Output Records............................................................ 71 B. Types of Fatigue..................................................*......... ,............................ ,-- 72 1. Exhaustion-Fatigue,. ...................................................................... . -- - 72 2. Tiredness-Fatigue____ T............................ ................................................ .. 73 3. Boredom-Fatigue........................................ *.............................. ...... ,, ., 74 C. Reduction of Fatigue......................................-............................... ,, . 74 1. Occupational Fitness............................................................. ............... ........ 75 2. Motion Economy..................................... ........................................... - 76 3. Time Relationships............................................................ .................... -- 77 4. Between-Meal Feeding................................ ........................................... .. 8Q 5. Music in Industry............................................................................... .. 83 IV. Problems of Maintenance........ ............................... .....................................,,... 88 A. Nutrition........................ --............................... .......................................... .. 88 1. Caloric Requirements............................ ............................. ........................ 88 2. Special Dietary Requirements......................................................... ........ 88 3. In-Plant Feeding......................................... -............................................... 91 B. Personal Adjustment.................................................................. 91 C. Morale.................. 95 V. Comment............................... .......... .................................................................... .. 103 V. Environmental Factors in Fatigue and Competence. By W. N. WITHERIDGE 105 I. Air Conditioning...................,,....................................................................... ........... 107 A. Comfort and Efficiency. ,'.T............... 107 B. Physiological Response............................................ 107 C. Effective Temperature Index.............................................................................. 108 D. Temperature Differentials in Hot Weather........................................... 112 E. Excessive Heat in Industry................................................................................. 112 ` F. Loss of Salt from the Body................... 113 G. AirvConditioned Crane Cabs.......................................................................... 114 H. Low Temperature............................................... 114 I. High and Low Humidity............................................................... 115 J. Air Movement and Drafts.......................................................................... 115 K. Acclimatization in Air Conditioning............................................................ 116 DUP 0813687 DU 009665 CONTENTS XIX L. Psychology of Air Conditioning 77....................................................................... 117 M. Air-Conditioning Complaints. ....................................... ..................................... 117 N. Measurement of Air Conditions................................ .......................................... 118 II. Light Conditioning............. ........................................................................................ 119 A. Requirements for Comfortable and Efficient Seeing.................... ................. .. 120 B. Natural Illumination or Daylighting.................................................................. 124 C. Artificial Illumination................ _........... .................... ................................. ..... 125 D. Measurement of Illumination............................................................................. 126 III. Sound Conditioning.................................................................................................... .. 127 A. Effect of Noise on Human Beings....................................................................... 127 B. Prevention of Noise and Vibration........................... ........................................... 128 C. Measurement and Analysis of Noise................ ................................................. 129 IV. Sanitary Conditioning...................... ..............,.................. ...................................... 130 VI. Physiological Effects of Abnormal Atmospheric Pressure. By HEINZ SPECHT 135 I. Introduction--Historical Background...................................................................... 135 II. Properties of the Atmosphere.................................................................................... 137 A. Composition................................. 137 B. Physical Attributes of Atmospheric Gases, and Fundamental Physiological Aspects.................................. ..........................................--..................................... 138 1. Mass and Weight............... ........................................................................... 138 2. Density............................... -......................................................................... 138 3. Compressibility.................... 138 4. Partial Pressures.................. 142 5. Solubility or Absorption........ ..................................................................... 142 6. Temperature of the Atmosphere, Its Origin and Variation..................... 145 C. Chemical Activity _____ _____ J.7.............................................................. .... 146 1. Oxygen and Carbon Dioxide......................................................................... 147 2. "Inert" Gases........................ ,,...................................................................... 148 III. Effects of Increased Atmospheric Pressure on the Body........................................ 149 A. Charging of the Body with Gases......................... ............................................. 149 1. Mechanical Effects................. ............................... ........................................ 149 2. Solution of Gases in the Body.............................. ....................................... 151 3. Rate of Change of Pressure.......................................................................... 152 B. Effects of Maintained Positive Atmospheric Pressure..................................... 152 1. State of Saturation of the Several Body Tissues....................................... 152 2. Effects on the Circulation....... .T..................................................... ............ 153 3. Oxygen Poisoning....................................................... ................................... 154 4. Inert Gas Effects.................. ...................................... .................................. 154 5. Effects of Temperature and Humidity....................................................... 155 6. Other Effects and Subjective Responses.................................................... 155 C. Discharge of Gases from the Body Following Exposure to Increased Atmos pheric Pressure: Decompression.................................. .. ..................................... 156 1. Mechanical Effects......... ..... .....,...... ........................................................... 156 2. Bubble Formation................ . .......................... ........................................... 157 3. Rate of Decompression................................................................................. 159 IV. Effects of Reduced Atmospheric Pressure on the Body......................................... 161 A. Discharge of Gases from the Body: Decompression........................................ 161 1. Rate of Ascent.........................._.................................................................. 161 2. Evolution of Gases from Solution in Body Tissues during Ascent......... 163 3. Mechanical Effects........................................... ............................................ 164 DUP 0813688 DU 009666 XX CONTEXTS B. The Effects of Maintained Low Atmospheric Pressure................................... 165 1. Hypoxia.............................................................................................,,........... 165 2. Hypocapnia............................................................... ....................TM...... 166 3. Water Vapor of the Lungs.......................................................... ...... ........... 167 4. Critical Altitudes. ............................... -....................................................... 168 5. Decompression S ickness.................. ............................................................. 168 6. Acclimatization.... T.................................. .................... ............................... 171 C. Charging of the Body with Gas in Descent: Recompression.......................... 171 1. Re-solution of Gases. Relief of Decompression Sickness....................... 171 2. Mechanical Effects of Recompression.......................................................... 172 3. Rate of Recompression................................................................................ 172 D. Comparison of Effects of High and Low Atmospheric Pressure.................... 173 VII. The Mode of Entry and Action of Toxic Materials. By FRANK A. PATTY... 175 I. Classification of Contaminants............................. ...................................................... 175 A. Physical Classifications................................. ........................................................ 175 1. Gases and Vapors............................................................................................ 175 2. Particulate Matter--Dispersoids.................................................................. 176 3. Particulate Matter--Condensoids................................................................ 176 4. Other Physical Classifications and Definitions......................................... 176 B. Chemical Classifications........................................................................................ 176 C. Physiological Classifications................................................................................. 176 1. Irritants............................................................................................................ 177 2. Asphyxiants............................................ .............................................. ......... 177 3. Anesthetics and Narcotics............................................................................. 177 4. Systemic Poisons.. ,,................................ .................................................. 178 5. Particulate Matter Other Than Systemic Poisons.................................... 178 II. Respiration........................ ............................................................................................ 178 A. Mechanics of Respiration..................................................................................... 178 B. Lung Structure, Vital Capacity, and the Dead Space.................................... 179 C. Regulation and Control of Respiration.............................................................. 180 D. Funct:on of Hemoglobin....................................................................................... 180 E. Circulation as a Factor, and Its Regulation...................................................... 181 III. Absorption, Distribution, and Elimination............................................................... 182 A. Modes of Expressing Concentrations.................................................................. 182 B. Volume-Pressure-Temperature Relations......................................... ............. 183 1. Partial Pressures.................................................................................. ...... 183 C. Role of Solubility in Absorption of Gases and Vapors.................................... 184 1. Solubility Coefficient.................................. ................................................... 184 2. Body Saturation................................................................................. ;........ 185 3. Effect of Intermittent Exposures................................................................ 189 4. Relative Concentrations of Vapor in Blood, Tissues, and Expired Air.. 189 D. Dusts and Fumes.......... ....................................................................................... 190 1. The Absorption of Particulate Matter........................................................ 190 2. Action of Suspended Particulate Matter.................................................... 191 E. Mists....................................................................................................................... 191 F. Other Means of Absorption............................. ....................................................192 1. Ingestion................ . ................................ .... ................................................. 192 2. Absorption through the Skin........................................................................ 192 IV. Standards of Physiological Response................ .. ......................................... ......... 193 V. Standards for Permissible Atmospheric Contamination and How They Are Set. 194 009667 DUP 0813689 . afeaAJBi iifcB, CONTENTS XXI VIII. Sampling and Analysis of Atmospheric Contaminants. By FRANK A. PATTY 199 Gases and Vapors...............................................................................................................-.200 I. Methods Giving Quantitative Results in the Field................................................. 200 A. Evaluating the Intensity of Odor and Irritation.......................................... . 200 B. Portable Rapidly Indicating Devices........................... ....................... ............. 203 1. Interferometer............... ... ... ...................................................... 204 2. Portable Orsat........................................................ ....................................... 206 3. Combustion Devices......................................................................................... 206 4. Ultraviolet Absorption Devices..................... 208 C. Collection in Indicator Medium.......................................................................... 208 D. Hand Piston Pump, Luer Syringe, and Rubber-Bulb Collection Devices... 210 II. Methods Requiring Laboratory .Vnalysis........................ ...................................... 210 A. Halogenated Hydrocarbons Combustion Apparatus................................ 210 B. Adsorption for Evaluation by Weight..........................................:................... 212 C. Condensation at Low Temperatures.................................................................. 213 D. Collection by Absorption or Adsorption for Laboratory Analysis................. 213 E. Sampling in Evacuated Bottles........................................................................... 213 1. Vacuum Bottle Samples................................................................................. 213 2. Samples in Partially Evacuated Bottles..................................................... 214 F. Spectrometry.......................................................................................................... 214 1. Infrared................................... 214 2. Ultraviolet.............................. 215 3. Light Absorption.................... 215 Dusts, Fumes, and Smokes........................... 215 I. Sampling................................................. 215 A. Impingement................................... 215 1. Greenburg-Smith Apparatus......................................................................... 216 2. The Midget Impinger.............................. 216 3. The Konimeter........................................ 217 4. Owen's Jet....................................................................................................... 217 B. Electrostatic Precipitation................................................................................... 218 C. Filtration.................. 219 D. Thermal Precipitation.......................................................................................... 219 E. Sedimentation................................................ 220 II. Evaluation of Dust Samples............................................. 220 A. Making a Dust Count................... ..................................................................... 220 1. Counting Impinger Samples................................... 220 2. Counting Konimeter Samples.......................... 224 3. Counting Owen's Jet Samples........................................................ .......... 224` B. Determining Particle-Size Distribution........................... 225 C. Weighing the Sample............................................................................................ 227 D. Analysing the Dust......... ....... '............................................................................ 228 1. Chemical Analysis for ToxicMaterials........................................................ 228 2. Determination of Quarts............................................................................... 228 Bacteria........................................................................... 232 Radiant Energy and Radium. By LEON F. CURTISS........................................... 235 I. Fundamental Concepts of the Production of Injury by Radiation...................... 235 A. Ionization as Cause of Injury.............................................................................. 235 B. Target Theory........................................................................................................ 235 C. Injuries in Higher Forms of life...........................................................................236 D. Genetic Effects of Radiation............................................................................... 236 E. Visible Evidence of Injury fromRadiation........................................................ 238 DUP 0813690 VC.''' . DU 009668 . xxii CONTENTS j II. Penetrating Ionizing Radiation........................................................................ .--. _ 239 i A. Tjfpes of Exposure and Injuries.................................................................. ..... 239 I 1.'''Latent Period............... ............................... ........................................ 239 i 2. 1 iterance Dose........... ......................................................................... .... 240 3. Methods of Measuring Exposure............. ................................................241 4. Blood Counts as Index of Injury......... ............................................ ... ,, 244 . B. Protection from Gamma Rays............................................. ........................... 245 1. Pre-employment Examination........................................................... .. 245 2. Protection of Personnel......................................................................... .-- 245 3. ^Storage of Radium ............................................................................. ........246 4. Manipulation..........._............................................................................... -- 247 5. Exposure Table for Gamma Rays............................................................... 248 6. Protection of Messengers...................... .......................................................249 7. Transportation by Common Carrier............................................................249 C. Protection from X-Rays. ................................................................................... 250 1. Special Features................................. ...................................................-- 250 2. Protection from Electric Shock.................... ............................................... 251 3. Shielding Materials for Protection against X-Rays.................................. 252 4. Shield of the X-Ray Tube.................... ................................................ 253 5. Screening Complete Rooms.......................................................... ............... 253 6. Ventilation................. ................................................................................ .... 254 7. Special Conditions............ ................................................. ........................... 254 8. Unnecessary Hazards............................................................................. ........ 254 III. Infrared and Ultraviolet Radiation....................... ....................................................255 I A. Infrared.......................... .......... ,............................................................................255 1. General Effect............. ................................. ................................................. 255 2. Protective Measures....................................................................................... 255 B. Ultraviolet.............................................................. 255 1. General Effect........... r................ .................................................................. 255 2. Protective Measures...................................................................................... 256 3. Tolerance........................... 257 IV. Corpuscular Radiation.............................................. TM^-257 Neutrons..................................................... 257 1. Types and Effects........................................ ................................. ................ 257 2. Measurement.............--.................................................................... .. . 258 3. Shielding............................................ 259 V. Poisoning from Radium or Thorium......... ..................... 259 A. Radium Poisoning........................................................... 259 1. Historical Summary........................................ 259 I 2. Radioactive Nature of Radium.................................................................... 261 3. Injuries and Symptoms in Radium Poisoning................................. ... 263 4. Tolerances..................................................................................... 264 5. Detection of Unsafe Conditions................. ................................................. 265 6. Protective Rules for Radium Dial Painting...............................................269 B. Thorium Poisoning............................................... 272 1. Industrial Use of Thorium............................................. ............................. 272 2. Tolerances........................................................................................i..............273 3. Methods for Measurement of Thoron........................................................... 273 4. Protective Rules for Handling Thorium....................................................... 274 X. Ventilation. By W. N. WITHERIDGE.................................................................... .... 275 I. Human Ventilation Requirements................................................ 276 A. Air Composition............... 276 DUP 0813691 DU 009669 its ( ONTE.NT.' XXI11 B. Carbon Dioxide as an Index of Ventilation Requi; tnents .. . C. Effect of Room Size on Per Capita Ventilation Rv. lirements D. Mines, Tunnels, and Underground Spaces, ... 277 2JS 270 II. General Industrial Ventilation. .................. A. Classification of General Industrial Ventilation. . 2S0 ......................2S0 1. Natural General Ventilation.... . . . , 280 2. Mechanical General Ventilation.................................................................. 280 B. General Ventilation Specifications.........................................................................281 1. General Ventilation Rates in Terms of Air Changes........................... 281 2. General Ventilation Rates Based on Floor Area..................... .......... 282 3. Dilution Ventilation (General and Local).................................................. 283 4. General Ventilation for Control of Solvent Vapors................................... 284 5. Vapor Equivalents of Liquid or Solvents................................................... 285 . C. Dispersion of Air Contaminants by General Ventilation................................ 286 D. Provisions for Make-Up Air. . ......................... .. ...................................... 286 1. Airbound Rooms and Buildings ................................................................. 287 2. Estimating Infiltration by the "Crack Method"...................................... 288 3. Cost of Heating Make-Up Air............................................. ........................ 288 4. Heat Loss Analysis.................... ................................................................... 290 5. The Degree-Day................. T_........................... --.................. .................. 291 6. Heat Loss Analysis Using Degree-Day Data. .................................. . 291 7. Heating Values of Various Fuels.................................................................. 291 E. Air-Supply Inlets and Exhaust Outlets.............................................................. 292 1. Air Inlets............................................................... ......................................... 292 2. Air Outlets....................................................................................................... 292 F. Short-Circuiting the Air Flow.. 2L...................................................................... 293 G. Successive Ventilation................................................. ........................................ 293 H. General Ventilation vs. Local Exhaust Ventilation................................... .. 294 III. Industrial Process Ventilation............ ........... .................................. 294 A. Industrial Process Enclosures............................................................................_ 295 1. Paint-Spraying Rooms or Booths...................................................................295 2. Welding Booths or Rooms......................................................................... 295 3. Abrasive-Blasting Rooms............................... -........................................... 296 4. Metalizing or Metal-Spraying Rooms........................................................ 296 5. Grinding Booths................. ................................. --.................................. 297 B. Local Exhaust Ventilation........ -....................................................................... 297 1. Exhausting vs. Blowing.. ............................................................................ 299 2. DallaValle's Equation for Unobstructed Hoods....................................... . 299 3. Flanges and Baffles Increase the Range of Exhaust Hoods.................... 300 4. Air Velocities for Control of Air Contaminants...................................... .- 301 5. Specific Gravity of Gases and Vapors.................. 303 6. Canopy Hood Ventilation................................... 303 7. Sidedraft or Backdraft Hoods................... 304 8. Downdraft Hoods.................. 306 9. Face Velocity.................................................................................................. 306 10. Slot Exhaust Ventilation for Tank Processes........ .............................. ... 306 11. Tailpipe Exhaust Systems for Internal-Combustion Engines................. 308 12. Special or Irregular-Shaped Hoods.............................................................. 310 C. Ventilation in the Munitions Industry........................ ......................... .......... 314 IV. Air-Cleaning Methods and Equipment............................. ....................... ........ 314 A. Selection and Performance of Air Cleaners....................................................... 314 B. Types of Air Cleaners................ --..................................................................... 316 DUP 0813692 DU 009670 xxiv CO N'TEX l'.-- i 1. C '.ruritugui and Dynamic'C->: -: t'y-: nn - cud liu: .me*............. lilt) i 2. Wet Collectors: Spray Washer--, Scruhlier-. and Comleiw.r*................ 317 3. Filters: Cloth, Felt, Paper, GU--. ami Metal.......................... 318 i 4. Electrostatic Precipitators............... .............. .......... 319 C. Recirculation from Air Cleaners 320 D. Air Bacteria Control ................ 320 V. Aeromotive Methods and Equipment 321 A. Natural Aeromotive Forces................................................................................ 321 1. Wind Direction. Velocity,and Pressure........................................................ 322 2. Roof Ventilators.................................................................. 323 i 3. High-Temperature Stacks................................................... 324 B. Mechanical Aeromotive Forces.................. 324 1. Fans: Blowers and Exhausters.......................................................... ..........324 2. Ejectors, Venturi Ejectors, or Syphon Jets .............................................. 328 VI. Design of Ducts for Exhaust Systems............................................................ .. 328 A. Procedure for Design of Exhaust Systems............................................ ........ 329 B. Design Example......................................... ............................... ................... .. 336 C. Relation between Air Velocity and Velocity Pressure ........................., 336 D. The Wright Friction Chart................................................................................. 336 E. Reynolds Number....... ......................... ........ ................................................... 338 F. Flexible Metal, Canvas, or Rubber Ducts................................................. ...... 338 G. Adjustable Dampers or Flow Regulators.......................................................... 338 H. Pneumatic Conveying Systems....................................................... ................ 339 I. Construction Specifications for Ventilating Systems...................................... 339 J. Central vs. Unit Exhaust Systems........................................... ,............. ... 339 K. Maintenance of Ventilating Equipment.......................................... ............. ... 340 VII. Air Flow Observation and Measurement......................................................... .. 340 A. Visual Methods of Observing and Measuring Air Flow.................................. 341 1. Smoke Clouds......... .... ..............................-....................................... ........ 341 2. Floating Objects............................. ..................................................... .. 342 B. Static and Dynamic Pressure Indicators................................................... . 343 1. The Pitot Tube or Pitot-Static Tube......................................................... 343 2. Suction at Exhaust Hood Throat................................................................ 343 3. Venturi and Orifice Meters. Nozzles..... ................................................ 344 4. Propeller or Revolving-Vane Anemometer...................................... .. 345 5. Deflecting-Vane Anemometer................................................. .......... .. 345 C. Chemical Methods of Measuring Ventilation............................. .... .............. 346 D. Thermal and Electrothermal Measurements of Air Flow....................... ........346 1. Kata Thermometer (Standard and Electric)................... .................... . 346 2. Electrically Heated Thermometer Anemometer....................................... 347 3. Electrically Heated Wire Anemometer................................... ........... ........ 347 4. Electrically Heated Thermocouple Anemometer.................................... 347 E. Air Movement in Unconfined Spaces......................................................... . . 348 XI. Occupational Dermatoses. By LOUIS SCHWARTZ, M.D................................... 349 I. Historical Data........................................................................................ ........... _-- 349 II. Incidence................................_.................................. ........................................... 350 III. Causes of Occupational Dermatoses and Their Classification............................... 351 A. Predisposing Causes................. ............................................................... _.... 351 1. Base............................ -........... *............................................................352 2. Age........................... ^....... ............................... .............................352 3. Sex..................................................... .............................-......... -ttt. 352 ' DUP 0813693 DU 009671 10NTE.VT5 XXV I. Season of the Year................. 352 5. Perspiration........................... .. .. . ! '. . 352 0. Presence of Skin Disease....... .. ........................... ...................... 353 7. Uncleanliness.................................. . .................. 353 8. Allergy................................ ............................................. _ ...........................353 B. Actual Causes........................................ ............................................................... 354 1. Mechanical.................................... -............................ _.............................. 354 2. Physical..................................,... ,,............................... .............................. 354 3. Chemical...................................... ................... :....................................... ..... 354 4. Biologic Agents............................................................ ....................-------- - 358 IV. Clinical Types of Occupational Dermatitis.............................................................. 359 V. Diagnosis of Occupational Dermatoses..................................................................... 359 The Patch Test in Industry............... ................................................................. 380 1. Technique...................................... 361 2. Interpretation and Reading of Patch Tests,.. ........................................ 363 3. Complications of Patch Tests........................................ ................ .. 364 VI. Prevention of Occupational Dermatoses.............................................................. 365 1. Pre^mployment Examinations.................................... 365 2. Ventilation................................ 366 3. Protective Clothing....................^......................... . ............................. 366 4. Cleanliness........................................... 368 5. Protective Ointments.................... 368 VII. Treatment............................................ ........................................... 370 VIII. Occupational Cancer................................................... ............................................. 370 Prevention of Occupational Cancer............................................................ 371 IX. Methods of Investigation.................... ....._............................... .............................. 372 X. Skin Hazards According to Types of Workers or Occupations............................. 374 XII. The Visible Marks of Occupation and Occupational Diseases. By CAREY P. McCORD, M.D........................................................ 381 I. Introduction.................................................... 381 II. Stigmata of Degeneration........................................................ r-.............................. 383 III. Marks from Work and Work Diseases......................... ......... .................................. 385 IV. Summary................................................ .. ................................ ............................... 386 V. Common External Marks of Occupation or Occupational Diseases or Other Diseases (Table)..............;....................... .,............................................................... 387 XIII. Section One. Fire and Explosion Hazards of Combustible Gases and Vapors. By G. W. JONES........................................................................... ............................... .. 409 I. Limits of Inflammability......................... ...................... ......... ................................ 409 ... A. Factors Affecting the Limits of Inflammability................................................ 410 B. Limits of Inflammability of Gases and Vapors in Air..................................... 410 C. Calculation of Limits of Inflammability.................... ....................................... 415 1. One Combustible.................... ....................................................................... 415 2. Two or More Combustibles.......................................................................... 417 3. Complex Gas Mixtures............................................... ................................. 418_ D. Limits of Inflammability of Gases and Vapors in Oxygen.............................. 418 II. Ignition Temperatures............................................................................................... 419 A. Factors Affecting Ignition Temperature............................................................ 420 B. Minimum Ignition Temperatures of Gases and Vapors.................................. 420 C. Ignition Temperatures in Air and Oxygen.......... ............................................. 426 III. Flash Points.......................................... --........................,......... .............. ............ 426 IV. Temperature Range of Inflammability................................. .............................. 428 DUP 0813694 DU 009672 iamik jLifigjBaa--3iasiiai8iBK;, mam XXvi CllXTKXTS V. Methods of Minimizing Explosions............................................. .............. 429 A. Control of the Oxygen Content of the Atmosphere.......................... ........... 429 B. Operating Outside the Range of Inflammability........ .......................... 432 C. Use of Less Inflammable Materials. . .................... . . 433 D. Elimination of Ignition Sources.......... ............................................434 E. Segregation of Hazardous Operations.......................................................... .. 435 F. Provision of Adequate Ventilation..................................................................... 436 G. Release Diaphragms and Vents......................................................._............. 436 H. Combustible Gas Indicators for Inflammable Atmospheres............. ............. 43S XIII. Section Tujo. Explosion and Fire Hazards of Combustible Dusts. By IRVING HARTMANN.......................................................................................................................... 439 I. The Explosion Hazard................. ............................................................439 A. Factors Affecting Explosibility of Dusts.......................................................... 440 1. Composition of Dust.................................................................................... . 440 2. Fineness and Physical Structure of Dust................................. ................ 441 3. Concentration of Dust Cloud..................................................................... , 442 4. Composition of Atmosphere.......................................................................... 443 5. Type of Ignition Source............................................................................ ... 444 6. Characteristics of Explosion Space.................................... ........................ 444 II. Laboratory Data on Dust Explosibility............................................................. 444 A. Data on Ignition Temperatures........................................................ ........ .. . . . 445 B. Minimum Explosive Concentration............................................................447 C. Minimum Energy Required for Ignition........................................................... 448 D. Maximum Pressure and Rates of Pressure Rise in Dust Explosions............ 448 E. Relative Inflammability of Dusts........................................................... ...... 450 III. The Fire Hazard............................... -.................................................................... 450 Prevention of Dust Explosions and Fires........................................................ 451 XIV. Respirators and Respiratory Protective Devices. By FRANK A. PATTY........ 455 I. Historical R4sum5 and Present Approval Procedure........................................ .... 455 II. Types and Uses of Respiratory ProtectiveDevices................................ ............... 456 A. Air-Purifying Respirators......... ......................................................................... 456 1. Gas Masks (Canister Type)......................................................................... 456 2. Chemical Cartridge Respirators................................................................... 458 3. Mechanical Filter Respirators (for Dust, Fume, Fog, or Mist).............. 459 B. Atmosphere-Supplying Respirators.......... .. ...................................... ,.............459 1. Supplied-Air Respirators................... ........................................................... 460 2. Self-Contained Air- or Oxygen-Supplying Equipment............................. 461 3. Newly Developed Air- or Oxygen-Supplying Devices..............................461 C. Unapproved Equipment....................................................................................... 462 1. Filtering Efficiency against Paint Mist.................................................... ... 462 2. Unreliable Carbon Dioxide Absorbents............................................ .. 463 III. Selection of a Respirator........................................................... ................. .............. 463 IV. Cleaning and Sterilizing.................... ......................................................................... 465 V. Examining a Respirator.............................................................................................. 465 XV. Dust and Its Role in the Causation of Occupational Disease. By EDWARD E. DART, M.D........................................................................................................................ 467 I. Introduction.................................................................................................................. 467 A. Properties of Dust................................................................................................. 468 B. Atmospheric Dust Concentrations and Particle Size....................................... 469 II. Classification of Dust Based on Its Effect in the Body......................................... 470 a c u o 00 w 0to> 01 DU 009673 CONTENTS XXVII III. Anatomical Factors o! Importance in Injury by Dust...........................................471 IV'. Physiological Factors of Importance in Injury by Dust........................................ 475 V. Dust Causing Extensive Pulmonary Fibrosis (Silicosis and Asbestosis).......... .... 476 A. History.................................. ........... ............................................................ 476 B. Exposure to Silica in Industry.................-......................................................... -476 C. Etiology of Silicosis............... .... ... ................................................................... .. 478 1. Composition of Dust in Relation to Production of Fibrosis..................... -479 2. Number of Particles Inhaled in Relation to Production of Fibrosis.... 484 3. Particle Size in Relation to Development of Fibrosis.................... 485 4. Individual Predisposition... ....................................................................... 486 D. Pathological Anatomy and X-Ray Findings..................................................... 486 1. Nonspecific Pneumoconiosis...................................._................................... 486 2. Discrete Nodular Silicosis.............................................................................. 487 3. Modified Silicosis...................... 495 4. Nodular Silicosis with Localized Conglomerate Lesions.......................... 496 E. Tuberculosilicosis....................... ....................................... .................................. 496 F. Diagnosis of Silicosis..................... ................................. --................................... 500 G. Evaluation of Disability in Silicosis............................... ................................... 500 1. Statement of the Problem............................ 500 2. Pathological Physiology and General Principles........................................ 501 3. Terminology............................. 503 4. Tests for Ventilatory Efficiency................................................................... 504 5. Tests for Respiratory Insufficiency.............................................................. 507 6. Exercise Tests in General............................................ 508 7. Summary............... 508 H. Control of Silicosis in Industry.... ................................. *.............................. 509 1. Engineering Control................. ................. ................................................... 509 2. Medical Control........................................................ ................................... . 509 3. AluminumProphylaxis and Therapy........................................................... 510 I. Asbestosis................................... ...... ........ .................... ....... ............................... 511 VI. Dust Causing Minimal Fibrosis or No Fibrosis...................... ,............................. 513 A. Silicates..................................... ... ,,,......................... ....................................... 513 B. Nonsiliceous Dust.................... ..................................... --.............................. .. 514 VII. Dust Causing Chemical Irritation............................................................................. 515 VIII. Dust Causing Systemic Poisoning............................................................................ 515 IX. Dust Causing Allergic Manifestations such as Dermatitis, Hay Fever, and Asthma..................................................... ..........................., ...^......... ..................... 516 X. Dust Causing a Febrile Reaction (Acting in an Unknown Manner, Possibly as an Allergen)....................................... ............ ........................w................................ ... 516 XI. Summary........................................................................................................................ 517 Subject Index.................................................................. 519 DUP 0813696 _J DU 009674 (. HAFTER FIFTEEN. Dust and Its Role in the Causation of Occupational Disease EDWARD E. DART, M.D. I. Introduction The industrial hygienist and the industrial physician are concerned with dust because of its almost constant dispersion in air. where it may he inhaled and in some instances cause disease. This suspension of finely divided particles in the air may not ordinarily attract attention in rural areas but the smokiness of large cities is im mediately apparent. Clean country air may contain as much as 0.2 mg. dust per cubic meter of air, whereas the average amount in city air during the winter months is approximately 0.5 mg. per cubic meter of air.1 Thus, the cloud of dust that arises from a stonecutter's chisel is an excessive amounjrsuperimposed on that which is present in the already dust-laden air. __ _ In addition to the medical pioblems, the legal entanglements which may re- volve around dustiness are often of sufficient complexity that months of careful study are required to determine or fix responsibilities. In cities where general in dustrial smoke contamination is a perennial problem individual firms may be selected each year to bear the brunt of civic ire, and each year certain luckless corporations are forced to defend themselves in civil suits that are based almost entirely upon claims having no factual evidence for support. Medical-legal situations may be even more complex than the nonmedical problems and are complicated by numerous intangible factors, Not only does the exact nature of the disease and its relation to dust require proof, but the actual source_of exposure must be determined so that a nondusty industry will not be held responsible for dust disease that may have resulted from exposure many 5rears prior to the onset of the disease. This chapter is written as an attempt to bring together facts necessary for a general understanding of dust and dust diseases. The presentation in the first portion is somewhat general so that the contents can be readily grasped by physicians with- `J. M. DallaValle, Nicromentics. New York. 1948. The Technnjoqii /if Fi>'/ PnrUrh"--, 2nd cd., Pitman, 467 : I I |j i ,j a | j , ! ' f DUP 0813697 DU 009675 R.S Kinv.ua) K. DART . \u-n-i\e background in engineering >>r phy.-ies, anil hy -ngim-cr- am! :u.Ii;^_ rial hygieni.~i - without meilii'al training. In the later section- an u* >ui:pt i- m.:eie r . review pneumoconioses in sufficient detail to aid the phy>ician i-alled upon to oxamine employees whose work exposes them to dust. A. PRORKHTIKS OF IX'.ST The important physical and chemical properties of dust have been summarized by Drinker and Hatch,2 and much of the material presented here was obtained from that source, in) Settling rates. Suspended microscopic dust particles are attracted to the ea -th by gravity just as is any other free body. However, because of their small mass and the relatively great resistance of the air, they do not fall according to the usual laws of gravity. Settling rates are much greater for large than for small particles. A settled dust, accordingly, may contain a proportionately greater percentage of large particles than the contaminated air from which it settled and in which the fines predominate. Ore as it is found in mines may contain a certain amount of quartz, which is frequently harder than the other minerals present. Because of this relative hardness the quartz may be ground less finely in drilling operations. Much of this coarser quartz dust may settle out from the air in the working area with comparative rapidity, leaving a smaller percentage of quartz in the atmospheric dust than may be present either in the parent material or in the settled rafter dust. (b) Flocculation. Dust produced by crushing or grinding a material such as quartz-differs from fume such as magnesium oxide in respect to its tendency to flocculate. Freshly formed fume particles are usually well below 0.3 a and accord ingly exhibit marked Brownian movement. Because of this and perhaps other fac tors, they tend to collide and form floes which, because of their larger size, settle out relatively quickly. Such masses tend to adhere to vertical walls and projecting surfaces.. True dust is much less apt to flocculate than is fume, and any floes formed are much more loosely bound together. Settling of dust clouds is therefore much less pronounced than is settling of fume clouds. As a dust cloud clears, the size of the particles remaining in suspension decreases and the degree of dispersion increases, i.e., the ratio of flocculated to discrete particles becomes less. On the contrary, in a metallic fume both the percentage of floes and their size increase with the age of the cloud. Turbulence in the air increases floe formation in.fume clouds by increasing the collision frequency, but it does not improve the settling rate of dust. Humidity below saturation is said to have little effect on flocculation time. However, humidity to the point of supersaturation is an important factor, as the dust particles function as nuclei on which water may condense, thus increasing particulate size. (c) Wetting. Wetting is primarily an adsorption phenomenon in which the ' P. Drinker and T. Hatch, Industrial Dusts. McGraw-Hill. New York, 1936. o c a o co tcon 10 oo DU 009676 hi -i in nil. i \i -1 riiin "i m < ri' \ ri"N w. :'i-i. \ -mI;! -- "I tin- purtieli-- Ihtiiiih .proud "II plain- -url'aco. lull <1 ...... the ]>:irtit-lt-r- an- already M.-rounded liy a film "I air. Wottiim- i~ ni impm-- .11.-I in <lu*t r-umpliuu; ami in rontniMif iln-t. Tluvi- lartin- Itavi- Ihvii ili--i-i-ilu-it'hy Drinker ami Hatch as "f importance in :|u- wotting of dust. First, it is necessary to maintain iiit: -- -';,v....... ........ .,1 Iona duration between the dust and liquid. Second, i ihe liquid immediately at the dust source, because the producing dust by drilling or grinding hampers air adsoi mis flooding at the source excludes Air. Third, wetting crease the wetting power of water. V . [(/1 Electrical properties. Dust particles are elect}- ingly are attracted to oppositely charged particles. If. tl suspension are given an electrical charge, the tendency! increased. Attempts have been made to utilize electrical method of air purification but without great success. Ek the other hand, has been used quite successfully for eolle such precipitation depends upon the attraction of the el to an oppositely charged plate rather than upon floccuk (c) Optical properties. Dust or moisture particles light, reflected from dust particles otherwise too smalPtc visible when a beam of light enters a darkened room. T light by dust or mist is known as the Tyndall phenomei of suspended particles in air vary with their shape, the nally their size. With particles larger than the wave ler the strength of the Tyndall beam varies directly with pra cent ration: thus, for a given weight concentration ityjd tide size. Attempts have been made to utilize these opt surement of dust concentration, but variation in the size determinations unreliable. _ _ B. ATMOSPHERIC DUST CONCENTRATIONS A> Whenever a solid or liquid is ground or broken into the surface area is greatly increased. Thus if a etibe of.r dimensions is ground into small cubes 1 cu. /i in size, thei a total surface area of 0 sq. meters as compared with.O sc This great increase in surface area is largely responsible activity of finely ground materials and may be an impo tion of silicosis. -- Industrial dust concentrations may range from the air," in operations where no dust is produced or where t trol. to as high as 2 billion particles per cubic foot of air, i has pointed out that more than 50 per cent of industrial c DUP 0813699 DV 009677 ;ii sMiUMiB .li I. I > v\ \'.; [ -iZc v : '!' ill :i111i 11 11' '-In- meilmii Imuid l.-il Hilly "in per rrtU ''! 11 n * pari ii'li" : * 11 ul.* -mall.! liiali 1 H ali'l * I ml the I nt l i;i 11 -izi' :i- i .'> , I la I'l j 111 'ina l!i-l : I Hi I hi ill in ill-' I iaJ :: - ii.- >i .i m ail. la '-it! a ill ill'!..'" I ic->. In i\\ over. 'iirli a' pis UU: m pai'iii'li- ucll 1 h i11a. 1 m ill size an- prniinn i.r it. ~iiiiii,-~i,: n . i *. II. (.lassificalion of Dusl Based on ll' KH'rcl in tin1 Uinl\ Tin.- industrial hygienist ir- interested in dii'l lieraii.'i' m it - dYi-.-' mi ilir hum:,! lindy. Therefore. a limited classificationOf dust imin this vicu point may innu basis fur relating the chemical composition of dust to the anatomical and phydological reactions which occur in injury from dust. (/1 Dust causing extensive pulmonary fibrosis. This group includes all du.'i containing free silica or asbestos. Free silica is encountered in nature in the following forms: quartz--a crystalline form found in granite, schist, quartzite, sandstone, and sand; opal--an amorphous colloidal hydrate found in diatomaceuii' earth: lliut--a crystalline form found free or in association with chalcedony: chaindimy--a mixed form consisting of fibers of quartz and an interstitium of opal. Other less common forms are tridymite. cristobalite, and siliceous or vitreous glass. Axb< Hus is hydrated magnesium silicate. It is mined in Canada as the mineral chrysotile. (i'l Dust causutg minimal pulmonary fibrosis or no fibrosis. This group in cludes almost all inorganic dust except that containing free silica or asbestos. To the industrial hygienists the silicates, carbon, iron, and barium are the most important forms of dust in this group--the silicates because of their close chemical relationship to free silica, carbon because of its frequent occurrence in industrial atmospheres and its tendency to accumulate in the lungs, and iron and barium beeau'C of the unusual ruentgenographic findings produced. 131 Dust causing chemical irritation. This group includes obvious chemical irritants such as acids, alkalies, fluorides, and chromates. (Fluorides may also-lie included in group 4.i (41 Dust causing systemic poisoning. This group includes dust of certain metals such as lead, arsenic, drugs, and all systemic poisons that may occur in dusty form. (o) Dust causing allergic manifestations such as dermatitis, hay fiver, ami asthma. This group includes almost innumerable organic dusts such as pollens, synthetic resins, plastics, felt, fur. gums, kapok, leather, spices, tobacco, paper, rags, rayon, rosin, rubber, wood dust, starch, and wool. In addition to causing der matitis and other allergic manifestations, these dusts may irritate the skin and mucous membranes by purely mechanical means. (6) Dust causing a febrile reaction (acting in ah unknown manner, possibly as an JJ. J. Bloomfield. S. Pub. Health Repts., 48, 961 (1933). * T. Hatch and C. L. Pool, J. Ind. Hyg., IS, 177 (1934). o c TJ o CO w -ooJ DU 009678 n\r in i iii *\1 ". 111in 'H h i i i'_\ 11'i\ u. in-i: \'i 171 ,///,// , The tun <<nr-1;mi 1!!iii nn-ntim-r~ "i 'In- i-:ii -iiiir\' arc metal nunc '<>pc- i-i.-llly zillc n\ii|e ami rnttnll 11 ' i-' __ 111. \nal<miical Factor- <!' Impurtimcc ill Injury l>> I)u-t 'llic late of inhale. I dii.-l in I he I mily can lie uinliT.-twnil only by kn< .wing iimietliins nf t ho anatomical -t ruetjire- ami physh .logical reactions involvoil in respiration. The air passageway consi-tr- of the nos< pharynx, trachea, bronchi, bronchioles, and alveoli. The relationship of those various structures is shown in Figure I. t/) .Vo.sc. The portions of the nasal cavities just within the external nares are lined with skin containing hairs. The remaining parts of the nasal cavities are lined with mucous mem brane. composed on its surface of ciliated and mucus-secreting cells. This tissue is highly vascular and contains freely anastomosing venous channels. The nasal passages are connected directly with the air sinuses in the skull. The hairs in the entrance of the nose and the mucous material secreted by the lining membrane collect many of the larger inhaled particles. The cilia of the entire respiratory tract tend to move material toward the mouth, those of the nose tending to force the mucus and particles in it toward the pharynx. An indication of the importance of the nose as & protective mechanism has been shown by G. Lehmann.6 This investigator studied 426 miners, of whom 241 had silicosis and 181 were normal, and found the median efficiency of nasal filtering in the silicotics to be 27.5 per cent and in the normals 45 I'm. 1. Diagrammatic representation of the respiratory tract.5 per cent. He concluded from this that persons who develop silicosis do so, in part at least, because of a faulty filtering mechanism in the nose. __ (2) Pharynx. The pharynx is a common pathway for food and air, connecting 5 L. E. Hamlin, Rocky Mt. Med. J,, 41, 391 (June, 1944). `G. Lehmann, Arbeitsphysiol.. 7, 147 (1933); see also J. hid. Hyg., 17, 37 (1935). if DUP 0813701 DU 009679 o c L T3 O 00 CO >oto0 DU 009680 lm ,K> ill. II,, in fix -., uml l,, l>r....,l,iK o f ,!,, ItMB'tliiM-BiBtf iftiigfSiiRI -fff>qrn-i /j BailS" traaffgS- in-i i\ i * I . \i ' \: ; nr iMiri' \ rt> i\w. m-i.\-r. 17:1 till- nusil |>nv-ui><` \\ i 111 l lif i if: 11 j i:it ||V. a\ anil with tin- tra"iira. Ii- na-al j >* *i-t u iti i~ linnl illi filialril fpilhflimu. <! f.tii-'/n.r timl iruch< n. The larynx lies, lid ween the piiarynx and trachea. ii i- -rretitt'thetied !iy -trunn cartilage.-, cun lain.- the vocal mechani-m, ami ha- ai lhiopening to (lie oral pa--age a valvelik" -1 rueture---the epiglotti:--which elo-e- the tracheal opening during ^wallowing to prevent food from entering the respiratory pathway. The trachea is a tube I to 2 cm. in diameter, strengthened by cartilage rings and. like the nasal pharynx, lined with ciliated and mucus-producing cells. The relationship of the trachea and bronchi to the lungs as a whole is shown in Figure 2. ) bronchioles and alveoli. Macklin' divides the bronchial tree into two parts that may be compared to the trunk and branches^of a tree. The first part, which extends from the trachea to the terminal bronchioles inclusive, serves simply as an air conduit, and, like the branches and twigs of a tree, has no respiratory function. The terminal bronchioles are the last of a series of subdivisions of these nonrespiratory bronchioles. The muscular tissue in their walls is more highly developed than that in any other part of the bronchial tree and when fully contracted exerts a sphincterlike action which can completely shut off the air supply to the chambers beyond. The structures lying distal to the terminal bronchioles are the "leaves" of the bronchial tree. They have a respiratory function: the interchange of gases between air and bloodoceurs through their walls. The respiratory portion consists of the respiratory bronchioles, alveolar ducts, alveolar sacs, and pulmonary alveoli. The cluster formed by a related group of these structures constitutes a lung unit or primary lobule. This is the distensible or bellows part of the lung. The respiratory bronchiole as described in Best and Taylor5 has the same diam eter as the terminal bronchiole, of which it appears as a branch or a continuation. Five or six alveolar ducts arise from each respiratory bronchiole. Each alveolar duct after a variable number of rebranchings gives rise to from three to six dilatations, the alveolar sacs. The bays in the walls of the latter constitute the pidmonary alveoli, which are lined by a single layer of flattened epithelial cells cemented together. The alveolar walls-contain elastic fibers and a rich network of capillaries. Frequently a single capillary channel alone intervenes betiveemthe walls of adjacent alveoli. The blood in the capillaries is therefore separated from the air in the alveoli by only two membranes of the utmost delicacy--the alveolar and capillary walls, so the greatest freedom is afforded for the diffusion of gases from the blood to the alveolar air and from the alveolar air to the blood. The bronchioles, as they approach the periphery of the lung, branch and re branch repeatedly, diminishing in length with each subdivision. The first branchings -- : ; J. Sobotta and J. P. McMurrieh. Atlas uj Human Anatomy. Yol. 11. iru'diett. NYw York. 1933. 1 C. C. Macklin, Am. Rev. Tuberc., 25. 363 (1932). SC. H. Beat and X. B. Taylor, The Physiological Basis ot Medical_ Practice. 3rd ed.. William? & Wilkins. Baltimore, 1943. a^aaw DUP 0813703 DU 009681 171 i i.u . an- ;i I .1, ;mill, m !i :: u' i i a in i :: ' 111 i hi in 11. I 'in in. in * f........... T- niiiuT .. tv-pirm"i :<.i.i-11i,~ ri:< r*>m O.'J 'u ih'i nun. in Ii'iniM, m;: , ih,- limnHi-r : In- inniv .enti-il ~! 11 >< 1 i i-i- n i.'. Thai i-, 11 it- 1 .n<-l i : 7---- - i;. >i i " i i i"r r. i. ~i... . j>i;>*:i>-;i 1J\ Ini <-t- in ii.-inn-': - :Im-v 1 -- ;..v,->.i | M-fl I )1 II :; 'I i.i- ni' i.n'.WA rl\ i^ <- >n^i-1\- i'li-l '::!] . ' * hr < ~ Iory i)i` tin iiii lie til' iht- ai \ ri>iar iliii'I I n mi u hirii il u i i-o.-. 1 ir- piilim u - . a| \r< iii a M'lniii'lniiiiiai' anil 1 ia\'i diuim'iiT- ratiuinii inun I).ll7.`) in 0. IT' mm.: ' in tlif lu mi- ha> lu'cit or i main 1 liy Zunr v. al 77)0 mill inti. W i 1! ~i >n '-iial immi., .: r -- i i n epithelial -uifuce of the liin>!> at 70 .-<[. meter.-: of thi.-, prnlmhly .).') rneier-. we 2.5 times the -urinre area of the -kin. is respiratory. Fig. 3. Composite diagram (modified from Miller") of the primary lobule lvmphatic system, indicating the primary distributions or accumulation points for dust which will lead to predominant phases^of pneumoconiosis: b.r., respiratory bronchiole: d.al., alveolar duct: a.. atria: s.aL. saceruli alveolate; a.p.. alveoli opening into respiratory bronchioles and alveolar ducts in close relation with the origins of peribronchial and perivascular lymphatics; .4. branch of pulmonary arterv. accom panying the air passages: I'., branch of pulmonarv vein in interlobular septum: P.. pleura: P.B.. peribronchial lymphatics: P.Y., perivascular lvmphatics: 1, 2, 3, and other dotted areas, lvmphoid deposits. (By previous permission of Dr. \V. S. Miller.) " H. G. Willson. Am. J. Anai.. 30, 267 (1922). 11W. S. Miller, ai reproduced by Pendergrass in A. J. Lanza, Roentgen Diagnosis, Silicosis and AsbesLosis, Oxford Univ. Press, Xew York, 1938. o c TO O 00 -x CO o DU 009682 Ill - ! IN III!.' \! 'N i 11 ii. ! Vi `in l iii'M' I in-I - ii i- :i | ilia i vn i r i.:: ' Inna '.-- i'1 * (i < : - ' ' mi >fn- ln-' .'tnilimu <t ali\ in tin In Illy Ini' i lit1 al -- .| |>I i"l; : maliTl- - '!::ii 111:1;. :: in <> >1: * '.silh IJrintl,, /.v tttf/! J,, m j/h nhr*, l..\rrp' I. *! a :t 31'( ' .l'i'.'i ^ i he 1'] " M1 V('->cl- ala I ly nij ilia i a-.- it i - ii i i i ! t i-t-ly ' i.,. put 1, ; i n ii i. . n-r. flit- ; < !:i I n ui'liip in i)ii j-ripliiTy "i li.f lima i~ -In:. .t iii\ I/.^.iir> 3 Tla> lymphatic -v-lnn c,m>i>i~ ut vi'--el- Uuit carry ..'i .-imilur 'n l lie lilt mi l pla-ma alii I nodule^ unpt !-<< l la i'a< ly nf pi -c-i ive air: phagocytic cell.-.. The lymphatic ve-r-rls and lymphoid ti:--11<- arc imp''I'ant in o,.micotion with a -tudy m dust because most of the du-t particles finally ! in tin- peribronchial and inter stitial lymphoid tissues, carried there by wanuenng phagocytic cells. u;i Phagocyte. In the alveolar spaces there are large cells capable of ingesting foreign material and having the power of independent motion. A large number of these ameboid forms appear wherever foreign material enters the lungs. After ingesting the exogenous particles, some of these ceils pass into tiie blood stream and finally lodge in the spleen and liver or move,elsewhere in the lung tissues; the ma jority, however, make their way to the lymph vessels and eventually to accumula tions of lymph tissue, where they lodge. This re-ting place may be anywhere in the lung. Some phagocytes migrate peripherally to the pleura and others centrally to the hilus. In the lymph tissue the foreign materia! may be absorbed, may remain in an inert state, or may, by some chemical reaction, initiate pathological changes such as the formation of silicotic nodules. IV. Physiological Factors of Importance in Injury by Dust (1) Volume of air inhaled. Just as we are interested in the amounts of dust suspended in air, so are we also mtere-ted in the amount of air inhaled by men under different conditions. This has been discussed in Chapter 7. (2) Dust retention. .. Before we can arrive at a logical basis for determining maximum permissible concentrations, it is necessary to know what proportion of inhaled dust is retained. Since most dust-collecting apparatus imposes considerable, resistance to the passage of air from the lungs, satisfactory results were not obtained in such studies until Baumberger42 used an electrostatic precipitator with tubes large enough to reduce the resistance to a negligible factor. His studies on tobacco smoke yielded results considerably higher than those obtained later by Sayers,13 by Drinker, Thomson, and Finn,14 and by Brown.15 Baumberger found as much as So per cent retention of smoke. Sayers, working with tetraethyl lead in concentrations varying from 0.35 to 10.4 mg. per cubic meter oTliir, found that only 15 per cent was retained and attributed this limited retention to the small particle size. Brown's studies gave rather conclusive results, showing that the percentage retention is in versely proportional to the minute volume of air breathed and to the respiratory 15 J. P. Baumberger, J. Pharmacol., 21, 47 (1923). _ ** R. R. Sayers, L'S. Bur, Mines Repts. Investigations No. 2661 \ 1924). "P, Drinker. R. M. Thomson, and J. L. Finn, J Jnd. Hyg.. 10. 13 (192S). 15 C. E. Brown. J. Ind. Hyg., 13, 293 (1931). rtgMffifcaik gfaiMMMH ' 17'*> I l>w Mil* I.. M Mi r nili-. uln'ivii' :' -lin'd Iv pmpnmunal to tin- particulate size, dr: - ni '! ~U~p<-in it" I i!: air, all'! Ha' extent In which the duet is wcMcd while pa-ring ||,| water. He i.tinl that retention w:i- not affected by volume per respiration, capacity, m n-la;- humidity ot' inspired :tiI. .... Diisl (.ausing K\leiisi\e I'lilmoiiarj Fibrosis (Silicosis and Ashestosisi A. HISTORY Since ancient times it has lieen thought that dust caused disease. Perhaps tinearnest, reterence to disease caused by dust and fume is that of Plinius,"5 who dtscribed the devices used by refiners to prevent the breathing of "fatal dusts." In lood, in Dr rr mctallica, Agrieola17 stated: "On the other hand, some mines are so dry that they are entirely devoid of water, and this drvness causes the workman even greater harm for the dust which is stirred and beaten up by digging penetrates into the windpipe and lungs and produces difficulty in breathing." The best of the early writings on silicosis: is that of Ramazzini,1' translated in 1705 in".l Trealise of the.Diseases of Tradesmen, in which he stated: "For in hewing marble or stones out of the rock, in polishing and cutting them, they oftciitinnsuck in tiy inspiration the sharp, rough and cornered small splinters or particles that tty off: so ihat they arejisually troubled with a cough, and some of .them turn asthmatiek and consumptive . . . And in dissecting the corps of such artificers, the lungs have been found stuffed with little stone?. Diemerbrock gives a curious relation of several stone cutters that dv'd asthmatiek, and wenopened by him: in whose lungs he found such heaps of sand that in running the knife through the pulmonary vesicles he thought he was cutting some sandy body. He adds that he was informed bv a master stone cutter that in cutting stones there rises such a subtile dust, as is able to penetrate through ox bladders lumg in the shop . . . And this very dust he took to be the cause of the death of many Unwary workmen." In recent years the contributions to knowledge of silicosis have been sufficiently substantial, numerous, and varied to make this perhaps the most widely discussed 1 occupational disease. Silicosis is of particular interest to students of preventive. 1 medicine not only because of its general distribution in industry but more particu larly because of its tendency to increase susceptibility to tuberculosis--a characterI istic inherent in the disease. The limited space of this chapter does not permit ref1 erence to many sound contributions which have led to our present understanding ; of dnst disease. An exceedingly interesting and somewhat detailed review of the i history of diseases caused by dust may be found in the work of Lanza.19 , B. EXPOSURE TO SILICA IX INDUSTRY Since siliceous material makes up the bulk, of the earth's crust, it is not surp is! ing to fine! silica exposures in industry, where raw materials from the earth are used 14Cains Plinius Secundus, Xaturalis historic/, Bk. II. Trans, by Iv. C. Bailey under the title. Tin Elder PlinyChapter on Chemical Subjects, Pt. 1. Longmans. Green. Xew York. 1929. "Georgius Agrieola. Dc re mctallica, Bk. I. Trans, from 1st Latin cd. of 155b by H, (' Hoover and L. H. Hoover. Mining & Sci. Press. San .Francisco. 1912. j " B. Ramazzini. A Teat me oi the Diseases, oj Tradesmen. English 'ran?.. 1705. 13 A. J. Lanza. Silicosis and Asbestosis. Oxford Univ. Press. Xew York. 193$. DU 009684 a c -a o 00 w -si o CP l gjMBWBBtii BlMi.il A wijjajiiir; li.jfTiiagj iracaa r>1 T |\ nn; U'iATIilN 111 < X I'ri'.VVIOSAl. DISK.W. 177 / to make many of tin- i,nmnitiUjtio nvn.s.-ury to our daily livo. Unck- and nnr.iTm> arc often intimately a.-Miciated vith free silica and it is obvious that tho,-r occupa tions concerned with mining, rock grinding, or drilling may constitute silicosis hazard-, a- well as occupations concerned with the processing and industrial use of siliceous products. . According to Knopf-'" the. must common forms of free silica used industrially are massive crystalline quartz, quartzite, sandstone, flint, tripoli, diatomaceous earths and silica sand. Table 1, from kadoo.21 illustrates.the great variety of uses to which silica is put in industry and indicates the kind of silica adapted to each purpose. , TABLE i Industrial Uses of Silica and Types of Silica Used51 l.'.ics Types Abrasives In scouring and polishing soaps and powders. In sandpaper. In sand-blast work. Metal buffing, burnishing and polishing. For sawing and polishing marble, granite, etc. As whetstones, grindstones, buhrstoncs, pulp- stones. oilstones, etc. Tube-mill lining. Lithographers' graining sand. Tube-mill grinding pebbles. In tooth powders and pastes. Wood polishing and finishing. Quartz, quartzite, flint, chert, sandstone, sand, tripoll and diatomaceous earth; ah in finely ground state. Quartz, quartzite, flint, sandstone and sand; coarsely ground and closely sized. Quartz, quartzite, sandstone and sand, crushed into sharp angular grains uniform in size. Ground tripoli and other forms of ground silica. Sharp, clean sand graded into various sizes. Massive sandstone from very fine- to moder ately coarse-grained. Chert,"flint and quartzite in dense, solid blocks. Medium to fine sand or rather coarsely ground silica Shd tripoli. Rounded flint pebbles. Various forms of pure silica finely ground. All forms of silica ground to medium fineness. Refractories In making silica fire brick and other refrac tories. Metallurgy In making silicon, fcrrosilicon and silicon al loys of other metals, such as copper. As a flux in smelting basic ores. Foundry-mold wash. Foundry parting sand. Fairly pure quartzite known as gannister; not less than 97 per cent SiOi nor more than 0.40 perl*5nt alkalies, tightly interlocking grains desired. Moderately pure sand, massive crystalline quartz, sandstone, quartzite or chert. Massivejquartz and quartzite. Ground sandstone, quartz and tripoli. Fine sand and ground tripoli. Chemical industries As a lining for acid towers. As a filtering medium. In the manufacture of sodium silicate. In the manufacture of carborundum. Massive quartz or quartzite. Massive diatomaceous earth and tripoli, sand, finely granular quartz or quartzite, finely ground tripoli, diatomaceous earth and other forms of silica. Pure pulverized quartz sand, pure tripoli and diatomaceous earth. Pure quartz sand. - ---- , Table continued ;o A. Knopf, C.S. Pub. Health Bull. No. 187 (1929). :|R. B. Ladoo, Silica, Nahmetallic Minerals. McGraw-Hill, New York, 1925, p. 525. Ii i DUP 0813707 DU 009685 178 KDW'AKI) i:. IJAHT TABLE 1 continued1 I Types Paint A? an in-r. rxtendi-r. Mineral filler.* As a wood tiller. Finely ground crystalline quartz, quartzite and Hint, also finely ground sandstone, sand and tripoli. __ Finely ground crystalline quartz, quartzite. flint, tripoli and other types of ground silica. In fertilizers. ) In insecticides. | As a filler in rubber, hard rubber, pressed and } Finely ground silica of all types. molded goods,phonographrecords, etc. j In road asphaltsurfacingmixtures. j Ceramics In the pottery industry as an ingredient of bodies and glazes. " In the manufacture of ordinary glass. -- In the manufacture of fused-quartz chemical apparatus, such as tubes, crucibles and dishes. . Flint, tripoli and chert, and other amorphous silica preferred; also all other forms of verypure silica, all finely ground. Pure quartz sand. Very pure massive quartz preferred. Decorative materials In the manufacture of gems, crystal balls, table tops, vases, statues, etc. .-- Insulation Heat insulation for pipes, boilers, furnaces, kilns, etc. ... __ Sound insulation in walls, between floors, etc. Rock crystal, amethyst, rose quartz, citrine quartz, smoky quartz, chrvsoprase, agate, chalcedony, opal. onyx, sardonyx, jasper, etc. Massive and ground diatomaceous earth. Massive and ground diatomaceous .earth. Structural materials Sand-lime brick. , Optical quartz For the manufacture of lenses and accessories for optical apparatus. Moderately pure, sharp, angular sand, prefera bly finer than 20-mesh, together with a small percentage of finely pulverized silica. Clear, colorless, flawless rock crystal or massive crystallized quartz. C. ETIOLOGY OF SILICOSIS Silicosis has been defined by the Committee on Pneumoconiosis of the Indus trial Hygiene Section of the American Public Health Association22 as; "A disease due to breathing air containing silica (SiOi), characterized anatomically by generalized fibrotic changes and the development of miliary nodulation in both lungs and clinically by short ness of breath, decreased chest expansion, lessened capacity for work, absence of fever, increased susceptibility to tuberculosis (some or all of which symptoms may be present) and by characteristic x-ray findings." The definition adopted at the International Silicosis Conference in 1930 and reaffirmed at the 1939 conference is generally accepted and is somewhat simpler than the above. It is as follows: :: R. R. Sayers, Yearbook, Am. Pub. Health Assoc. (1932-33). ip DUP 0813708 DU 009686 SB 1 -i *\ i m. r.w i.r; . . .-i '* SincuM- a pa':. n'i*rh'ul .-oiiiliuijn >f limit- l'ir .`.nalfttM.:, 'ii <ii" L can b- produced cxpentr.-.-nmlly in animals." Lanza23 in "Etiology (>i`rfilicosi.s." as printed :n the National .Silk'iiM- Conference Report on Medical Control, .states: _____ "Simple or uncomplicated silicosis is a el.rvnic, tibro'r ..--as; of the . ..:.c- due Pi massive in vasion of the pulmonary tissue by silica siOp, inhaled in the form of jUst, In its early stages, silicosis may be symptom free: in its later Mages shortnessrof breath, decreased chest expansion. lessened capacity for work, may--one or more--be present, together w::h an increased susceptibil ity to tuberculosis. The disease presents the characteristicjeray appearance ot nodulanon. without which a clinical diagnosis may not be made." ,, The production of silicosis depends upon the following factors: the composition of inhaled dust, the number of particles of inhaled dust, the size of the particles of inhaled dust, the length of time during which particles are inhaled, and individual susceptibility. 1. Composition of Dust in Relation to Production of Fibrosis The fact that silicosis is caused by free silica (Si02) is attested by a great mass of clinical experience as well as by experimental observations. Gve and Kettle24 have shown that silica in solution, or in noncrystalline form, stimulates the proliferation of fibroblasts in tissues. Gardner25 produced a reaction in the lungs of animals in a period as short as two years by exposure to extremely high concentrations of dust. Miller and Sayers26 developed an intraperitoneal injection technique for testing the tissue response to dust, and their method has been used extensively by the United States Public Health Service, On the basis of this procedure it has been found that all dusts behave in one of three ways in the body tissues; they may disappear (be absorbed), cause cellular proliferation, or remain inert in the tissues. Dust Causing an Absorptive Reaction. XcTcasSs of pneumoconiosis have been reported and confirmed among workers exposed solely to .lust of the absorptive group. In experimental animals this dust disappears, leaving little or no scarring. A list of different varieties of dust investigated, which are absorbed, follows. These are of industrial origin unless otherwise stated. Calcile--essentially pure calcium carbonate. Precipitated calcium carbonate--containing 10.1 per cent magnesium carbonate, 0.1 per cent magnesium oxide, 0.6 per cent iron and aluminum oxides and 0.4 per cent total silica. Gypsum--the unealcined, natural mineral composed essentially of calcium sulfate with 1.3 per cent total silica. Limestone--not less than 82 per cent calcium carbonate, less than 12 per cent total silica, and not more than 10 per cent free silica. Portland cement--containing 74.4 per cent.calcium oxide and 21.1 per cent total silica. Free silica not reported. Pyrolusite--composed of 54.9 per cent manganese with no quartz reported, "A. J. Lanza, Report on Medical Control, Xational Silicosis Conference, U.S. Dept. Labor, Div. Labor Standards, Bull. No. 21, Pt. 1 (1938). -- M W. E. Gye and E. H. Kettle, Brit. J. Exp. Path., 3, 241 (1922). " L. U. Gardner, in A. J. Lanza, Silicosis and A*b<*tnsis. Oxford Univ. Press. New York, 1938. :`J. W. Miller and R. R. Sayers. L'A. Pub. IhaithMepl*.. S6. 264 (1941). Reprint 2234. j 1 1 DUP 0813709 DU 009687 480 HOWARD K. DART l/i,.-./ l in,.-, ni) a ihi h rulin' h'iiirtwH. Kach typt* oi < h i-t cxainiivi that fit!!- info tlu' proliforarivc group is known to produce nodular, pulmonary tihm-i- a:.,i each is a t'nrm of free silica. In experimental animals such dust produces nodu!i ~ which projin---ively increase in size until a maximum is reached, in about.<K) ,|::vAt first the nodule is similar to that produced by dust which is absorbed. Later the fibroblasts are replaced by macrophages, which become filled with du-t particleMiller and Sayers give the following examples of this group: Bisque ware--ground semivitreous pottery bisque ware, fired at a relatively low temperature Total silica. 72.0 per cent: quartz, about 40 to 50 per cent: the remainder semifused clay and feld spar. Chert--total silica. 76.1 per cent; quartz about 25 per cent; other forms of free silica. 35 per cent. Diatomile--total silica, 92.5 per cent: aluminum oxide, 3.5 per cent; ferric oxide, 1.5 per centcalcium oxide, 0.4 per cent; magnesium oxide, 0.7 per cent; essentially pure diatomite. Greenware--ground vitreous unfired pottery ware. Porcelain enamel frit--total combined silica, 35 to 50 per cent; the remainder is oxides of antimony, zinc, and aluminum, and fluorides of sodium, aluminum, and calcium. Quartz--a pure mineral dust; normal crystalline quartz of high purity (SiCh). Quartz--identical with the above sample but treated with 0.6 per cent crude pine fatty acids. Quartz-sericite--the source of this dust is unknown. Chemical analysis: total silica. 81.04 per cent; calcium oxide. 0.3Q per cent; magnesium oxide, 0.45 per cent; sodium oxide, 0.10 per cent; potassium oxide, 0.98 per cent; iron oxide, 0.25 per cent; aluminum oxide. 14.25 per cent; total water, 2.61 per cent. Petrographic examination: quartz, about 50 per cent; muscovite (variety, sericite), about 45 percent; fibrous sericite, less than 5 per cent. Bisqueware, chert, greenware--containing from 69 to 76.1 per cent total silica and 25 to 50 per cent of this as quartz. Diatomite--essentially pure and containing 92.5 per cent total silica. Quartz--samples of pure mineral dust and industrial dust containing over 99 per cent SiO-. Quartz-sericite--about 50 per cent quartz and 50 per cent varieties of sericite. Tripoli--total silica, 9S.9 per cent; chalcedonic silica (crystalline aggregates) with an occa sional crystal of normal quartz. Dust Causing an Inert Reaction. Pneumoconiosis resulting from some of the forms: of dust that are inert in the peritoneum has been reported. Clinical and pathological examples of the reactions show modified nodular fibrosis if the dust contains appreciable quantities of free silica; with other types of inert dust, diffuse interstitial fibrosis may sometimes result. The nodules produced in experimental animals become gradually flattened, and the dust is dispersed into the adjacent connective tissue, often to a considerable distance. Inert dust must be considered as a possible potential cause of pulmonary fibrosis. It is much less likely to cause pneumoconiosis than is dust that produces cellular proliferations in the peritoneum. Dust samples of the following descriptions were shown by Miller and Sayers to be inert: Aluminum--pure aluminum bronzing powder of the finest grade. Alundum--total silica, 4.6 per cent; aluminum oxide, 88.4 per cent; ferric oxide, 6.9 per cent. Asbestos--total silica 37.5 to 50.86 per cent. Anthracite coal--total silica, 6.6 to 8.6 per cent. Bentonite--clay, variety montmorillonite, about 97 per cent; feldspar, about 2 per cent; quartz, none observed. DU 009688 nr>T in tiii: i'Ar> tTP>N ok m-ivr.vTiON.u. di>k\'K I''! H -7ni roo--ground vitreous pottery bisque ware, Iiivj at :t rrlultvciv high temperature, ijuarz. abuti; 30 in 10 por cen*: t ho particles were wholly nr partially covered i >v the glass phase. iThis is absent in semivitreous bis<juo ware. ' />'-' ninrutt,< nn!--total silica. 0.S to 3.-3 p*T cent. t'.fi. phiis/il,,!',. --petrographic examination: earthy phosphates tnm apatite', about 97 per r1:!': normal and rledrcdonir quartz, about 3 per cenu_ Chromite--total silica, 7.8 per cent: quartz, less than .3 per cent. Diamond flits/--pure bortz diamond dust used as abrasive. Feldspar--total silica. 65.9 per cent; calcium oxide. 0.81 per cent; magnesium oxide, 0.10 per cent: aluminum oxide. 19.55 per cent; iron oxide, 0.2S peF'eent; potassium oxide, 8.98 per cent; sodium oxide. 3.18 per cent. Petrographic examination: feldspar (plagioclase-microcline), about 95 per cent; normal quartz, about 5 per cent. Fuller's earth--filtral clay, containing from 55.7 to 62,1 per cent total silica and 1 to 10 per cent quartz. Glass teool--finely ground sample of commercial hard glass wool. Hematite (jewelers' rouge;--total silica, 1.5 per cent; iron oxide, 98.3 per cent. Kaolin--china clay and hydromica predominant; quartz and feldspar, a trace. Lanthanum sublimate--from the burning of white flame electrodes. Lanthanum, 40.0 per cent. Petrographic examination: particles too small to identify. .1Hea--silica. 46.92 per cent; magnesium oxide, 0.86 per cent; aluminum oxide, 34.95 per cent; ferric oxide, 2.65 per cent; potassium oxide, 9.54 per cent; sodium oxide, 1.02 per cent; manganese dioxide, trace. Petrographic examination: mica, both as plates and fibers, plates pre dominating, about 98 per cent; a very small amount of quartz and feldspar. Precipitator ash--composed of siliceous material, magnesium, iron, aluminum and calcium oxides, or rare earth oxides of the cerium group. The total silica content ranges from 0 to 48.3 per cent and the quartz from 0 to 5 per cent. .-- Pyrophyllite--predominantly pvrophvllite, with a small amount of rutile and a small un determined quantity of quartz. Rock wool--a finely ground sample of commercial, insulating rock wool. Sele7iium--selenium. 98.8 per cent; tellurium, 0.01 per cent; ash, 1.16 per cent. Selenium--a chemically prepared sample of highest purity. St. idle--a pure mineral dust. Total silica, 51.74 per cent; calcium oxide, 0.61 per cent; mag nesium oxide, 1.74 per cent; sodium oxide, 3.40 per cent; potassium oxide, 4.48 per cent; iron oxide, 5.83 per cent; combined oxides, 31.82 per cent; total water, 6.26 per cent. Petrographic examina tion: sericite and feldspar residues (fibrous sericite predominates), about 95 per cent; quartz, less than 5 per cent. Shale--silica, 61.0 per cent; aluminum oxide, 12.4 per cent; calcium oxide, 4.5 per cent; ferric oxide, 5.0 per cent; magnesium oxide, 1.3 per cent; sodium oxide, 2.3 per cent; potassium oxide, 1.5 per cent; moisture, 10.3 per cent. Petrographic examination: about 35 per cent quartz; the majority of the particles appeared to be coated with clay. Silicon carbide--pure manufactured silicon carbide. Silicon, 67.5 per cent. Petrographic ex amination showed no impurities. Soapstone--total silica, 36.8 to 49.9 per cent; calcium oxide, 1.7 to 5.0 per cent; magnesium oxide, 22.7 to 26.2 per cent. Petrographic examination: talc, about 55 to 65 per cent; dolomite, about 5 to 30 per cent; tremolite, about 15 to 30 per cent. No quartz observed. Talc--total silica, 49 to 56.54 per cent; calcium oxide, 6.25 to 8.8 per cent; magnesium oxide, 22.6 to 30.74 per cent; calcium silicate, 0 to 11.00 per cent; calcium carbonate, 0 to 1.88 per cent; iron and aluminum oxides, 0 to 1.04 per cent; ignition loss, up to 4.60 per cent. Petrographic examination: talc, mostly fibrous, about 40 to 75 per cent; tremolite, about 25 to 60 per cent; oalcite and (or) dolomite, up to 1 per cent. Titanium oxide--a finely divided, high-purity sample. DUP 0813711 DU 009689 !>2 !:i)\vaki> :. ! >t/'u . >ih -- a i:tbi)rai<>!'y-[i!,'`p:t!v'l sampi-- - "li'ni; -liti-M. Ili-i.-r rat in.- ul > uxidr killed tin.- u:.::t.al~. Tni/i rocl:--silica. 51.7 per cent; aluminum oxide. lii.O > terrie .Aid-. 2.0 per ,, lerrous oxide. 9.0 per cent; calcium oxide, 10.0 per cent. mu-.-- xide. >1.2 ;.-.t araplnc examination: feldspar. some slightly decomposed, at." 45 j>-r -eu': pvt'ixvae ab.v;- per cent; magnetite, about 10 per cent:_biotite. about 1 per cen Volcanic ash--silica, ,54.4 per cent; aluminum oxide. 14.5 pet . -m; ferric oxide. 3.S per cent magnesium oxide, 2.6 per cent; calcium oxide, 0,7 per cent; ash, 7s2 per cent. P.rrosrapiiic exam.nation: fine volcanic ash partially altered to montmorillonite. No .plan/, observed. Volcanic ash--a specially treated sample. Silica. 74.3 per cent; mixed oxides. 1G.S per cent; ferric.oxide, 2.2 per cent; calcium oxide, 0.5 per cent; magnesium oxide. 2,2 per cent. Petrographic examination; glass.only. No quartz or calcite observed. The immediate response of body tissue to any dust is essentially a foreign-body reaction, but the subsequent behavior of the tissue to any given dust determines whether such a dust is harmful. In the peritoneal injection experiments of Miller and Sayers only dust contain ing free silica caused fibrous proliferations. Although it has been well established that silicon dioxide is the cause of silicosis, there has been little satisfactory explanation for its action. Earlier it was thought that the fibrous nature of the proliferation was related to the hardness or sharpness of the particles. However, Gardner27 found that no fibrosis was produced by experi mental inhalation of carborundum dust, which was even harder and sharper than silica. Thus, the action is clearly chemical, but the exact chemicophysiological re action that takes place is still unknown. The mixed reaction sometimes produced by dusts of the inert group in which silicaTis mixed with other minerals emphasizes the possible effect of mixed dusts on the development of silicosis. The probable importance of concomitant exposures has alsa been indicated by clinical experience. Chapman.2' MacDonald and hi: asso ciates,28 and Kilgore30 have reported cases of rapidly developing silicosis caused by breathing air with high concentrations of silica and alkali dust. Kettle31 and Mc Cord32 failed to demonstrate such action experimentally. McCord, on the basis of extensive investigations of workers in six plants where there was exposure to silica and alkali dusts, found no evidence of an accelerator action by alkalies. In fact, the absence of silicosis in this group suggested an inhibitor action which he believes may have resulted from the marked increase in solubility of silica in the presence of alkali. Peritoneal injection in animals yielded no results to prove either an accelera tor or inhibitor action of alkali in the formation of silica nodules; but alkali did cause silica to spread from the point of injection and increased its primary toxicity. The absence of silicosis in ganister-brick manufacturing was thought at first due to an inhibiting effect of accompanying dusts; more recently it has been found " L. U. Gardner, Am. Rev. Tuberc., 20, 883 (1929). " A. M. Chapman, J. Am. Med. Assoc., 30, 9 (1939). " G. MacDonald, A. P. Piggot, and F. W. Gilder, Lancet. 2, 836 (1930). " E. S. Kilgore, J Am. Med. Assoc., 93, 1414 (1932). " E. H. Kettle, Proc. Inst. Mining Metallurgy (London) 43rd Sess., 1934. " C. P. McCord, Ind. Med., 5, 17 (1936). D C TJ O 03 to DU 009690 i ilWBlift i i;.ar t>r-x iv nn: > .\"-.\riox nr nivnunnwi. !i-: ,-< I'!:5. 'Imt tin- `-(.inn mration m iY<v in the work nimivqmeiv .'.a- ,,,>.v m .iuim- iibrosi>. Silitxc-i.-. as ioun<! in i-i.-nl miners ^anlhraeosisi ami in im.mii;, num may he quite different in x-ray appo-araner and in its course from that observed in quartz minder.-. (iarunor;i investigated these efforts experimentally using ferrugunm- chert and mixtures of quartz and calcined gypsum. He found that the percentage of free silica in air-borne dust may not be the same as in the parent substance. This fact may explain the slowness in development of silicosis inlworkers in certain areas and in certain types of work. When a mixture of calcined gypsum and quartz was present in air, particles of both minerals flocculated and the rate of settling of the mixture was greater than that of either dust in the pure state. Injection experiments with ferruginous chert showed that the iron in the mixture temporarily inhibited the action of silica. Gardner's summaries of these experiments follow: 1. Artificial mixture of equal parts of calcined gj-psum and quartz. Materials ground sepa rately to respirable sizes and mixed in a dusting hopper. Quartz content of parent mixture.............................. .......................................... 49.7% Quartz content, air-floated dust in cages........ ...... ...................... .. 29.6% Average light-field count, air inside cages, 336 million particles per cu. ft. Xo exposed animals developed silicosis within 25 months although only 15 months were required to produce nodulation with average concentration of 120 million particles pure, quartz per cu. ft. of air. Of 17 animals exposed more than 25 months and up to 30 months, 7 showed nodular fibrosis of modified type. Remaining 10 developed only chronic pneumonitis. 2. Artificial mixture of 2 parts of calcined gypsum and 1 part of quartz prepared as above. Quartz content of parent mixture................................................................ - 31.4% Quartz content, air-floated dust in cages..................zr.................................... 17.1% Quartz content, lung ash of exposed animals. . . . .................................... 15.4% Average light-field count, air inside cages, 245 million particles per cubic.foot of air. X'o animal developed silicosis until exposures had been continued for 24 months. Mature nodules found in only 3 of 16 guinea pigs exposed 24-29 months. These lesions were of modified type. The other 13 showed nonnodular pneumonitis. _ 3. Ferruginous Chert I, a natural mixture ground at a mine to such size that a majority of the particles were less than 10 microns in diameter, but there were a considerable number of larger ones. Free SiOj of parent mixture...................................................................... .. 54.6% Free SiOi of settled rafter dust...............................--.......................... ........... 38.4% Free SiCh of air-floated dust in cages.............. ................................................... 10.4% Free SiOs of lung ash of exposed animals............................................................ 3.3% Average light-field count, air in cages, 776 million particles per cubic foot. ! X'o suggestion of silicotic reaction but merely pigmentation of lungs of animals exposed for maximal period, 18 months. --. "" 1 4. Ferruginous Chert II. A similar natural mixture jffom the same source as that used in : exp. 3 but ground until all particles were 5 microns and less in diameter. Free SiOi of parent material............................. .... ................................. .. 67.5% Free SiOi of settled rafter dust................................ --............--....................... 61.0% Free SiOi of air-floated dust in cages.................... ___.............................*... 33.5% Free S1O2 of lung ash of exposed animals............. ....................... ..................... 16.3% ' " L. U. Gardner, "Reactions, to Mixed Dusts," in Fourth Saranac Laboratory Symposium | on Silicosis, B. E. Kuechle, ed.. Employers Mutual Liability Insurance, Wausau, Wis., 1939. mm DUP 0813713 DU 009691 Pig iflgq Miiimmi n_Mi\ .\s\ .!>\v Wilt !,. I > \K r Avf'!':u:v ;tir id **:i*j;*T7t> million pai'Ui`[o< per rub; : >o. So >ihrnH" in uuy uninuiT' lun^s i \{u>.-l un-lrr 'A yeti's: in S <>i 1 ' iniimiis ---l for! :-.;u .. iocU. nxurn* prvsotu. Tin* oihrr 7 clrvrioiird only purnirnuiu-.n and rhr.:.:.- ..n.... moni'.is. Tims we luive both laboratory and clinical demonstration of the h.:i;:eunexerted by other dust uii the development of silicosis. 2. Snmbir of Particles Inhaled in Relation to Production of Pibrosi* From the findings of Gardner, quoted above, and from the discussion of tioceulationand settling, in the preliminary section,'it is apparent that the type of dust may play an important part in determining the number of particles in the workroom atmosphere. Xot only may some components of admixtures flocculate and thus change the character of a dust, but silica itself, being a hard material with a ten dency to form large particles as compared with those formed by softer minerals, may settle out more quickly than other components of a mixed dust. However, at this point we are somewhat more concerned with the concentra tions of dust that are harmful than with the factors that have produced any given concentration in the air. Determinations of free and total silica in the lungs of patients who have died after fibrosis developed and in those without fibrosis have been made by incinerating the lungs and chemically analyzing the ash for its silica content. Although there have been some variations in published data on the amount of silica in pulmonary tissue necessary to produce silicosis, Sladden,34 McNally,56 Badham and Taylor,30 and Fowweather37 found fairly comparable amounts. Drinker and Hatch36 sum up the present knowledge somewhat as follows: as a rough guide, a total silica content as high as 0.2 per cent of dried lung can be considered normal. A content over 1 per cent is definite evidence of dust exposure, and this amount is usually accompanied by fibrosis. There is too much overlapping of data and variation in technique to be sure from published data of the significance of quantities between 0.2 and 1 per cent of ashed lung. This fact is of especial signi ficance, as pointed out by Cummings .3a Since there is usually no evidence of silicotic reaction in lungs containing less than 1.5 to 2 gms. of silica (1 per cent of weight of dried lung), it may be inferred that the contraction of silicosis does not necessarily follow the inhalation of silica. Silicosis occurs only after the inhalation of amounts in excess of a minimum. In any control program we are of course concerned primarily with the amount "A. F. Sladden, Lancet, 2, 123 (1933). ** W. D. McNally, J. Am. Med. Assoc., 101, 584 (1933). ** C. Badham and H. B. Taylor, Med. J. Australia, 1, 511 (1933). " F. S. Fowweather, Chem. Industries, S3, 713 (1934). MP. Drinker and T. Hatch, Industrial Dust--Hygienic Significance, Measurement and Control. McGraw-Hill, New York, 1936. *D. E. Cummings, "The Etiology of Silicosis," in Fourth Saranac Laboratory Sym posium on Silicosis, B. E. Kuechle, ed,, Employers Mutual Liability Insurance, TVausau, Wia., 1939. a c TJ iO --00k co -4 DU 009692 /111 - ! I N 1 11 I ; . - \ I 11 i N I i: .. I 1 \ I 11 ,\ . :. 11, - ' '< -J i^ Hi' dii't in llit- air 11 ml will (Suim- !;iwii.~, Tin- ni<-tii >tt~ . >i drtrrniininii atnnt'plwr''- tiiml niiwent ratimi- an- <iix-i. i in l liaii'ri1 lliuihl. < im.nntm> MiutwMfd tlu>.i atmir-plmrie concent rat ii n> nl -:lwu duM -!i 11< 1 lie <- m'i<It-ni in term.- <-I i v. 11 in "I i oh I': the prim: rv 11, rt -i i- NC-:: level a' 11 it 1: a I wail liy man '-an In- employed itir hi.- lifetime will,i m h:,rni. al- ut a.cmi.mui |TiT;irK' per eiil.ie I ligin-iiei,: count i; ami tlw sect,Hilary tlm-hold. a level :;i which a healthy man will inevitably develop silicti.-i>. ill>tHit lnO.llUO.Ofld particle- pal' cubic Pint tliyilit-tiflt 1 mini . Tlw National Silicor-is ('onforence summarize- >lw .-ftuation as follow.-: "There is evi dence that lor prolonged exposure a coiwenrration of more than 5 million particles per cubic loot, of a highly siliceous dust, is dangerous. Therefore it is now considered good practice to hold concentrations of highly siliceous dust at 5 million particles per cubic foot, or less," as based on light-field counting methods. Since standards of safe atmospheric dust concentration based on medical find ings have been suggested tentatively for only a few industrial dusts, anil since considerable study is necessary to form a basis for such standards for other industrial dusts, a tentative arbitrary measure of what is good practice may be used. This should be within the limits of good engineering practice and yet low enough to control the silicosis hazard for most industrial exposures. The following formula is frequently used to express the maximum permissible concentration of silica in air. Multiply the percentage of free Plies by the ml .lust particle count per cubic foot ,lightfield technique!. If the result is over 5 million, the ecunentration may be considered too high. For example: a dust containing 10 per cent free silica wirli an average total concentration of 30 million particles per cubic foot would give 0.10 time.- 30 million, which equals 3 million good practice): a dust containing 30 per cent with an average total concentration of 50 million particles per cubic foot would equal 0.3 limes 50, or 15 million unsaiiMaetorynThis formula is not applicable to any dust containing less than 5 per cent free silica. The Division of Industrial Hygiene. National Institute of Health,40 has sug gested that an attempt should be made to haveJiighly siliceous dusts kept at a concentration below 4,000,000 particles per cubic Toot since considerable silicosis occurred in the pottery industry even with low dust concentrations. Dust may also be simply a nuisance. It is considered good practice to control even relatively harmless dust sufficiently to prevent concentrations in excess of 50,000,000 particles per cubic foot (by light-field count! in the workroom air. 3. Particle Size in Relation lo Development of Fibrosis We have already mentioned the fact that large particles settle more rapidly than small ones and that particle size is importanFas a determining" factor in the actual amount of dust in air. Particle size is even more important in determining the chemical activity of the dust and physiological responses to it. Chemical activity is, of course, increased in small particles because of the increased surface area. McCrae41 "R. H. Flinn, W. C. Dreessen, T. I. Edwards, E. C. Riley. J. J. Bloomfield, and R. B Sayers, VS. Pub. Health Bull. No. 244 (1939). " J. McCrae, Pub. S. African Inst. Med. Research. Report No, 3 U9I3;. DUP 0813715 DU 009693 (Mi i:d\v \iu> r.. n \ fill 111' I l ii:ii 7H IIIT '-I'LlI ' 11 I !|r |):ll'l ifll" ill 'ili'-oi ir llllli.' I i'-- ' ; .. ; mull Ini i ill.-l;u-o.-~l ui-ivii"! greater than II)..V- An u |-i >.-i i i i: i:' In..,-- ;..... - -izi' l lull " ill pr-idm-e 'ilii-o'i> has been ~iltrfi<`^1 <1 I M-i-ail'-- : g- - par1 i-v- .tj . iilv illi-i-ii-il 1 iy imti-us in tin- iipprr rr-pii'iiinry 11-art mi-i ii .-n: i - ciliary yi-timt. The importance of small particles in tin- pio-l-mi i-.n .>i . liccn well ilcnnmst rateil hy Tehhens. Schulz, anil Drinker.-' The-r iim-^i ... produced liver fibroids in experimental animals hy intraven.ni' iiije.-t|..|> - ... pended silica and t'ounil that particles less than O.ii g in diameier i-mM-.l nni.-h n..-, fibrosis._than larger particles. Briefly, silicosis is caused by the inhalation of silica particles less than 111 ,, diameter. Recent work suggests that particles of less than O.ii m may he of greati-si importance in this respect. Individual Predisposition Detailed discussion of the role of individual predisposition in the etiology silicosisds hardly necessary. Race and sex seem to play little part, although race may be a factor in the development of tuberculosis just as financial status may he a factor. Certainly it is known that of two persons working in the same dusty ex posure one may contract silicosis in a few years while the other may wholly escape it. We have already mentioned the possible influence of differences in nasal filtration as a factor in causation of silicosis. It is likely that there are sound explanation.' lor the many variations in individual susceptibility, but clarification is lacking. D. PATHOLOGICAL ANATOMY AND X-RAY FINDINGS Gardner," whose descriptions of pathological anatomy have been used a,' a basis for much of this discussion, has classified the pneumoconioses as follow.-,: Nonspecific pneumoconiosis, including all forms except silicosis and asbestuoi.', silicosis of the classical discrete nodular type, modified silicosis caused by the inhala tion of dusts containing free silica mixed with certain other minerals, and silicosis with conglomerate lesions, in which healed or active infection probably plays a dominant role. 1. Nonspecific Pneumoconiosis All dust other than that containing free silica and asbestos produces the same general reaction. X-ray Examination. There is simply an accentuation of the normal, branching, treelike shadows cast chiefly by the pulmonary blood vessels. As an occasional varia tion in this picture there may be superimposed fine reticulations. These reticulations are thought to be caused by thickening of the sheaths of the pulmonary arteries and thickening of the interlobular septa. See Figures 4 and 5. "B. D. Tebbens, R. Z. Schulz, and P. Drinker, J. Ind. Hyg. Toxicol., 27, 199 (1945). " L. U. Gardner, in Fourth Saranac Laboratory Symposium on Silicosis. B. E. Kucchlr. ed., Employers Mutual Liability Insurance. Wausau, Wis., 1939. D C "O o 00 oo -'4 0) DU 009694 !m - I IN I II I. i \! -A 111 IN i 'I ' h i 1'1'A l'l"N \ i 11 -1. \ -l ;n, Il'nisi Exon ./Hlliiill.Kv<|(.`] t witll [mill Hill'll mill ili(i-Il.~l\ i` ''N|l' >~u r< '111' rileurui .-urlartv- m lung> witIi iitm.-pecifie pneumucimiosii- >hm\ uiily inral ami nii'-m 'illiH'iinn,- of pisinii'iit that arc Mitt in con.-i.-tcncy and not rai-ml almvc tlie >uiti mmi ll si ti'-ucN. t Mi -' -iiriaro. arn-N r\aininatiim n'vcaKi'iiuiiiii'il llc-lv- ut pkir.'ii; 2 I o nun. in 'liana ter. Inn a Imis >hnw.- liner linear depiisit- in the iutrrhiimlar -' ]>:a nul in the miter walls ofthe lilood vessels. The entiivTimg may lie rnlored liy pia- ment a- in the black lungof siitt-coal miner.-, hut no fibrosis I- foundunless there ha- net'll exposure to tree silica. There may be small patches ot emphysema in or ad jacent to pigmented areas. Scars of healed infections differ from the usual sears by the presence of pigment. Microscopic Examination, If death occurs during exposure, dust particles are found free in the peripheral air spaces or ingested by alveolar phagocytes that are found adherent, to alveolar walls and in loose areolar tissue about the bipod vessels, especially the arteries, and in the interlobular septa. These last two linear depusits are referred to as perilymphatic deposits because of their close relationship to the lymphatic trunks. The bronchi show relatively little-dust; when any is present, however, it is found in the connective tissues just beneath the epithelium. If there has been no recent exposure (years), the intrapulmonary dust tends to be removed from the air spaces and deposited along the lymph trunks; in severe exposure large amounts of dust-filled phagocytes may remain in the alveoli. Nearly all pure sub stances other than silica cause little cellular reaction. Coal and some silicates, espe cially mica, may cause minor irritation without producing fibrosis. Unless the linear reaction is fibrous and caused by free silica, there is_.no altered susceptibility to tuberculosos. - . 2. Discrete Xodular Silicosis X-Ray Examination. This form of dust diseasejs characterized in the x-ray by small discrete nodular shadows, uniformly distributed throughout all parts of both lungs with the possible exception of small emphysematous areas in the costophrenic region. In the absence of infection, the nodules are of .uniform size, rarely exceeding 4 mm. and never more than 6 mm. in diameter. The nodules are sharp with well-defined borders. See Figures 6 and 7. Gross Examination. The pleurae are studded with slightly elevated, grayish nodules 2 to 3 mm. in diameter, and around these there may be a flat zone of black, gray, or brown pigment. No pleural adhesions are present. The lungs are stiffer than normal but crepitus is present. There are palpable shotty nodules. The cut surfaces are seeded with black or gray nodules, 2 to 4 mm., or rarely 6 mm., in diameter. The edges of the nodules are well defined, but a lens shows pigmented strands radiating from their periphery. There is little confluence excepUwhere scars or infection are present. Usually some gross emphysema is present, but this condition may be apparent only with microscopic examination. For differentiation from perilymphatic pigmentation there must be definite pleural nodulation in an appreciable amount. Some nodules may arise along the peripheral branches of the pulmonary arteries. '^`ftiiilifV 1 DUP 0813717 DU 009695 "*rr-w DU 009696 DUP 0813718 ivl Fig. Increased linear markings. Increased linear markings may be seen in the roentgenograms of apparently healthy subjects, and they may result fronunfeetion, exposure to irritants or dust or from other causes. Increased linear markings may also be demonstrated in patients who later develop nodular silicosis, A definite diagnosis of pneumoconiosis can not ( made from roentgeno grams showing only increased linear or vascular markings DU 009697 DUP 0813719 *&** *mn.La.:^JiitiLit.; -I l:-U-i_ I'.'n -*- ra-t-wr-ws- DUP 0813720 Fig. 6. Nodular silicosis, uncomplicated < courtesy L. E. Hamlin., nn DU 009698 I'.li Fig. 7. Nodular silicosis with infection in right upper lobe (couihiy L. E. Hawhn i I DU 009699 DUP 0813721 Fig. S. Increased linear markings and indistinct nodulation. This typo of abnormality is some times seen in roentgenograms of subjects exposed to mixed dust. This roentgenogram is about mid way between that seen in nonspecific pneumoconiosis and that seen in nodular silicosis. ;i it DU 009700 DUP 0813722 Fig. 9. Xodular silicosis with conglomerate lesions. It has been, pointed out in the text that con glomerate lesions are ordinarily associated with infection, ustj&lly tuberculous. Itjs of inteie'-t to note that this patient was negative to tuberculin tP-P-D. first strength; and that he hau had eleven sputums that wore negative and none positive for tubercle bacilli Icourtesy L. Hamlini. DU 009701 DUP 0813723 iv; #r 0 Fig. 10. Xodular silicosis with conglomerate If.-ion^ and infection {courtesy L. E. Hamlin*. DU 009702 DUP 0813724 m ~r in rm . \i -ii'Mi nr m rvnovu. dim-: v-i. I'.i'i The lr;ti'hr'ihrnnfhi:il lymph wh- ;i;< al lil'' rithtrilrd and linn. i.-in-i -uttii: ,:wl i`\t rrincly hard. Srrtinn- <>f thr-c w >d>'< reveal > 1-n^( leutherlike t i->uo. \\ hidi i--ilky in texture berau.-e 'if tho deerea>e in <>1 faitt-ii'ni~ mnnective tissue. M iri nsrn/iir Examination. M'iM upic examination -Ii.iw-n layer- of > 11'11 -< 11y:11 i111> collagenous libel- with mu-lei ,-n rumple--ed in? to be almost in\ i-il>1<` ar times. The borders are dear eut, .with no exudation,. There may he pigment either nhout the periplierv or in focal points within the nodule itself. The nodule may he calcified, occasionally to the point nt hone formation in its central portion. Nearly all nodules are associated with branches of the pulmonary arteries, as demonstrated bywax reconstruction of the arteries; they may form spherical or spindle-shaped masses around the arteries. Pigmentation occurs about the lymphatic trunk just as in non specific pneumoconiosis, but there is always some fibrosis. The air spaces immedi ately adjacent to the nodules are distorted and frequently dilated. There may be widespread emphysema, most marked in the costophrenic angle, where nodulation is most sparse. The emphysema is fine, not coarse or bullate. Ordinarily there is no leukocytic reaction. Early silicosis resembles nonspecific pneumoconiosis; the re action, however, is more extensive and is fibrous rather than cellular. The closely related pathological pictures in early silicosis and in the nonspecific reaction would be expected since the x-ray findings in the two conditions are almost identical. Neither in early silicosis nor in nonspecific pneumoconiosis are the x-ray findings associated with any disability. 3. Modified SilicosisT Modified nodulation results from breathing dust containing free silica mixed with other minerals. Although a great deal is not known about mixed dust reactions, there have been sufficient examinations of the lungs of hard-coal miners to deter mine that lung tissue responds differently to the dust.of coal mines than to pure silica dust. - X-Ray Examination. Long experience in interpretation of roentgenograms of silicoties with varied exposures may enable one t.o_.conjecture with a reasonable degree of accuracy the general type of exposure. Large amounts of nonsiliceous or silicate dust in the mixture tend to induce perilymphatic deposits of the linear type. Free silica intensifies this reaction and causes it to become fibrous. At times hyaline nodulation occurs, perhaps when there is enough free silica in the dust, but this reaction is atypical. Gross examination of the modified silicotic nodules may reveal heavy deposition of pigment with or without dense fibrosis. With a hand lens hard elevated nodules may be seen in the centers of some of the pigment deposits. See Figure 8. -- Microscopic Examination. On microscopic examination it will be seen that many of the nodules consist ofnothing but coarse, heavily pigmented fibers devoid of organized arrangement. Such nodules max- have Irregular peripheral extensions, which fuse with those of others. (This fusion of.nodules may be partly responsible for the appearance produced in the conglomerate reaction.) 1 -1 " tl i < ! j ' i { j; jb !'[ DUP 0813725 DU 009703 lltflMUBiiaHi mu XI.O I Sntinhl:' Sobri/.w ' l,urn : t nr., ,i;i Lynn-* X-lt'ih/ E.aimiiiiiliuii. \-ruy i\nmin:ii 3 -lam- i~->;.> t < ! nr biliii orally -yn,inclrir.-il m:i--i\< .-hailouv u-tially '.alyyl in '; uppur !iai; >t 'hr lung... 1.n,(1 illH`- ill (hr lower lliinl. Tll'-e !h; -- ivt!_>lui`; - may i Vrml il'nm llir innl in ihr pleural Mirl'iiev. nr they may lit- T-.-p ill the ;Mivnchylna, Serial x-ray- may .~ii<i\\ that the lesions remain stationary over aperin.i ni live to -ix year-; or they may -how an increase in .size on successive pictures UUltin'.ately central rarefaction. interpreted as cavitation, may develop with subsequent evidence ni infection in other part- of the lung (see Figures 9 and 10). Gardner14 presents the Pillowing working hypotheses with regard to conglomerate lesions: '1. In tuberculo-silicosis the infection may hca! -o completely that its tuberculous origin is no longer recognizable. Such an outcome has been ub-crveil in experimental animals exposed to ferruginous chert and infected with attenuated tubercle baeilfi. "2. Conglomerate lesions in the upper lung fields, particularly when they are bilateral, are in the great majority of cases due to an underlying tuberculosis in healed or latent form. In persons not exposed to dust, bilateral disease in this location proves to ho tuberculous in 95 to 9S cases out of every hundred, and even unilateral disease can safely be considered tuberculous in 90 per cent of cases. ` 3. Large isolated or bilaterally .symmetrical eonsrlomeratiuns in t he lower lungs should be considered tuberculous unless this origin can be excluded. In that ca-e the possibility of organizing pneumonia due to Friedlander's bacillus or other organism? should receive consideration. "4. The character of the fibrosis resulting from the combined activity of an infectious organ ism and silica dust with or without other minerals may suggest a relationship between the time of exposure to dust and the development of the infection. "a) When I he silicosis is already e-rablished lief,.re tiil>errui"-is supervenes the infection localizes in and about the nodules which retain their form but increa-e in size. Bronchial obstruc tion caused by the infection may produce widespread atelv msis with a consequent approximation of the nodules in the involved area. In such eases the uu'hiic? of large individual nodules in the re sultant conglomeration are distinct and clearly defined. "(b) When silicosis and chronic tuberculosis have developed -itmihaneo.usly the nodular character of the conglomerate fibrosis is less obvious. Nodules are pre-vat but they are surrounded by a matrix of more diffuse fibrosis produced by the action of the silica upon an organizing pneu monic process. "(c) When the scars of a healed infection are.already present before employment in the dusty industry, the inhaled particles accumulate in particularly large quantities in their immediate vicinity. Continued accumulation in the localized area produces many nodules, which are small because they are closely packed together but typically spherical in outline because there is no activity in the underlying infectious process to produce diffuse fibrotic reaction." Manj- patients with conglomerate silicotic fibrosis are dvspneic, but the toxic symptoms of the associated infection may be absent. This is reasonable, since healed tuberculosis does not cause symptoms and even active infections may be so well encapsulated by dense fibrous tissue that.no tissue reaction is possible. E. TCBERCULOSILICOSIS The relationship between silica exposure and the development of tuberculosis has been well demonstrated in the United States as well a.- in other countries where 44 L. U. Gardner, "Pathological AnatomyM_in Fourth Saranac Laboratory SymposiumOn Silicosis, B. E. Kuechle, ed.. Employers Mutual Liability Insurant. Wausau. Wis.. 1939. DUP 0813726 009704 PER CENT OF POPULATION WITH MINER'S PHTHISIS in 'r i\ mi. i vi > \ mis hi i ii i i l1 v rii is u. i>:-1. vm. . ibT `ii'lv I. i- i"-i 11 ' l>-h i'\|iitliv. 1 Hu- "I ilir fii.-i i k.-c! ilc-ii-im ni'i ml inn,' nl In* rel;i- ''"U ii' 'll ii ri'i 111 i'i - tn -i I it-a ilu>l c\|i(j.~iirc> i.~ imp: .ii ill'' a'irk "i' .Miivi'iitriii'iliitiik' i 1!ii:-- ' ,-n i'-vi in J )i i i<-a! !,v in I'l nil lv I 1. Ti.i- >ymiH'iniaiiii"uy ami vliitirtil fiiulaisi:-- in -ilicu'is ami in silicosis complicated Iiv tillii'iriiln^is have lieeu .saiinnarizcd in the National Silicosis Conference Report of the Committee oil Medical Control, and these have been condensed by Lanza46 as follows: SrB.IF.rnVE SYMPTOMS: Dyspnea--The complaint most frequently mentioned is shortness iil'breirh. Depending upon the extent of the involve ment. till?, varies from slight dyspnea, following exer- ion. in marked dyspnea upon the least exertion or even when at rest. The shortness of breath noted in silicones promts one peculiarity in that it is seldom accompanied by orthopnea, the individual being no more short of breath lying down titan when in an upright position. This may not be so, however, when silicosis is complicated by cardiac disease or by true Fit;. 11. Dust control and silicosis in South Africa. asthma. Silicosis Noted as a rule only after sudden or extra inser tion. Seldom so marked as to interfere with routine duties. However, in cases with extensive pulmonary fibro>t>. it may limit the individual's "Silicosis with infection If complicating infection is not widespread, may lx? no more marked than in cases of simple sili cosis but as~infection anti fibrosis increase, it becomes disabling, "Cough. Many silicotics complain of a troublesome cough. This cough differs from that resulting from simple irritation due to dust which clears up upon removal from exposure. When present, it is more pronounced in the morning or upon beginning work after a rest'period. Silicosis The rvpical silicotic cough is dry and nonpro ductive. It usually parallels shortness of breath in decree and may contribute to disability. Silicosis with infection The cough usually becomes more troublesome and is productive. The sputum varies from thick,, tenacious, mucous material to that of a foul, purulent or purohemorrhaeic consistency. Microscopic examination or animal inoculation frequently reveal tubercle bacilli or. in some cases, organisms of the fusiform spirochetal group. In advanced cases, coughing attacks are often.of such severity as to leave the individual exhausted.. Chest Pain. This symptom is complained of by a majority of silicotics. It varies from a feeling of tightness m the chest to the sharp pain typical of pleurisy. (Since chest pain is offered as a complaint in many conditions, it cannot be stressed as especially characteristic of silicosis.* * A. Mavrogordato. Pub. S. African Inst. Med. Research. Report No. 19 (19261. * A. J. Lanza, Silicosis and Asbestosis. Oxford TTnivT Press, New York. 193S. MMM* 4US r.i>\vAHI> K. D\IU \ i:il v *\ mpi'tm m of miii pit mH'^m.v Him . rnotv t hail a ^`tisi* of t iglit in*-- . ,r fr.-ling ot suii>0`rnal piv^Min- Finin' v pain i> m i\ < "1 a *'*;*[ii-m'; ,u t**<*# ion. 1' i- innva*- *i lv .no i . coughing ami may ! >h.Miv--ing in a*l\ao.'.-.j c;iM*> Wri, t-XU-llMVc Uilrrlioll. "If, '>)>!js.s. Trim lirtin.pt v m.- "''Itiom Ft.-at.!<' ly. t h** v'ltum inn\ 1.iu.nl--tirakr.l fulkiwing a >evnr <<>>iiiiiin5 a'tack. ll.'tm*p` \ m> mu-r aovay** ! '<:iM'l--:-"i ... suggestive of nihereulosis. "ili.osis Min-.uP w;*h Oeeaiuhai blood-sileaked sputum. May result May he die fir>t imliration of tuhemiloii> in- from alveolar rupture following sudden exertion_ feet ion. Mav he eonsequeut upon t he develop- in advanced rases. merit of pneumothorax. May orcasionaJIv hr excessive if cavities are present. *General Complaints. Weakness, loss of weight, digestive disturbances, night sweats, insomnia. dizziness, and edema of the extremities are not characteristic of uncomplicated silicosis but are apt to be present, if infection supervenes, especially when the infection becomes extensive.. "OBJECTIVE SYMPTOMS*. Changes in the general appearance are infrequent in simple silicosis unless far advanced. Such changes as._are manifested arc usually due to complicating '`onditions. Silicosis Silicosis with infection Early cases appear unchanged; in fact, it FT . The appearance sooner or later becomes that of common to find these individuals showing a chronic phthisis. The bony landmarks of the slight increase in weight, possibly because they thorax become prominent and there is an in* are less active. As the disease progresses, respir- crease in the anterior-posterior diameter of the atory.embarrassment is noticeable and there is-" chest, possible hypertrophy of the accessory a general loss of muscle tone. .. respiratory muscles of the chest, and in the linal stages, retraction of the supra and infra clavicu lar spaces. Cyanosis and clubbing of the fingers are not prominent except in those cases of lung standing, with cardiac disturbances. "Chest Expansion. Decrease in the expansion of the chest may be demonstrated in cases with extensive pulmonary fibrosis. Silicosis Silicosis with infection In early cases it is usually not possible to Decrease in expansion may not be noted in demonstrate decreased expansion. In advanced early silicosis with slight infection but as the cases, expansion may be lessened by 20 to 30 Y" condition progresses, a definite decrease is per cent but remains equal on both sides. --.readily observed. When infection is more pro nounced in one area of the lung, expansion may be more markedlv decreased on the affected side, particularly if there is pleural involvement. "Prolonged Expiration. In most cases, decreased chest expansion is preceded and later accompanied by a definite change in respiratory' rhythm. Close observation reveals that even at rest there is a distinct tendency to prolongation of the expiratory phase, which, as silicosis advances, becomes more marked. Following exercise, the silicotic may breathe less rapidly than the normal person under similar conditions as the lungs cannot be emptied rapidly enough to permit more rapid respiration; but although the respiratory rate is not so rapid as in the normal person, itfwill persist for a longer period. Silicosis Early in the development of a simple silicosis, prolonged expiration may be evident only after exertion. Later the degree of prolongation us-., ually parallels the increase in pulmonary. fibrosis. Silicosis with infection In cases of early silicosis with slight infection, prolongation of the expiratory phase may be no more marked than in simple silicosis. As the condition progresses and fibrosis increases, it may simulate characteristic asthmatic respira tory rhvthm. I a a 1 I r, t o 1 b a r iv )c l t id *a 1a t Ja ,d X If ! i DUP 0813728 DU 009706 aifipg; p-jjjiiiia as ami ^ja.,132 iilittlj^|||||Hi HI Vi ; \ ! ill-: \\ - \ ! !.>s nr m . I I' \ rmvvL n(MuW. 4i>y n ini >" m t >m> a t'h mn-'" uni. H * l'> lv pauu'Mn >M hr *-h Hi .\rvvr. wh.wr : :t I" a m \i- l.'.dkr d iv.r* - ill eX- Mati'Mii. on* ina> u>ir ov palpation ti.aT i;> >11 ion;.- i loti, the :tu' \i > -m 'l A.ili i** s11;*; 1 - *\ M:.- ;p . ridiM-ic*. n!` :wpiuif toil. - , .. \.| I,.ill-'' IlMlr.i ' u Ii 'aki-n plu'V. 'A hrsi Ui' i'f a'iil.* irctmui*' ai-nrruliv. ti-i\ ` i I !i;i' U* aii iinJva-- iu .................. w.O. I lull \Yltrtl im-'iTt.iH W r\T I'li-l W. Uftllr iV. : t U' U- 1< iucivaM'd aii*l M,t,a**i<.*iially iii**TI**i nu> tu;tv ! elicited. KxteitMve thickening ut` tin* pleura or pneumothorax may result in a decrease or absence ot' tactile fremitus over affected areas. "Pemwshu. There is usually an impairment of tlie percussion noted over the whole chest but unless one is narticuiarlv observant, this mav not be detected. Silk AS1S Silicusis witli infection Since impairment in resonance is general over all lung areas, it is difficult to demonstrate until advanced fibrotie cluing"* have developed. De crease in diaphragmatic excursion may sometimes he revealed by percussion. Increase in Joss of normal resonance. When massive areas of fibrosis have developed, this may amount- to absolute dullness over areas involved. Amphoric resonance may be dieted where there, is pneumothorax. Decreased dia phragmatic excursion may readily be shown in advanced infection. 11 Auscultation. . Breath Mjutids arc usually decreased in intensity and the characteristic prolongation of expiration is readily noted. Silicosis Decrease in breath sounds general and more marked as the condition progresses. Suberepitant rales, which clear up after coughing, are occasionally heard. Silicosis with infection Usually heard, some of the following: Persistent post-thssie crepitant anti subcrepitant rales; coarse rhonchi associated with productive coughing, wheezing or musical rales increased bv exertion and coughing, amphoric breath sounds over cavities and areas of pneumo thorax; pleural friction rubs occasionally." Part of the symptomatology associated with silicosis may be due to pathological processes other than fibrosis. Filley. Hawley, and Wright," using isolated perfused lungs of guinea pigs found that colloidal silica produced bronchia! constriction, although soluble silica did not. This at least suggesEsdhat part of the disability' in silicosis may result from bronchial constriction. Such findings also offer the first rational approach to a basis for explaining the improvement of symptoms in patients with silicosis after aluminum therapy. The inability of soluble silica to cause bron chial constriction, however, raises a question as to the validity of the assumption that this same reaction occurs in workers exposed to silica. _ That exposure to silica dust may increase the tendency to contract respiratory diseases other than tuberculosis has been suggested by Sayers.1* He concludes from a survey of the mining industry that: _ "1. The principal pulmonary diseases to which the miner is subject are bronchitis, influenza and pneumonia, pulmonary tuberculosis, anthraeosilieosis, and silicosis. "2. Statistics indicate that much higher morbidity and death rates from pulmonary diseases are experienced in dusty than in nondusty industries, especially where silica dust is used or pro duced. "3. Investigations by the Public Health Service reveal that hard-coal miners suffer a high 4TG. F. Filley, J. G. Hawley, and G. W. Wright, J. Ind. Hyg. Toxicol., 27, 37 U945). 4* R. R. Sayers, VS. Bur. Mines Circ. Xo. 7146 (1941).,_J DUP 0813729 DU 009707 'll III iiin.-- ll :nliii''li/;i mi.` ,1. Iii ini.'* C:i :u,.l IlKIti l ill' . .1; '11:1111> :mI'll!n inU'J-i'iml I iilin u- i' i*ii^-iii' 1 in pui-ui1' ii'iii ,11. 1 -I- .Min .m.' i \ l.llW \ |>|> I, |l \ l( ! 1 .-''iii in 'in- a nut nia': F. IPACXOSIS 1)1 SI Lit i ISI> Tii uiaU'' u definite dingim-i- "I rilim-i- uue mu-( li;i\ e u a rni-m hi mm: tlie appearance cluti'iU'lic of fibrous nmlulatinn and >, prim; m i |{c exposure to significant amounts of dust containing I'rcu -iliea. 1 iur<ini`i ' piu,; the importance of an occupational history since a nodular or mottled \-rav paHiaii may occur in other conditions, including so-called "arcwolder's .-idem.-i.-" and li.'intosis, in which no fibrous nodulation can lie demonstrated by pathological examina tion. Organic iron from the blood may cast shadows that simulate silicon.-. A -unk ing example of the effect of blood is seen in roentgenograms of men trapped under ground in mine explosions; serial films demonstrate the sudden appearance of fine modulations, which disappear in a few weeks,. Pulmonary sarcoidosis, a tuberrlelike infection of unknown cause, occurring throughout the population at large, nmv pro duce similar shadows. Another condition to be considered is miliary calcification of the lungs, commonly called "wheatena"; the dense, not uniformly scattered noduie.are thought to represent a stage in the healing of some infection of unknown nature. Likewise, cardiac decomposition may, by the accompanying pulmonary congestion, produce an x-ray picture that somewhat resembles silicosis. All of this suggests the difficulty in diagnosing silicosis unless full detail,- of all findings are available to the examining physician. G. LVALUATIOX OF DISABILITY IX SILICOSIS 1. Stah-men! of the Problem To both management and labor the term "silicosis" has become nearly synon ymous with the term "total disability." Accordingly, some time should be devoted to the details involved in evaluating pulmonary "ability" or "disability" in this diseaseAActually, uncomplicated silicosis Is almost notorious for its lack of svmptoms even in relatively advanced stages. In fairness to both employer and employee it is necessary to go beyond simple diagnosis. In examining a patient with, silicosis an attempt should be made to answer certain questions: Does his chest x-ray suggest that he has silicosis? Does he have a history of sufficient exposures to free silica dust to account for any roentgenographie changes present? Does he have complicating tuberculosis of other infection? Is he incapacitated or disabled by the condition? The first three of these questions are usually answered by the examining physician. Too frequently, however, not enough attention is paid to the fourth question, con cerning disability. As a result of this an employee may be dismissed from work " L. U. Gardner, Am. Ind. Hyg. Foundation, Annual Meeting, Pittsburgh. November 14. 1945. D C TJ O 00 CO vl co o DU 009708 _--iSSiasIL:. .geatiffl, DUST IN THE fAI^ATIliN ill- m iL'I'ATIi'N AE DISEASE 501 unjustly i.r lie may collect confutation l'<r disibility .m.iu.-ily. I .,r :m>. -i:>-:.!-l.ii,iil purposes :)< well as for the purpose ,f fitting each alilitiuri fiuployec inio work within his capacity it is helpful to have ivords of progress on individual patients over a prolonged period, preferably many'years. Industrial medicine may make some contribution to an understanding of pulmonary physiology by accumulating specific data on large groups of people, and in the final analysis this can best be done by men closely associated with employees, with management, and with the problems of industrial medicine. \- _ We have already summarized the diagnostic criteria for silicosis and have dis cussed the findings indicative of complicating tuberculosis. It is necessary to bear in mind the fact that cardiac insufficiency, anemia, and other diseases'may produce symptoms not readily differentiated from those of pneumoconioses. In establishing a diagnosis of decreased functional capacity from a pneumoconiosis, these diseases must first be ruled out. Dyspnea as a symptom of disease has long been recognized by all physicians, and diagnostic aids such as ordinary laboratory procedures, electrocardiographic studies, and other tests are available for diagnosis of complicat ing diseases with pneumoconiosis. After a definite''diagnosis of silicosis has been established, physiological measurements of pulmonary function may be used as an aid to the usual clinical examination in determining the extent of disability. 2. Pathological Physiology and General Principles A great deal of work on the physiology of respiration has been done in this country and in Europe. Contributions of especial significance have been made by Cournand and his associates and by McCann and the group working with him. These sources have been drawn upon heavily for the material in this section. Cournand and Richards''1' have suggested a simple, yet useful, classification of the types of pulmonary insufficiency and discussed the. mechanisms involved in each type. Their grouping is as follows: {l) ventilatory pulmonary insufficiency, which is concerned with defective air movement into and out of the lungs: (2) respiratory pulmonary insufficiency, which is concerned with defective gaseous exchange be tween the blood and alveolar air; (3) combined ventilorespiratory insufficiency; (4) combined cardiopulmonary insufficiency. Ventilatory Insufficiency. The ventilatory aspect of pulmonary function is largely mechanical. Adequate ventilation is dependent upon the movement of sufficient air into and out of the lungs, that, is, upon a breathing capacity great enough to supply the body with the oxygen necessary for its needs. The flow of air to and from the lung is dependent on the chest bellows, regulated by a well-co ordinated neuromuscular mechanism, the tracheobronchial pulmonary air passage way, and the state of pulmonary tissue, particularly as related to the amount of elasticity and fibrosis. The breathing requirement, or the amount of oxygen required at any given " A, Cournand and W. Richards, Jr., Am. Rev. Txtberc., 44, 26 (1941). i f DUP 0813731 DU 009709 KDWXRIi ! . via.- - .uii jnviab"ii.-ni. posiure, oxygen an.; -..rjon d; . ..... ; "i ... :>t; mil nervous -tatcs, and c;xt.r> i'i'. I: i- prim:.: MW: :.V.1 :!e\ -1 is. ,.:rion of the respiratory center.-. 'i'i.v . : i.m.i :gu in ventilatory insufficiency i> it;. , ivai nia : Ifni.,: ' :.t -vm; ' :n, d.. -plica. /ujfp. iiury Laufficuney. Tiie respiratory function i> com-cna.-d with im.-eous interchange between the alveolar air and the blood. 'Ihis is dependent upon the degree of ventilation of the individual alveoli and the relative number of alveoli that are well ventilated, the number, size, and distribution of capillaries in contact with the alveoli, and the rate of blood flow through these capillaries, as well as the oxygen-carrying capacity of the blood, the gradient of pressure of respiratory gases across the alveolar-capillary partition and the physical properties of this partition. The cardinal sign in respiratory insufficiency is cyanosis. However, if the insufficiency is slight, cyanosis may not he present and hypercapnia may predom inate. In such instances measurements of oxygen removed from inspired air or carbon dioxide added to expired air or of the oxygen saturation of arterial blood mav be necessary to determine the actual extent of the respiratory failure. Cardiocrrculatory Insufficiency. The cardiocircuiatory function may be affected along with the respiratory and ventilatory functions. The causes of disturb ance in the heart and circulation that may be encountered in connection with chronic pulmonary disease are: hypertension in the pulmonary circulation and subsequent right-heart hypertrophy; obstruction to the flow of blood by displace ment of the mediastinum, increased pressure in the thorax, or disturbance in the mechanics of breathing; decreased cardiac function due to the effects of anoxia on the heart muscle and cardiac regulatory centers; and independent heart disease of any type. It must a'ways be borne in mind that patients with heart disease respond to pulmonary function tests similarly to those with pulmonary fibrosis and emphy sema."1 The fact, demonstrated by Enzer, Simonson, and Evans,52 that recovery of pulse rate during and after exercise is of little value in the segregation of normal persons from those with silicosis may be significant in differential diagnosis of purely pulmonary disease as compared with cardiac disease. However, Enzer himself points out that his tests were performed by subjects who worked until fatigue . developed. Enzer's normal subjects actually did more work than his silicotic pa tients before fatigue occurred, which may account for the lack of difference in the pulse rates. He found, nevertheless, a definite trend toward prolonged recovery time in his patients when certain types of work were done. At any rate there was a greater correlation between lung disease and pulmonary functions than between lung disease and pulse rates after exercise. We believe that information based on some standard form of exercise such as the Master Two-Step Test,53 which has been " N. L. Kaltreider and Wm. S. McCann, J. Clin. Investigation, IS, 23 (1937). " N. Enzer, E. Simonson, and A. M. Evans, J. Ind. Hyg. Toxicol., 23, 147 (1945). " A. M. Master and E, T. Oppenheimer, Am. J. lied. Sci., 177, 223 (1929). DU 009710 iipjj?ii mw ' -SriSijiTij aaftsfi il. Ill 4iiai:Lirii-,IiiiiaaB7Mit2lilBiflii:jim;. Jaiatati invr i.\ thl i .a'.'.ri'is ok oo.tiutiovu. ;>iv!:.v--i. ")<)3 aivnilly ,-t andardized for age and sex. would be helpful in making such an analysis, i A fundamental concept necessary to an understanding of symptoms in any disease is that symptoms develop only when the adaptive mechanism ot the hotly is ret (Hired to function in a degree beyond that normally required for adaptation. In other words, symptoms appear when the adaptive mechanism is put under strain. This is particularly true in pulmonary disease. As an example, Harrison54 found that "a person becomes short of breath when his actual volume of breathing be- ,. comes more than a certain, fraction of his maximum possible volume and the closer the actual volume approaches the maximum possible ventilation, the more severe the dyspnea becomes." Accordingly, measurements that indicate the relative degree of ventilation or aeration required under given circumstances in comparison with the total ability to ventilate or with other known lung capacities are of more value than measurements that indicate merely a particular capacity. Likewdse, as pointed out by Hurtado and Boiler,55 there may be wide normal variations from the median when any one function such as vital capacity or residual air is measured, whereas if this function is taken as a percentage of total capacity the normal variations are much closer to the median. Thus again is demonstrated the value of expressing a capacity in terms of percentage of another capacity. 3. Terminology A serious drawback to the proper comparison of different series of observations on respiratory functions has been the use of different terms and even of different meanings for the same term. It is therefore essential to adopt, if possible, a single nomenclature in order to have a clear understanding of the subject. Christie and Meakins56 have proposed a fairly satisfactory usage, which we shall adopt here, except for the suggestion of Hurtado and Boiler that the term "functional residual air'1 be replaced by the term "mid-capacity," and with the addition from later authors of terms describing ventilation and its components. The classification as suggested may be summarized as follows: _ 1. Residual air is the amount of air remaining in the lungs after fullest possible expiration. 2. Reserve air is the amount of air expired from the mid-capacity position to the maximum possible deflation. 3. Mid-capacity is the amount of air remaining in the lungs after a normal expiration. Christie and Meakins speak of this as the resting respiratory level. Hurtado and Boiler comment on this as follows: "The term 'functional residual air' is synonymous with this term. It appears to be more convenient, however, to use the term mid-capacity as being more descriptive and more com monly used. The term 'functional residual air' may be easily confused with residual air, or it may suggest that it is a subdivision of the latter. Mid-capacity represents the sum of the residual and reserve air." 4. Complementary air is the volume of air inspired from the position of mid-capacity to that of the maximum possible inflation. It includes the tidal air. 5* K. R. Harrison, Failure of the Circulation. Williams & Wilkins, Baltimore, 1935. " A. Hurtado and C. J. Boiler, J. Clin. Investigation, 12, 793 (1933). "R. V. Christie and J. C. Meakins, J. Clin. Investigation, II, 1099 (1932). | i DUP 0813733 DU 009711 504 KDWAUD L. DART 7. 7 m! ':i :i. Vi':; i;v. >f -h.- nim;ii' -:i::i rc-ridu.il air .-m l r moving in out during <jsih-t i.un in t.'li.'V:'- and M-iAin- Ml r In I'im-oi,: o; si mien hat more dynamic measurements. Command and Richard.' ami Kahreiiicr and Mc< :nmv have dc.-cribed ventilatory measurements. TIiom-. >v Ivlieve. shouldJie added to the above terminology: 8. Minute volume is the volume of air ventilated per minute under any givrn I'onditionis. T!n> is the same as the breathing requirement. 9. M-azimum ventilatory volume is the maximum volume of air that can be ventilated per unit of time (usually expressed in liters per minute). This is svnonomous with the maximum breathing capacity of Cournand and Richards.'0 -- 10. Breathing reserve is the excess of breathing capacity beyond the actual ventilation in anv given state, that is, maximum minute ventilation minus minute ventilation. This may be expressed as percentage of maximum ventilation. 11. Ventilation equivalent for oxygen is the amount of air ventilated in order to yield 100 ml of oxygen to the bod}-. 4- Tests for Ventilatory Efficiency The ventilatory function is tested by determinations of chest capacity and breathing volume. Probably the most revealing and important measurement is that of maximum ventilatory volume, at least when it is used as a basis for comparison with other measurements. Actually, Peabody57 has shown that dyspnea is more1 closely related to vital capacity than to total ventilation. There are three common methods for the determination of maximum ventila tory volume: (a) maximum ventilation in exhausting exercise51; (b) maximum ven tilation with carbon dioxide rebreathing58; (c) maximum ventilation by performing maximum ventilation effort, using voluntary rate and volume.50 The method employed by Kaltreider and McCann appears to give rather uni form results. They measured the air breathed from a spirometer during the last one and one half minutes of exhausting exercise. A test requiring this much co-operation on the part of the patient, no matter how valid its results, is somewhat beyond the scope of what may be employed in general in the examination of industrial patients, whose subjective reactions are extremely variable. Furthermore, the results ob tained by this method (average 71 liters per minute for normal male subjects) are somewhat lower than those obtained by the voluntary forced breathing test of Hermannsen59 as. adapted by Cournand and Richards50 (average 154 liters per minute for males, 100 for females). The method of carbon dioxide rebreathing is rather difficult to control in the ordinary, outpatient clinic and has the added disadvantage of the inaccuracies that develop during rapid breathing in a closed system. "F. W. Peabody, Harvey Lectures, 12, 248 (1916-17). "R. Goiffon, R. Parent, and J. Waltz, Ann. med., 35, 362 (1934); 3B, 57 (1934). ** J. Hermannsen, Z. ges. erptl. Med., 30,130 (1933). DUP 0813734 DU 009712 IK'ST IN THF. CArsATIuN tWP '.TioXAI. I' 505 The voluntary rapid- and d<vp-lking metluHi drsviiOc -, !ir. ' by iDncunn- sen"s and later adapted by Cournand, lthhurdr. and Darling' Oy \\ right' abo depends on effort by the patient. There i.-. however, greater hke:ih"..d ol obtaining reliable results by this method than by those in which maximexlmuying elbut is required. The technique has the advantage of being rather s;::ipie to pernrm. and according to the author its results are readily reproducible. In this method maximum deep breathing is measured by having the patient breathe turn a spirometer as deeply and as rapidly as possible but with emphasis on depth - that the individual breaths are somewhat short of vital capacity. The patient is tested again for rapid breathing. This time he breathes as rapidly as possible and as deeply but the em phasis is on rapidity. In these tests the author states that a surprisingly uniform pattern is produced. The breathing is carried on for 12 to 15 seconds. As a substitute for spirometry the exhaled air may be collected in a Douglas bag.60a The equipment essential for this technique includes only a close-fitting face mask, a two-way valve of low resistance, a two-way cock, some large rubber tubing, a large Douglas bag, and a flowmeter such as_jnay generally be found in a gas laboratory. The subject inhales room air as deeply and rapidly as possible, but with emphasis on depth, and exhales directly into the Douglas bag for a period of thirty seconds. The volume of air in the bag is then measured. It is desirable to have several men perform this test in a group so that maximum effort can be fostered by competition. Results obtained with this type of maximum effort are ordinarily more consistent than are results obtained by measurement of tidal air. in which psychic factors play a dominant role. When maximum ventilation is used as a basis for comparison, notation should be made of the method used in determining it so that the results may be compared with those found in the literature. The functions usually compared with total breathing capacity are vital capac ity, minute volume and pulmonary reserve, at a given amount of work or at dyspnea. Vital Capacity. Peabody57 in a study of dyspnea in patients with heart disease, and Hurtado and his associates61 62 studying patients with pulmonary fibrosis and emphysema, showed that the degree of dyspnea was closely correlated with the vital capacity. Harrison and his co-workers63 found that the degree of dyspnea in heart disease was more closely related to the expression total ventilation than to vital capacity either of these factors alone, and this has been corroborated by Kaltreider and McCann.51 Vital capacity can be determined simply by spirometry. Various formulas "A. Cournand, D. W. Richards, Jr., and R. C. Darling, Am. Rev. Tuberc., 40, 487 (1939). ""G. W. Wright, personal communication, 1947. "A. Hurtado, W, W. Fray, N. L. Kaltreider, W. D. W. Brook;, and W. S. McCann, J. Clin. Investigation, 13,102 (1934). " A. Hurtado, N. L. Kaltreider, and W. W. Fray, W. D. W. Brooks, and Wm. S. McCann, J. Clin. Investigation, 14, 81 (1935). "T. R. Harrison, F. Turley, E. Jones, and J. A. Calhoun, Arch. Internal Med., 12, 833 (1931). DUP 0813735 DU 009713 500 have ui.-o been devised. based on height. werTnt. budy Mirfaee area. and x-ray measure mont,- in currolati'm with i,v. I'lu'.-t Measurements,': The closest correla tion of predicted values with actual findings wa- obtained by Ilurtado and Frav with the chest measurement.-, and x-:uy rindint>. However, it would appear some what simpler and more accurate to use spireme!ric methods tor routine work inas much as the equipment is needed for determinations of total ventilation. Ivaltreider and McCann found that the vital capacity, the arterial saturation of the blood, and the ability to expand the chest decreased as dyspnea increased. Dyspnea is experi enced when the expression t0<-af ^ emulation .g greater tiian (.ot:a[ ventilation vital capacity determined by exercise method), and when this value is exceeded at low levels of work it is an indication of pathological dyspnea. The maximum ventilation is only roughly proportional to vital capacity in normal subjects, but in patients with pulmonary disease the relation is closer. Minute Volume. The significance of minute volume is rather striking when it is considered as the breathing requirement of a person at a given time and under given circumstances relative to rest, work, emotional state, and metabolism. This concept of minute volume is ably developed by Cournand and Richards.50 Minute volume may be measured with a spirometer or by collecting air in a Douglas bag. This measurement is important because from it and the maximum ventilation we obtain the breathing reserve (Maximum Ventilation minus Breathing Require ment). Minute volume may be compared directly with maximum ventilation as a percentage, i.e., (minute ventilation)'(maximum minute ventilation) x 100. In studies by Ivaltreider and McCann51 it was found that dyspnea was first noted by normal individuals at values between 46 and 70 per cent, with an average of 59 per cent. In patients with pulmonary disease the percentage often may exceed this value and at rest may even be well above it. Pulmonary Reserve. The excess breathing capacity beyond the actual ventila- tiom (minute volume) in any given physical state is the breathing reserve. Cournand and Richards have discussed this concept as follows: The maximum breathing capacity in each subject is a fixed value and the breathing reserve varies inversely with the breathing requirement. For comparative purposes this may be expressed in per cent of maximum breathing capacity. Thus, in a subject whose maximum breathing capacity is 150 liters per minute, and ventila tion at rest is 5 liters per minute, the breathing reserve is 150 -- 5 = 145 liters; and the ratio breathing reserve 145 X 100 at rest = ^ x 100 = 96.6 per cent. maximum breathing capacity Similarly, in the same subject, if the ventilation during exercise is 25 liters per minute, the reserve is 150 -- 25 = 125 liters per minute and the ratio is 83.3 per cent. In 37 patients out of 105 who were given a standard exercise test without " A. Hurtado and W. W. Fray, J. Clin. Investigation, 12,807 (1933). D C TJ O 00 CO -sj W 0> DU 009714  v ri* s vi. him: \m: .',07 exporienrmg ily.-imm. rit,. ix^crvc .even in the first minute folluwing exerci.se) was 73 per com >:'; he maximum breathing capacity. Although d\mpncu was complained of by a few patients when the.reserve was 75 per cent of maximum breathing capacity, the threshold of dyspnea was almost always, between GO and 70 per cent of the maximum breathing capacity. It is of interest if possible to predict, from findings in a patient at rest, whether dyspnea will occur easily. These authors found that if breatliiuir reserve X 100'at rest is above 93 maximum breathing capacity no dyspnea will develop with the standard exercise used, 7 Tents for Respiratory Insufficiency The respiratory function is best evaluated by determining the oxygen used from inspired air, the carbon dioxide given off in expired air, or the oxygen content of arterial blood, Ventilatory Equivalent for Oxygen. The oxygen used is usually determined as the ventilatory equivalent, that is, the number of liters of air breathed in order to supply 100 ml. of oxygen. Such measurements can be made by analyzing samples of expired air for their carbon dioxide and oxygen content by a method such as that described by Van Slyke and Sendroy,65 or a fairly accurate determination may be made by rebreathing an air-oxygen mixture from a closed system spirometer, re moving the carbon dioxide chemically and measuring the oxygen used by the de crease in the spirometer content. There is considerable variation among normals in oxygen consumption, and it is probable that oxygen saturation of arterial blood is the better indication of aeration of blood as it passes through the lungs. Oxygen Saturation of Arterial Blood. When lung capillary perfusion by oxygen is satisfactory there is usually a high percentage of oxyhemoglobin in the blood and this usually does not fall below 95 per cent even with severe exercise. (See Oxygen, Volume II.) A decrease in oxygen saturation of arterial blood may be due to various causes. In chronic pulmonary disease anoxemia may be caused by the flow of blood through capillaries that are unventilated or poorly ventilated. In heart disease pulmonary congestion may produce inadequate capillary ventilation. Also in heart disease the general circulation may be so retarded that the blood is seriously de pleted of oxygen when it reaches the lungs. Determinations of the oxygen and car bon dioxide contents may be performed on the Van Slyke apparatus. This is, of course, somewhat too tedious and time-consuming for routine work in industry. Recently there has been developed a spectrophotometric method66 for determining the oxyhemoglobin count of blood in the ear lobe. The procedure is simple and is apparently within the same degree of accuracy as chemical methods. It might well be adapted for investigations into blood oxygenation as there is a time lag of only about five seconds and continuous readings may be obtained. " D. D. Van Slyke and J. Sendroy, Jr., J. Biol. Chem., 95, 509 (1932). " G. A. Millikan, Rev. Sci. Instruments, 13. 434 (19427. DUP 0813737 DU 009715 50 <? edwaisd e. part F..o re:sc Texts in' licncrnl Tests depending upon either maximum effort or moderate effort a:-.- emp, .\V.; in measuring pulmonary or cardiac efficiency. Maximum effort or ptT : ;o and dyspnea tire- sometimes used and have their place in the study ulna mar. physiology. Fur a study of the effects of maximum effort, the most '..v.sfa. ti.rv equipment for measuring the amount of work performed is the bicycle ergometer. However, for most investigations in industrial clinics moderate exercise may give valuable information as to the state of the patient. In moderate exercise the patient may b; asked to squat, hop fifty times, lift a weight repeatedly, etc. None of these tests, however, is weighted to take into consideration normal variations in age and sex. In this respect the Master Two-Step Test67 has definite advantages as it has been well standardized at least for cardiac function as to age and sex, is simple tu perform, and is almost quantitative in terms of foot-pounds of work per given time, 7. Summary An attempt should be made by plant physicians and those charged with the management of workers in industries in which silicosis is a hazard to determine actual disability in patients. By the use of simple respiratory equipment, such as a slightly modified basal metabolism apparatus,60 the vital capacity and maximum pulmonary ventilation can be determined. The breathing requirement at rest and in standard exercise can be measured with a Douglas Bag or a Tisot Spirometer. Such examination should be possible within a reasonable time even for a busy indus trial physician, especially if clerical help is utilized for occupational history taking and nurses are available for the routine portions of the examination. If ventilation is measured by modern methods commonly employed industrially by physicists, as deflection of a wire or alterations in heat conductivity, pneumotachograms6s'6'a can be included in the data without requiring any additional time. In this way con siderable information on a new diagnostic procedure for lung and chest diseases (measurement of changes in rate of air flow during the different phases of the respira tory cycle) might be obtained. True, the appraisal of disability by pulmonary func tion testsjis no substitute for appraisal by sound experienced clinical judgment; but it furnishes records for year by year comparison, and it gives definite facts on which to base medical-legal opinion as to disability. In any consideration of disability in pneumoconiosis one fundamental concept must be emphasized. From an economic and sociological point of view it may be wrong to consider a patient as having dis ability if experience demonstrates that he is capable of doing his daily work. This is especially true if conditions are such that aggravation of an existing condition is unlikely. A. M. Master and E. T. Oppenheimer, Am. J. Med. Sci., 177, 223 (1929). "A. Fleisch, "Neuere Ergebnisse uber Mechanik und propriozeptive Steueritng der Atmungsbewegung." Ergebn. d. Physiol. 3S, 249 (1934). "" I/. Silverman, J. Ind. Hyg. Toxicol., 28, 183 (1946). D C O o 00 -W4 W 00 DU 009716 JMfei,j MMfek .;.,L~JjalaliiTILJBiiaai ICJri HapfT aTM mm DUST IN THE iaL.'ATIciN uh DCl'UDA IlON >.L DlsUA^K .">( M.i If. COXT^'lI. OF SILK us IS IN' IN!>I'S i'll'i V7, Entfinciriny Cojitrot The fundamental basis for blicosis prevention is engineering control. Enclosed processes, exhaust ventilation, weKjnethods. and other engineering techniques can be used to insure safe concentrations of du.-t_in the air breathed by w-i.rkinen. Engineering control of dusts is discussed in Chapter Ten. Personal protective equipment such as filter respirators and air-line or suppliedair respirators (See ChapterSjPourteen) will under some circumstances afford protection, but such devices are poor substitutesj'or air sufficiently free of dust to prevent the development of pneumoconioses. 2. Medical Control All employees with potential exposure to dangersous concentrations of free silica should be given annual medical examinations. These should include x-ray films of good quality competently interpreted, clinical examinations, laboratory examinations in cases where it is necessary to determine infection or concomitant disease such as cardioeirculatorv dysfunction, and pulmonary function tests. When there is a question of tuberculous infection, the patient should be examined with sufficient frequency and detail to determine the exact status of the disease. The type of routine x-ray examination used will be a major factor in determin ing the cost of the program to the medical department. Most roentgenologists feel that the standard 14-in. X 17-in. film is necessary for definite diagnosis. However, as a screening procedure, several less expensive films are available. Paper film is sometimes substituted for ordinary transparent film. Roentgenograms of this type usually show too little detail to be satisfactory even as a screening process. Roent genograms of the 35-mm. or 4-in. X 5-in. size, on the other hand, may be used rather successfully for differentiating normal from pathological chests. The 35-mm. film is cheaper and requires less time for developing than the 4-in. X 5-in. It must, however, be used purely as a screening device^ as there is not sufficient detail for diagnosis of abnormal findings. Films of the 4-in X 5-in. size frequently may be interpreted directly, necessitating the re-x-raying of fewer employees. The approximate relative cost of the different sizes of film in the amounts used by large industries is as follows: Size of 61m Cost per patient (approx.) 35-mm. film.................... ..........,,........ 4-in. X 5-in. film................ .................. 14-in. X 17-in. film.................................. 414 <f 7t 80 t The number of employees to be examined would alter this but the relative costs should remain fairly constant. The value of the routine chest survey in the control of silicosis cannot be overstressed, and if photoroentgenograms are used for screening purposes costs may be reduced to a level that can be absorbed by most industries. am DUP 0813739 DU 009717 510 kimvard e. dart i: '! ..ii-'i "i' nut .\ ^ jrlv;; i;s.n i .. .,:'y mid iv. purer great cure or. the part ul tin- x:i:nin:n_ ; t,-.-ient'>, as v.eli uf a ihei'numi understanding ot' working conditions in tin- particiii;.;- retipa- tion ui.'l a :i a pi i; <::* rii n. nt puJ *!i(r health and. mum! fCsnnnsk-duy 1 e u - . t|>(> dividiidrand V.. hi' ,i..-iji'iniis. Asa guide tor management of the ; ati--n* 1. dii, or itil>.*: i.m./.a'-' ha,' i'.rnrulr*toil the toll.nv.tt" rules tor 'i.e vari. -ctieral groups 'i-on : "I, Partial disability due to silicosis without infection: ";ai May continue at usual occupation, if environment is satisfactorily controlbu a., regards dust concentrations and tuberculosis contact; "b; Degree of fibrosis and rate of development may require that the individua: -ook loss arduous employment and avoid even minimal exposures to silica-containing atmosphere. ' ll. Partial disability due to silicosis with complicating pulmonary infection: "iaj Primary silicosis. Infection mild and nontuberculous. In most instances, after successful treatment of nontuberculous complicating infection, may be allowed to return to usual work, provided environment under which they are working is safely controlled. "(b) Primary silicosis with pulmonary tuberculosis as complicating infection. Those individ uals with silicosis who develop pulmonary tuberculosis are considered totally unfit for further employment in an industry affording even minimal exposures to free silica. This disability is obviously total so long as active tuberculosis is present. Following successful treatment, these cases regain their health to the point where they can be safely employed at other work." 3. Aluminum Prophylaxis and Therapy The use of aluminum for the prevention of silicosis was first reported by Denny, Robson, and Irwin70 in 1937. At about the same time similar investigations were un dertaken by Gardner and his associates. Since that time considerable attention has heen focused on aluminum and its compounds both in laboratories and in clinics. Tabershaw and Tebbens7` summarized the principles that have evolved from laboratory work on both finely divided metallic aluminum and amorphous hydrated alumina as follows: If alumina and silica localize in. the same phagocytic cell the effect of the silica is neutralized. Further progression of the tissue reaction character istically produced by silica is then arrested. Mature silicotic nodules become static, and immature lesions (inflammatory and early fibrous changes) are resolved. Aluminum may remain in the tissue and protect the individual for a long period-- over a year. Aluminum does not ordinarily produce toxic effects in the tissues, al though it appears to increase the susceptibility of experimental animals to tubercu losis when large doses are given. Occasionally, allergy to aluminum has been reported,72 but this is apparently a rare occurrence. Denny, Robson, and Irwin have preferred to use metallic alumi num, but Gardner has found that certain hydrated aluminas are more satisfactory. McIntyre Research Limited, the United States agency created for licensing the use "A. J. Lanza, Silicosis and Asbestosis. Oxford Univ. Press, New York, 1938, p. 56. "J. J. Denny, \V. D. Robson, and D. A. Irwin, Can. Med. Assoc. J., 37, l (1937): <0, 213 (1939). 111. R. Taberahaw and B. D. Tebbens, J.Ind. Med.. 14,709 (1945). "L. H. Cotter, J. Ind. Hyg. Toxicol., 2B, 7 (1944). D C o o 00 w o DU 009718 Dl'ST I.\ THE l\U SATION OF OCCUPATIONAL DISEASE Ol mi aiumitmm by physicians tor therapeutic or prophylactic purposes, uiaaes oim in.-i nllic aluminum available. Some investigators, notably Iiannon/'' have reported marked success in the treatment of patients with severe disability. However, when purely tibjeflivo criteria have been used to measure disability the results have been 'imieuhat les> striking. Gardner. Dworski, and~Delahant71 have suggested that variat ions in response to aluminum therapy may be due in part to the nature of the dust that lias caused the silicosis. They suggest that dust which is primarily free silica may react with aluminum more readily than dust which contains high per centages of iron. The use of aluminum generally in industry for the therapy or prophylaxis of silicosis should be contemplated only with the utmost caution. I. ASBESTOSIS Asbestos is a hydrated magnesium silicate. More than 90 per cent of the raw mineral used in this country and Great Britian is produced in the Canadian chrysotile mines. Asbestos is used in two general types of manufacturing processes. It may be used either by itself or mixed with other insulating materials such as diatomaceous earth for fireproofing, packing, or insulating; or it may be combined with cotton and woven as a textile for fireproof and heat-resistant clothing and other substances. Lanza78 estimates that there are about 10,000 persons exposed to asbes tos in the United States. Most observers feel that the incidence of asbestosis in American asbestos workers is quite low\ Asbestosis has, however, been reported more frequently in England and Canada. Lanza, McConnell, and Fehnel76 concluded from their study of asbestosis that: Prolonged exposure to asbestos dust causes pulmonary fibrosis different from that produced in silicosis and demonstrable by roentgenogram. Clinically it appears to be milder than silicosis. Definite cardiac enlargement frequently was found to be associated with asbestosis. A predisposition to tuberculosis, due to asbestos dust, was not indicated al though it was not known to what extent asbestosis may add to the mortality from pneumonia and acute nontuberculous pulmonary infections. Symptoms. The onset of asbestosis, as of silicosis, is slowr although symptoms are apt to be somewhat more marked than in silicosis. In silicosis there may be marked x-ray findings with little complaint of symptoms, whereas the opposite is likely to be the case in asbestosis. As in silicosis, dyspnea is the cardinal symptom. Anorexia occurs frequently in advanced stages, and cyanosis and clubbing of the fingers are apt to appear with greater constancy in asbestosis. Pathology. The fibrosis in asbestosis is diffuse and tends to predominate in the basal portions of the lungs in contrast to the generalized nodular fibrosis of silicosis " J. W. G. Hannon, Trans. Can. Inst. Mining Met., 48,180 (1944). "L. U. Gardner, M. Dworski, and A. B. Delahant, J. Ind. Hyg. Toxicol., 2B, 211 (1944). " A. J. Lanza, J. Am. Med. Assoc., JOS, 368 (1936). " A. J. Lanza, W. J. McConnell, and J. W. Fehnel, US. Pub. Health P.epU., SO. 1 (1935) DUP 0813741 DU 009719 t 512 kdward k. U.U1T .'iiptv-I-'iaitianve in the upper portions of tin; lung. Jir-efiiieftaM* and bronehio!t-ri.;,'i.- are i;";}itent, e.~peeially in the more fibrous portion:-. Whereas tin- prolifera tion of til irons tissue is caused by chemical action in silica exposure, it is induced by uv'-lmnical notion in asbestos exposures. Gardner77 found that the fibrosis-producing 'i'.aracter of asbestos could be almost eliminated by grinding the fiber:-.so that no p.:rifles more than 2 y, in length were present. As previously mentioned, asbestos is classified among the inert dusts. Microscopic Anatomy. Johnstone75 described the microscopic appearance of the lungs somewhat as follows: in the early phases of the disease there is thickening of the alveolar septa which results from fibroblastic proliferation. The alveolar spaces contain numerous phagocytes. With progression of the disease fibrosis be comes more marked; the alveolar structure gradually disappears, and in its place there is now dense fibrous tissue. The few alveoli that remain in the area of fibrosis are lined with low cuboidal epithelium giving them an almost glandular appearance. Scattered throughout the lung in both the diseased and healthy parts are spindle-shaped structures described first by McDonald.79 These bodies are 20 to 100 pAn length and are bulbous on one or both ends so that they appear club- or dumbbell-shaped. They are brownish in color, do not stain, and give a Prussian-blue reaction for iron. Simson80 has produced these bodies in guinea pigs by experimental exposure to atmosphere containing asbestos. Lynch81 concludes that these "curious bodies'' signify exposure to asbestos dust but do not necessarily indicate asbestosis. X-Ray Examination. For an excellent review of roentgenographic findings in both silicosis and asbestosis the reader might well refer to Pendergrass.82 Character istic differences in the roentgenographic findings in silicosis and asbestosis are tabulated below: Aabestoiia Silicoaia Fibrosis diffuse (film may have ground glass appearance from pleural involve ment). Findings may be either bilateral or uni lateral. Lesions largely in the lower one half or two thirds of the lung fields. Fibrosis nodular. Findings characteristically bilateral. Lesions predominately in the upper twothirds of the lung fields. Emphysema in lower portion of lung fields. Control. Prevention of asbestosis depends entirely upon preventing exposure to concentrations of dust sufficiently high to produce the characteristic reaction. " L. TJ. Gardner, Ind. Med., 9,45 (1940). TM R. T. Johnstone, Occupational Diseases. Saunders, Philadelphia, 1942. "S. McDonald, Brit. Med. J., 2, 1025 (1927). *' F. W. Simson, Brit. Med. J., i, 885 (1928). K. M. Lynch, J. Am. Med. Assoc., 109,1947 (1936). "E. P. Pendergrass, "Roentgen-Ray Diagnosis in Silicosis and Asbestosis," in A. J. Lanza, Silicosis and Asbestosis. Oxford Univ. Press, New York, 1938. o c -o oo 00 -J -NCa) DU 009720 m-- 1)1 ST IN trn; ' Al'-A'I'MN OK i II '(.Tl'ATklX.U. 1 >L."i:\~-tl bid Dree-sun. DallaVnllu, IMwanU. Millar, and Sayei>v' have round cvidenoe to indicate that j.GOO.OOU particles par cubic foot of air is a sat i-factory figure for the maximum permissible atmospheric concentration of asbestos to which workers may be exposed. Definite permissible standards, however, have not been established. VI. Dust Causing Minimal Fibrosis or No Fibrosis Gardner77 has pointed out that any known inorganic dust other than free silica and the asbestos silicates may produce nonspecific dust reactions, as described on page 48G. X-ray markings may be found in other conditions such as chronic infection and heart disease. No interference with pulmonary function or disability is produced by dust of this type and there is no influence on susceptibility to tuberculosis. A. SILICATES McCord,54 from a number of sources, has compiled a list of the commonly used silicates, which is presented here: - Olivine--a magnesium silicate widely present in all basic rocks. Many varieties of this stone are known. Calcium silicate--nonexistent in nature, but a common product of industry; may be found at blast furnaces and in production of cement and hydrated limes. Other silicates of calcium are known. Willemite--a zinc silicate (rare). __ Sodium silicate (mela)--the well-known water-soluble silicate, commonly called water glass. This is widely used in industry, notably as a filler in soaps. This is the only crystalline silicate of sodium, the others being amorphous glass. Tremolile--a magnesium-calcium silicate. 7 Asbestos--tremolite, aetinolite, chrysotile, or amianthus, all of which are essentially mag nesium silicates. Jade--another form of magnesium-calcium silicate. Crocidolile--``blue asbestos.'' It is a sodium iron silicate. Talc--a hydrated magnesium silicate with extensive industrial application. Soapstone--a form of talc. Agalite--a variety of talc resembling asbestos. It is used in the coating of paper, and as a paper filler. Meerschaum--also called sepiolite. It is closely akin to talc. Serpentine--hydrated silicate of magnesium. It is a common building stone. Sillimanile--aluminum-containing silicate. The source of many stone tools of the stone age Topaz--a semiprecious stone of silicate origin. Chemically it is an aluminum fiuosilicate. Fuller's earth--a hydrated silica-aluminum compound, associated with ferric oxide. Kaolin (kaolinite)--many related silicates of mixed constituency. Clays--hydrated aluminum silicates containing iron. Titanium, quartz and mica, are likely to be present in clays. "W. C. Dreessen, J. M. DallaValle, T. I. Edwards, J. W. Miller, and R. R. Sayers, UK. Pub. Health Bull. No. 241 (1938). " C. P. McCord, Ind. Med., 2, 4 (1933). DUP 0813743 DU 009721  iU i; i j v.- ' armrja--n '*li*-;t*t* .it !' .- wi i a _ vitnt'i'.'f, including Muo.-. rcas. grcf'iis. yb v: mi! wiiiti-. :u: i , m.* Mii-n- :i s:riiui> i.f-.!! .i'"-! 'hi'ira i;. .' in elcctri'-jil '.vurk inr i.-1'. U:nr Lim.-nr./vi . ~! i - - ' - r - t.-.v: : in i :s-ry. Unmet--complex silica-lee ui aluminum. i.'<jn. ealeimu. and [Uagn*-.~ium. liesides being a semi precious coni 'lore-- garnets are used as '-Mile:: Ocarina', in a-.-in culling. pouching, etc. /' i'/sp'O' --a large group of aluminum silicates entering into many minerals, for exampl granite. . Permulite--a sodium-aluminum silicate of complex structure, much used in narer softeningLava--mixed silicates of volcanic origin. Pumice--volcanic, glassy, spongy lava. It is primarily used as a polishing agent. Shale--a loose term applied to clays and other silicates that have been subjected to high pressures in the earth. Slaie--a substance of clay or shale origin, that has been subjected to high pressure and has metamorphosed. It contains or may contain much free silica. gj/ags--Products of metal blast furnaces that contain native impurities as well as minerals such as dolomite introduced as Huxos. etc. Almost all forms of silicates may be included. Free silica may be present. Silicon carbide--carborundum, a synthetic mineral. Silundum--another form of synthetic silicate, akin to carborundum in chemical structure. Ftbrox--silicon oxycarbide. It closely resembles carborundum and is somewhat similarly made. It may be stated with some certainty that none of these dusts, unless- in com bination with free silica, will produce nodular fibrosis; and proof of disability from breathing such dusts is lacking. B. NOXSILICEOUS DUST Xonsiliceous dusts such as calcite, calcium carbonate, gypsum, limestone, Portland cement, and pyrolusite dusts have been listed in the classification of Miller and Sayers85 as among those causing Anhabsorptive tissue response and, ac cordingly, are not considered as producers of pneumoconiosis. Apparent X-ray Nodulation without Fibrosis. Only brief mention will be made of baritosis and siderosis. Pendergrass82 reports having seen several patients ex posed to barium dust with widespread dense nodulation typical of that seen in simple silicosis. The individuals examined were symptom-free and not incapacitated. Sander86 has described a similar condition caused by the inhalation of iron oxide fumes at welding operations. Exposure to iron dust or fume may produce an x-ray picture characterized by generalized nodulation. Autopsy specimens have revealed that the nodules are collections of iron with no tissue reaction or fibrosis. " J. W-Miller and R. R. Sayers, US. Pub. Health Repts., SS, 264 (1941). " 0. A. Sander, J. Ind.Hyg. Toxicol., 2$, 79 (1944). a c TJ O 00 wvj DU 009722 -ii. iferMitfeML Miai m i I II. Du>l (aiii'ini: (ihemicul Irritation It i> hardly necessary to onur..in dftaiLrho chemical irritants. These ar- -willy either alkaline or acid in ':i"; : ti, j-.v.nmnlu- of the a.lkalinc ur's: p arc vriroxides. ci'ment. and - ..-.p: a!., .: ';> 1 'UP. :sr;t!:*. fiuorid c-. and chr a: `.at os. Such chemicals mav iirita'- *; 'kiit .ii'ii.'imj: uryri.c]nut or iburns. even : <> the point of necrosis. Injury to the n injunct ivae may occur with laerimulion anti con junctivitis; or this type of'clu.-: way produce inflammation of the nasal mucosa, sometimes to the extent of ulceration of tlic^nasal septum. These substances also may irritate the remainder of the respiratory tract sufficiently to induce coughing and, in more severe exposures, to cause bronchitis or pneumonitis. There is little evidence to suggest that prolonged exposure to irritant dust, in concentrations that are too low to produce symptoms at the time of exposure, will cause chronic disease or increase susceptibility toTnfection. Local irritation by dust may result from purely mechanical as well as chemical characteristics. Mechanical injury may result from breathing long sharp fibers ns of lint or other vegetable materials. A severe and even fatal pneumonitis may follow the inhalation of cadmium dust or fume. This is particularly, important since the dust does not produce any immediate irritation or warning symptoms. A few hours following exposure symp toms of gastritis may develop and subsequently pulmonary edema and pneumonitis may occur. Beryllium has recently been considered as a .cause of occupational disease be cause of the occurrence of acute and chronic manifestations in beryllium workers. The acute phase has been officially named'*'1 ''Acute pneumonitis of beryllium workers" and the chronic phase has been named56" "Pulmonary granulomatosis of beryllium workers." The acute reactions are characterized by dermatitis, conjunctivitis, irritation of the upper respiratory tract and, in some instances, pulmonary edema. Such lesions may be associated with exposure to the acid compounds of beryllium and may arise in beryllium extraction plants. The chronic lesions in the lungs are granulomatous. There is associated thicken ing of the walls of the air spaces and subsequent interference with gaseous exchange, producing dyspnea. Cor Pulmonale may develop. Chronic cases have appeared in persons engaged in the manufacture of fluorescent lamps and in the casting of beryllium alloys in which the percentage of beryllium was relatively high. The subject has been well reviewed in the Saranac Symposium on the Beryllium Prob lem, Sept. 29, 1947. VIII. Dust Causing Systemic Poisoning It is not possible to list here the thousands of minerals, drugs, and chemicals that may exert a harmful effect on the body. One need only recall the great surface '*"0. A. Sander, Summary of Saranac Symposiumlon the Beryllium Problem, Industrial Hygiene Foundation, 194S. DUP 0813745 DU 009723 510 EDWARD E. DART areaojf tlie lungs to realize that they may act as a gateway to the body for entrance of any material that is suspended in the air. If this suspended material is toxic, pathological reactions may result, providing sufficient dust is inhaled to cause injury. Dust counts ordinarily are not used to measure the degree of air contamination by poisonous substances. With a toxic dust, air contamination is usually defined in terms of weight per unit volume, such as milligrams per 10 cu. meters or milligrams per cubic meters (10 cu. meters is frequently used as the unit of air because this volume roughly approximates the average lung ventilation during an eight-hour working day). Such measurements correspond more closely to measurements used in pharmacological practice. Large particles of a toxic dust may be of greater im portance than are large silica particles since the former may be absorbed, in some instances, from the mucous membranes of the upper respiratory tract. Perhaps the classical example of a dust or fume causing systemic poisoning is lead (see Chapter Twenty-One, Volume II). IX. Dust Causing Allergic Manifestations such as Dermatitis, Hay Fever, and Asthma The layman who has consulted his doctor for allergy tests is well aware of the almost innumerable kinds of dust that may cause hay fever, ranging from pollens to house dust or chicken feathers. Since this is not the place for a discussion of im munology, it is sufficient to say that lacrimation, watery nasal discharge, asthma with its difficult expirations, or dermatitis may develop when a person inhales or contacts a material to which he is sensitive. This allergy is usually the result of a previous sensitizing dose or doses and symptoms do not develop, as a rule, until some time has elapsed following the sensitizing exposure (days or weeks). It is probable that any organic dust may be allergenic. Habeeb87 has attributed bronchial constric tion in silicotic patients to silica allergy. This conclusion is based largely on his own findings of eosinophiiia in patients with silicosis, and the in vitro evidence of bron chial constriction by colloidal silica.88 A high incidence of eosinophiiia has not, how ever, been found associated with silicosis by other authors. Gardner88 has reported attempts to use-silica on skin tests but was forced to conclude that any reaction was the result of the primary toxicity of silica rather than of allergy to silica. In the light of these findings, further proof would be necessary to show that symptoms asso ciated with silicosis are allergic manifestations. X. Dust Causing a Febrile Reaction (Acting in an Unknown Manner, Possibly as an Allergen) Examples of febrile reactions caused by inhalation of dust or fume are metalfume fever, which is discussed under metallic poisons (Vol. II), and "cotton fever." " W. J. Habeeb, Ohio State Med. J., 41, 1101 (Dec. 1945). "G. F. Filley, J. G. Hawley, and G. W. Wright, J. Ind. Hyg. Toxicol., 27, 37 (1945). " L. U. Gardner, personal communication. DU 009724 ! J8IPSs & - - DFST IN THE CAUSATION OF OCCUPATIONAL DISUASK O 17 / \\ others exposed to zinot oxide fumes, as in the welding or burning of galvanized iron, arc subject to a pec 'liar reaction, consisting primarily of chills and fever occurring some hours after excessive exposure. Details of this reaction are discussed elsewhere, but there is some evidence to suggest that it may be similar to the foreisro protein type of reaction. A similar reaction is found in cotton mill workers, in whom a condition known as "cotton fever" or "Monday fever" occurs. Employees experience a sudden attack of coughing with breathlessness following exposure to cotton lint, after a week end away from the work environment. This reaction is of fairly short duration, and if affected persons usually show no further trouble during the week but may have a recurrence of the same condition on the following Monday. Eventually, though, they suffer continually and may have to give up work. Prausnitz80 has shown that this condition results from allergy' to the protein fraction of cotton dust. The febrile response described may be a different entity from the similar condition reported first by Neal, Schneiter, and Caminita81 and by Ritter and Nussbaum.82 They found symptoms similar to a cold, with fever and complaints of sinus trouble, occurring in the first few weeks of work-rather than consistently on Mondays. The cause of this malady is described as an endotoxin liberated by the bacterium Aerobacter cloacae which grows in the cotton. A similar condition may occur in hemp handlers and those exposed to bagasse. cr XI. Summary The fundamental principles of anatomy and physiology necessary to an understanding of the pneumoconioses have been discussed. Dust has been considered as a cause of extensive pulmonary fibrosis, minimal or no pulmonary fibrosis, chemical irritation, systemic poisoning, allergic reactions, and febrile responses. An attempt has been made to "present pertinent data on these subjects in a way that will help engineers and industrial hygienists to understand the physiological problems in volved in dust diseases, and in addition to give sufficient medical data to assist physicians in diagnosis and examination of employees exposed to dust. "0. Prausnitz, Med. Research Council (Bril.), Special Rep. Series No. 212, (1936). " P. A. Neal, R. Schneiter, and B. H. Camimfa, J. Am. Med. Assoc., 119, 1074 (1942). " W. L. Ritter and M. A. Nussbaum, Ind. Med., 13,966 (1944). J . p || r; ; ' j 1 I * DUP 0813747 DU 009725