THE MEDICAL DEPARTMENT OF THE 
    
    UNITED STATES ARMY IN THE WORLD WAR
    
    
    VOLUME XIV 
    
    MEDICAL ASPECTS OF GAS WARFARE
    
    PREPARED UNDER THE DIRECTION OF 
    
    MAJ. GEN. M. W. IRELAND 
    The Surgeon General 
    
    By 
| COL. WILDER D. BANCROFT, C. W. S.  | CAPT. E. K. MARSHALL, JR., C.W.S. | 
| MAJ. H. C. BRADLEY, C. W. S. | MAJ. WALTER J. MEEK, C. W. S. | 
| MAJ. J. A. E. EYSTER, M. C. | MAJ. A. A. PAPPENHEIMER, M. C. | 
| COL. H. L. GILCHRIST, M. C. | MAJ. JAMES E. POORE, M. C. | 
| CAPT. SAMUEL GOLDSCHMIDT, C. W. S. | TORALD SOLLMAN, M. D. | 
| CAPT. PAUL J. HANZLIK, M. C. | SERGT. JESSE TARR, C. W. S. | 
| CAPT. ROBERT A. LAMBERT, M.C. | LIEUT. COL. F. P. UNDERHILL, C.W.S. | 
| A. S. LOEVENHART, M. D.   | ALFRED S. WARTHIN, M. D. | 
| CAPT. D. W. WILSON, C.W.S. | 
 | 
    WASHINGTON: GOVERNMENT PRINTING OFFICE, 1926
  
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LETTER OF TRANSMISSION 
  
I have the honor to submit herewith Volume XIV of the history of the MEDICAL DEPARTMENT OF THE UNITED STATES ARMY IN THE WORLD WAR. The volume submitted is entitled "MEDICAL ASPECTS OF GAS WARFARE."
?M. W. IRELAND, 
      Major General, The Surgeon General. 
The SECRETARY OF WAR.
3
  Lieut. Col. FRANK W. WEED, M. C., Editor    in Chief. 
  LOY MCAFEE, A. M., M. D., Assistant    Editor in Chief. 
   
  EDITORIAL BOARD a 
   
  Col. BAILEY K. ASHFORD, M. C. 
  Col. FRANK BILLINGS, M. C. 
  Col. THOMAS R. BOGGS, M. C. 
  Col. GEORGE E. BREWER, M. C. 
  Col. W. P. CHAMBERLAIN, M. C. 
  Col. C. F. CRAIG, M. C. 
  Col. HAVEN EMERSON, M. C. 
  Brig. Gen. JOHN M. T. FINNEY, M. D. 
  Col. J. H. FORI, M. C. 
  Lieut. Col. FIELDING 1H. GARRISON, M. C. 
  Col. H. L. GILCIHRIST, M. C. 
  Brig. Gen. JEFFERSON R. KEAN, M. D. 
  Lieut. Col. A. G. LOVE, M. C. 
  Col. CHARLES LYNCH, M. C. 
  Col. JAMES F. MCKERNON, M. C. 
  Col. S. J. MORRIS, M. C. 
  Col. R. T. OLIVER, D. C. 
  Col. CHARLES R. REYNOLDS, M. C. 
  Col. THOMAS W. SALMON, M. C. 
  Lieut. Col. G. E. DE SCHWEINITZ, M. C. 
  Col. J. F. SILER, M. C. 
  Brig. Gen. W. S. THAYER, M. D. 
  Col. A. D. TUTTLE, M. C. 
  Col. WILLIAM H.. WELCH, M. C. 
  Col. E. P. WOLFE, M. C. 
  Lieut. Col. CASEY A. WOOD, M. C. 
  Col. HANS ZINSSER, M. C. 
  ______________________________________________________________________________ 
  a The  highest rank held during the World War has been used in the case of  each officer. 
  4
PREFACE. a 
   
  In  this volume attempt is made to deal with only such problems of gas  warfare as  concerned the Medical Department directly, or through affiliation with  the Chemical Warfare  Service. The material seemed naturally to fall into three sections,  involving: (1) Organization  and administration of the gas service; (2) clinical features of gas  poisoning, including certain  statistical considerations; (3) experimental researches with respect to  the physiology, pathology,  and therapeutics of noxious gases.  
  The  connection of the Medical Department with the early development of the  defensive  aspects of gas warfare has been briefly detailed in Volume 1, which  gives the administrative  history of the Surgeon General 's Office. That account is elaborated,  with certain necessary  repetitions, in the present volume.  
  Reports  by the laboratory investigators concerning the progress of their  experimental  studies were submitted from time to time during and after the war, many  of which formed the  basis of contributions which appeared in professional journals or in  book form. A considerable  part, therefore, of the third, or experimental, section of the present  volume has been published. The purpose of this section is to assemble,  in one place and in convenient form the accounts of  the work of our most prominent students of the various aspects of gas  poisoning, as  experimentally investigated. The immediate editorial supervision of  this volume, in the earlier  stages of its preparation, and until official orders separated him from  the Historical Division, was  exercised by Lieut. Col. S. J. Morris. M. C.  
  ______________________________________________________________________________ 
  a For  the purposes of the History of the Medical Department of the United  States Army in the World War, the  period of war activities extends from Apr. 6. 1917, to Dec. 31, 1919.  In the professional volumes, however. in which  are recorded the medical and surgical aspects of the conflict as  applied to the actual care of the sick and wounded,  this period is extended, in some instances, to the time of the  completion of the history of the given service. In this  way only can the results of the methods employed be followed to their  logical conclusion. 
  
TABLE OF CONTENTS 
   
                        
  PREFACE
  INTRODUCTION  
   
  SECTION I.-    ORGANIZATION    AND ADMINISTRATION OF GAS DEFENSE 
      CHAPTER I. Organization    in the United States. By Maj. H. C. Bradley, C. W. S. 
    II. Organization in the American    Expeditionary Forces. By Col. H. L. Gilchrist,      M. C  
     III. Classification and methods of use of war    gases. By Col. H. L. Gilchrist, M. C 
    IV. Field arrangements for gas defense and    the care of gas casualties. By      Col. H. L. Gilchrist, M. C 
   
  SECTION II.- CLINICAL    FEATURES 
    V.    Physiological action of war gases. By Maj.    H. C. Bradley, C. W. S  
     VI. Pathological action of war gases. By Maj.  A. M. Pappenheinmer, M. C .
         [part 1, pages 87-137]
         [part 2, pages 138-188]
   [part 3, pages 189-249] 
    VII. Symptoms and treatment. By Col. H. L.    Gilchrist, M. C 
     VIII. Statistical consideration of gas    casualties:  
      (1) Gas casualties. By Col. H. L. Gilchrist,      M. C.
      (2) After-effects of gas poisoning. By Maj.      James E. Poore, M. C  
   
  SECTION III.-EXPERIMENTAL    RESEARCHES 
    IX. The chemistry of war gases. By Col.    Wilder D. Bancroft, C. W. S
    X. Physiological action    of phosgene,    chlorine, and chloropicrin. By Lieut. Col.      Frank P. Underhill, C. W. S 
    XI. Physiopathological action of acute    phosgene poisoning. By Maj. J. A. E.      Eyster, M. C., and Maj. Walter J. Meek, C. W. S
    XII. Physiological action of    dichlorethylsulphide (mustard gas). By Capt. E.      K. Marshall, jr., C. W. S. 
     XIII.    Physiological action of miscellaneous    gases. By Lieut. Col. Frank P. Underhill,      C. W. S 
    XIV. Experimental pathology of war gases,    exclusive of mustard gas. By Capt.      Robert A. Lambert, M. C. 
    XV. Pathologic action of mustard gas    (dichlorethylsulphide). By Alfred S.      Warthin, M. D 
    XVI. The    comparative skin irritant properties    of mustard gas and other agents. By      Capt. Paul J. Hanzlik, M. C., and Sergt. Jesse Tarr, C.      W. S.  
    XVII. The influence of solvents, adsorbents,    and chemical antidotes on the severity      of human skin lesions caused by mustard gas. By Torald Sollman,      M. D 
    XVIII. Ointment protection against mustard    gas. By A. S. Loevenhart, M. D. 
    XIX. Experimental treatment of poisoning by    lung irritant or suffocallt gases. By      Lieut. Col. Frank P. Underhill, C. W.      S.
    XX. The influence of oxygen administration on    the concentration of the blood which      accompanies the development of lung edema. By Capt. D. W. Wilson,      C. W. S., and Capt. Samuel Goldschmidt, C. W. S. 
    XXI. Researches of pathological and    physiological sections of Hanlon Field (experimental      gas field), American      Expeditionary Forces  
   
  APPENDIX.   
  
   Summary of    production, field supply section,    Gas Defense Service 
   Instructors in gas    defense methods, field    training section, Gas Defense Service 
   Quiz compend on the    use of gas in    warfare 
   A suggested    organization of the gas service    of the American Army (Church) 
   Gas defensive    organization of the British    armies in France 
   Abstract of plan for    organization of gas    service in United States Army (Flandin) 
   Gas and Flame    Service, offensive and    defensive (statement of action taken) 
   Inter-Allied gas    conferences (first, second,    and third) 
   The physiological    effect of warfare gases on    the human being, including symptomatology and general      treatment
   Circular No. 34,    American Expeditionary    Forces résumé of symptoms and treatment of poisoning by irritant gases) 
    Report of    lectures for division medical gas    officers held in Paris in October, 1918  
   Report on gas    hospital, Justice Hospital    Group 
  
  LIST OF TABLES 
   
   1. Admission for gas    poisoning, by    organization, American Expeditionary Forces Absolute numbers and percentages of      total      number 
   2. Admissions for gas    poisoning, by months of    occurrence, American Expeditionary Forces. Absolute numbers and      percentages of      total number 
   3. Admissions for gas    poisoning, by gas,    American Expeditionary Forces. Absolute numbers, deaths, and case mortality rates 
   4. Admissions for gas    poisoning, by gas,    officers and enlisted men, American Expeditionary Forces  
   5. Deaths from    exposure to gas; by groups and    by months of occurrence 
   6. Medical and gas    officers' record of the    type of gas to which the fatal cases coming to autopsy had been      exposed 
   7. Series of fatal    cases coming to autopsy, by    groups, and by the gas believed to have been cause of lesions      found 
   8. Character of gas    attacks    sustained 
   9. Duration of life    after gassing, by groups
   10. Causes of death
   11. Associated    diseases other than those    mentioned in Table 10, as cause of death 
   12. Principal lesions described    in the autopsy protocols of Groups A and B 
   13.    Distribution of burns and pigmentation as    described at autopsy, by region and by group 
   14. Bacteriology of    cases    studied  
   15. Organisms    isolated in the series of    cases 
   16 A study of 3,014    gassed cases, American    Expeditionary Forces (1917-18), with a view to determining after-effects.      Numbers      and percentage of the total number of cases of the series and of certain      specific classes for each result. Average percentage of disability in specific      classes 
   16. A study of 3,015 gassed    cases, American Expeditionary Forces (1917-18), with a view of    determining after-effects. Numbers of percentage of the total numer of    cases of the series and of certain specific classes for each result    Average percentage of disability in specific classes continued
   17. Toxicity of    chlorine gas 
   18. Toxicity of    phosgene    gas 
   19. Toxicity of    chloropicrin    gas
   20. The influence of    chlorine poisoning Upon    the composition of the urine- 
   21. Chlorine    experiments 
   22. The influence of    chloropicrin poisoning    upon the composition of the urine
   22. The influece of    chloropicrtin poisoning upon the composition of the urine continued
   23. Hemoglobin    changes in the blood in    phosgene poisoning 
   24. The influence of chlorine gassing    upon    the leucocyte count 
   24. The influence of chlorine    gassing upon the leucocyte count continued
   25. Chloride content    of blood plasma and    pulmonary exudate after phosgene gassing
  26. Blood volumes in phosgene poisoning 
   27. Pulmonary    aeration during phosgene    poisoning 
   28. Irritating    effects of    dichlorethylsulphide applied locally 
   29. Irritating    effects of    dichlorethylsulplhide applied locally 
   30. Time of exposure    to vapor tests required    to produce a visible reaction 
   31. Skin irritation    from local application of    dichlorethylsulphide 
   32. Effect in    individuals of local    application of dichlorethylsulphide 
   33. Sensitivity of    negroes to    dichlorethylsulphide 
   34. Susceptibility of    skin of animals to    dichlorethylsulphide 
   35. Removal of    dichlorethylsulphide from skin    by washing with kerosene 
   36. Effects of    evaporation after application    of dichlorethylsulphide
   37. Effects of    evaporation after application    of dichlorethylsulphide 
   38. Effect of    covering dichlorethysulphide    burns 
   39. Effect of    covering dichlorethylsulphide    burns 
   40. Effect of    covering exposures of varying    lengths  
   41. Effect of    covering exposures of varying    lengths  
   42. Transfer from    skin to skin of    dichlorethylsulphide burns 
   43. Sensitivity tests    of dichlorethylsulphide    burns
   44. Persistence of    gas after    dichlorethylsulphide burns 
   45. Animals gassed    with cyanogen    chloride 
   45. Animals    gassed with cyanogen chloride continued
    46. Animals gassed    with cyanogen    bromide  
   47. Toxicity of    diphosgene on dogs  
   48. Effect on the    respiratory tract of    different concentrations of diphosgene
   49. Dogs gassed with    chlorine  
   50. Dogs gassed with    chlorine  
   51. Dogs gassed with    phosgene  
   52. Dogs gassed with    phosgene 
   53. Degree of    increase in lung weight after    gassing  
   54. Pulmonary    complications in dogs gassed    with phosgene  
   55. Dogs gassed with    chloropicrin  
   56. Dogs gassed with    chloropicrin-percent    showing pneumonia
   57. Dogs gassed with    chloropicrin-degree of    edema of lungs  
   58. Blood changes    following gassing with    arsine  
   59. Relation of the    edema of lung and the    concentration of blood in gassed animals
   60. Animals gassed    with    phosgene 
   61. Dogs dying of    malnutrition 
   62. Dogs dying of    chloropicrin    poisoning  
   63. Mean course of    experimental lesions
   64. Effect of    venesection on chlorine    poisoning after standard gassing 
   65. Effect of    venesection and infusion of    salt solution
   66. Influence of    various salt solutions in    the treatment of chlorine poisoning- 
   67. Treatment of    chlorine    poisoning 
   68. The influence of    various strengths of    sodium chloride solutions in the treatment of      chlorine poisoning  
   69. The influence of    the volume of fluid    injected in the treatment of chlorine poisoning 
   70. The influence of    repeated infusion in the    treatment of chlorine poisoning 
   71. The influence of    dextrose and acacia    solutions in the treatment of chlorine poisoning 
   72. The influence of    calcium and other salts    in the treatment of chlorine poisoning 
   73. Effect of    morphine in treatment of    chlorine poisoning 
   74. The influence of    subcutaneous injections    of calcium in the treatment of chlorine poisoning  
   75. Effect of    environmental conditions    (temperature) on the efficacy of the prescribed      treatment  
   76. The influence of    the element of time of    bleeding in the treatment of phosgene poisoning 
   77. The influence of    multiple small bleedings 
   78. Influence of    early infusion (recorded by    percentage)  
   79. Influence of    early bleeding and delayed    infusion  
   80. Influence of    various types of treatment    (recorded by percentage) 
   81. Modified treatment 
   82. Influence of    water intake upon treatment 
   83. Effect of    bleeding upon goats gassed with    chloropicrin 
   84. Effect of    bleeding upon goats gassed with    chloropicrin 
   85. Chloropicrin    treatment 
   86. The influence of    oxygen administration    upon the mortality of dogs gassed with phosgene  
   87. Comparison of    toxicity figures for    phosgene and those obtained by oxygen administration 
   88. The influence of    oxygen upon gassed dogs    treated by venesection 
  89.    Influence of    oxygen upon dogs gassed with    sublethal concentrations of phosgene and      treated by venesection 
   90. The influence of    oxygen upon dogs gassed    with chlorine treated by the standard method 
   91. The arterial and    venous oxygen content    and percentage saturation breathing air as compared with breathing oxygen      (approximately 50 percent). The capacity of the blood (oxygen-combining      power)      is also given  
   92. The influence of    oxygen administration    upon the percentage saturation and oxygen content of the blood of dogs gassed      with      phosgene (71 to 80 parts per million) (0.31 to 0.35 mgm. per      liter) 
 93. The    influence of oxygen administration    upon percentage saturation and oxygen content of the blood of dogs gassed with      phosgene (50 to 60 parts per million) (0.21 to        0.26 mgm. per liter) 
   94. Comparison of    calculated amounts of fluid    lost from blood and extra fluid in the lungs of      gassed animals  
   95. Alteration in the    blood count, following    the intravenous injection of dichlorethylsulphide 
   95. Alteration in the    blood count, following    the intravenous injection of dichlorethylsulphide      continued
   95. Alteration in the    blood count, following    the intravenous injection of dichlorethylsulphide continued
   95. Alteration    in the    blood count, following    the intravenous injection of dichlorethylsulphide continued
   96. Effect of    dimethyltrithiocarbonate upon    animals  
   97. Pathological    report  
   97. Pathological    report continued
  
  LIST OF    CHARTS   
  
   I. Factory protection    section, Gas Defense    Service, Surgeon General's Office
   II. Medical Division,    Chemical Warfare    Service, July, 1918
   III. Gas Service    organization, American    Expeditionary Forces
   IV. The Medical    Department in the    organization for gas defense, training research and treatment, American      Expeditionary Forces  
   V. Organization chart    of Hanlon Field    (experimental gas field), American Expeditionary Forces, November 23, 1918 
   VI. Changes in total    solids of blood after    phosgene gassing, showing characteristic differences in the three gas      concentrations selected
   VII. Changes    in total solids of blood, after    phosgene gassing, showing characteristic differences in the dogs that      died      acutely and those that survived the acute period  
   VIII. Comparison of    the changes in total    blood solids of dogs gassed with phosgene and those gassed      with chlorine 
   IX. Comparison    of total solids and    hemoglobin after chloropicrin gassing 
   X. Comparison of the    characteristic changes    of blood solids induced by chlorine,      phosgene, and chloropicrin      gases  
   XI. Comparison of    erythrocytes and hemoglobin    content of blood after chlorine gassing 
   XII. Comparison of    erythrocytes and    hemoglobin content of blood after chloropicrin gassing
    XIII.    Changes in the chlorides    and total    solids of the lungs      after phosgene gassing  
   XIV. Changes in the    total solids of the blood    and lungs after phosgene gassing  
   XV. Water content of    lung tissue after    chloropicrin and phosgene gassing 
   XVI. Relation between    the changes of plasma    chlorides and lung solids after phosgene      gassing
   XVII. Changes in the    chlorides of lung    tissues and blood plasma after phosgene gassing  
   XVIII. General    changes in the oxygen capacity    and content of the blood after phosgene gassing 
   XIX. Composite curve,    from 10 experiments, of    the changes in arterial blood pressure      after acute phosgene gassing 
   XX. Arterial blood    pressure record from a    case of acute phosgene poisoning 
   XXI. Composite curve,    from 14 experiments, of    the changes in the      heart rate after acute phosgene gassing 
   XXII. Composite curve    from 16 experiments, of    the changes in hemoglobin concentration after acute phosgene      gassing 
   XXIII.    Composite curve, from 9 experiments,    of the changes in the red blood      cell counts after acute phosgene gassing 
   XXIV. Duration of    life after chlorine    gassing 
   XXV. Duration of life    after phosgene    poisoning
   XXVI. Degree of    pulmonary edema after    phosgene gassing, as determined by lung-heart and lung-body ratios 
   XXVII. Duration of    life after chloropicrin    gassing
   XXVIII. Comparison of    the degree of pulmonary    edema and concentration      of the blood in gassed animals. Cross-hatched        columns represent percentage of increase in lung weight and are        arranged        in order. Solid black columns represent percentage of increase          in          red blood corpuscles. This chart clearly shows that there is no          relationship between the two 
   XXIX. Changes in    hemoglobin of the blood      after gassing with chloropicrin, 1 to 8,500, for 25 minutes. Solid      line, animals receiving extra oxygen; broken line, control animals
   XXX. Changes in    hemoglobin of the blood after    gassing with chloropicrin,      1 to 8,500, for 30 minutes. Solid        line, animal        receiving extra oxygen; broken line, control animal  
   XXXI. Changes in    hemoglobin of the blood    after gassing with chloropicrin, 1 to 8,500, for 25 minutes. Solid line,      animals      receiving extra oxygen; broken line, control animals 
   XXXII. Rabbit No. 12,    serial No. 97, and    rabbit No. 13, serial No. 55 leucocyte counts, showing fluctuations due to      experimental changes of outside temperature. Counts plotted by      hour of day, space after each date representing 24 hours 
   XXXIII. Rabbit No.    20, serial No. 96
   XXXIV. Rabbit No. 23,    serial No. 141, and    rabbit No. 24,      serial No. 104
   XXXV. Rabbit No. 25,    serial No. 168
   XXXVI. Rabbit No. 26,    serial No. 174
   XXXVII. Rabbit No.    27, serial No. 177
   
  LIST OF PLATES  
   
   I. Mustard-gas    inhalation. Diphtheritic    inflammation, with      formation of false membrane, upper respiratory tract 
   II. Mustard-gas burns    of external genitals,    with vesiculation and pigmentation
   III. Experimental    mustard-gas burns (negro),    612 hours. Early      vesicle formation.        Absence of inflammatory reaction 
   IV. Experimental    mustard-gas burns (negro),    24 hours. Vesicle      formation, with necrosis of overlying epidermis, and        inflammatory reaction at margin of vesicle  
   V. Case 86.    Mustard-gas burn of scrotum, 18      days duration. Hyperkeratosis, hyperpigmentation, with irregular        distribution of pigment, chromatophores in corium  
   VI. Case 6. Mustard    gas, 2 days. Lung  
   VII. Mustard-gas burn    (contact) of neck
   VIII. Mustard-gas    burns of body  
   IX. Case 24. Mustard    gas, 5 days. Section    through wall of small bronchus, showing false membrane replacing the      necrotic      epithelium, hemorrhage into adjacent alveoli, and      fibrinous exudate into      the alveoli external to the zone of hemorrhage 
   X. Gross changes in    larynx of a soldier who    died four days after inhalation mustard gas  
   XI. Heart and lungs    of dog dying 24 hours    after phosgene gassing. Light      colored patches of emphysema alternate with deep        red        congested and partially collapsed areas in the voluminous lung. Heart is        dilated, particularly the right side 
   XII. Lungs of dog    killed 14 days after    phosgene gassing. There      is marked emphysema with irregular patches of atelectasis. Microscopically a        widespread obliterative          bronchiolitis is present
   XIII. Multiple    hemorrhages in wall of    bronchus of dog killed 6 days after exposure to chloropicrin  
   XIV. Higher    magnification of bronchus shown    in Plate XIII. Note      particularly the flattened character of the regenerating bronchial epithelium. A mitotic figure is seen on the left  
   XV. Pneumonia    complicated by multiple abscess    formation and pleurisy 5 days after exposure to      dichlorethylarsine. Only one lobe      is consolidated; others are relatively emphysematous  
  
  LIST OF FIGURES   
  
   1. Plan of mobile    degassing station  
   2. Case 2. Lung.    Poisoning with phosgene and    Blue (Cross gas. Intense alveolar edema, dilatation of atria, stasis of      leucocytes in capillaries. Epithelium of small bronchi is intact  
   3. Case 2. Large    bronchus. The epithelium is    in part lost, in part altered, the superficial cells being non-ciliated,      and      showing hyaline degeneration. There is marked congestion of the capillaries      of      the submucosa  
   4. Case 8.    Mustard-gas burn of skin, of 2    days' duration. Necrosis of epidermis with beginning of intra-epidermal      vesicle      formation  
   5. Case 89.    Mustard-gas burn of 20 days'    duration. Regeneration of new epithelium beneath crust of necrotic      original      epithelium. Hyperemia. Absence of inflammatory reaction 
   6. Case 18.    Mustard-gas burn of 5 to 6 days'    duration. Section through vesicle. Overlying epithelium is necrotic. The      contents of the vesicle consist of homogeneous, slightly fibrinous coagulum      with      moderate numbers of leucocytes.       The underlying corium is edematous  
   7. Case 18. Another    section, showing    condition similar to that seen in Figure 6  
   8. Mustard-gas    poisoning. False membrane    extending from epiglottis through entire trachea into bronchi 
   9. Diphtheritic    necrosis of mucosa of upper    respiratory tract after mustard-gas inhalation 
   10. Diphtheritic    necrosis of mucosa of upper    respiratory tract after mustard-gas inhalation
   11.    Diphtheritic necrosis of upper      respiratory tract after mustard-gas      inhalation  
   12. Mustard-gas burn.    Deep-seated necrosis of    bronchial mucosa 
   13. Case22.    Mustard-gas burn,5 days'    duration. Deep necrosis of trachea mucosa
    14.Case 21. Mustard-gas burn, 5 days'    duration.    Necrosis and exfoliation of tracheal epithelium, exposing basement    membrane. Fibrinous edema of submucosa 
   15. Case 61.    Mustard-gas burn, 9 days'    duration. Epithelial regeneration of trachea, proceeding from the mucous ducts 
   16. Case 41.    Mustard-gas burn, 7 days'    duration. Metaplasia of tracheal epithelium into squamous cell type. Numerous      mitoses 
   17. Case 24.    Mustard-gas burn, 5 days'    duration. Between the false membrane and the congested subepithelial tissue,      are      interposed hydropic epithelial cells of the        squamous type  
   18. Case 89.    Mustard-gas burn, 20 days'    duration. Trachea, the regenerating epithelium is growing beneath the old      swollen      basement membrane, which covers the exposed surface  
   19. Case 86.    Mustard-gas burn, 18 days'    duration. Bronchus. Proliferation of epithelium of ducts of mucous glands 
   20. Case 28.    Mustard-gas burn, 4 to 5 days'    duration. Lung. Intense congestion, hemorrhagic edema, aplastic exudate. The      leucocytes are filled with minute Gram-negative        bacilli  
   21. Case 103.    Mustard-gas burn, 58 days'    duration. Lung. Organizing and interstitial pneumonia  
   22. Case 81.    Mustard-gas burn, 15 days'    duration. Lung. Dilatation of atria, with hyaline necrosis
   23. Case 22.    Mustard-gas burn, 5 days'    duration. Lung. Pneumonia with necrosis of alveolar walls and nuclear      fragmentation  
   24. Case 53.    Mustard-gas burn (history of    exposure also to green and blue cross shells), 8 days' duration. Lung, small      bronchus, lined with dense granulation tissue; thickening of septa of adjacent      alveoli, which contains plugs of dense fibrin undergoing early organization 
   25. Case 100. Death,    51 days after exposure    to mixed vesicant and suffocant gases. Section through dilated bronchiole,      containing a vascular organized plug  
   26. Case 74.    Mustard-gas burn, 12 days'    duration. Lung. Proliferation of alveolar epithelium over a mass of fibrin      and      agglomerated red-blood corpuscles 
   27. Case 6.    Mustard-gas burn, 2 days'    duration. Lung, showing patchy alveolar edema, stasis of leucocytes in      capillaries,      beginning lobular pneumonia, with areas of necrosis, dilatation of atria 
   28. Case 16.    Mustard-gas burn, 4 days'    duration. Trachea. Low-power view, showing laminated false membrane      attached to      openings to mucous ducts
   29. Case 25. Yellow,    blue,    and green cross    shell, exposure 5 or 6 days before death. Dilated bronchiole lined with laminated      fibrinopurulent membrane. Complete        loss of epithelium 
   30. Case 47.    Mustard-gas burn, 8 days'    duration. Longitudinal section of bronchiole, completely occluded by      fibrinopurulent exudate. A few shreds of epithelium        are still present 
   31. Case 61.    Mustard-gas burn, 9 days'    duration. Pharynx. Localized superficial      necrosis of epithelium with      inflammatory reaction  
   32. Case 67.    Mustard-gas burn, 9 days'    duration. Section through bronchus, showing regeneration of metaplastic      epithelium, fibroblastic thickening of bronchial wall, epithelial      proliferation,      edema, of adjacent alveoli  
   33. Case 75. Death,    probably 10 to 12 days    after exposure to mixed gases. Bronchiectases filled with purulent exudate.      Peribronchial and periarterial edema and beginning fibrosis 
   34. Case 88.    Exposure to yellow, blue, and    green cross shell gas. Death after 20 days. Lung. Section passes through      interlobular septum, which is edematous and in which there is active growth of      fibroblasts, and plasma cell infiltration. There are organizing plugs in the septal      lymphatics
   35. Case 89.    Mustard-gas burn, 20 days'    duration. Lung. Area of bacterial necrosis with fibrinopurulent material      in the      adjacent alveoli  
   36. Same as Figure    35. Larger area of    gangrene in lung  
    37. Case 94. Death, 26 days    after exposure to mixture of    suffocant and vesicant gases. Obliterative bronchiolitis 
   38. Case 103.    Mustard-gas burn, 58 days'    duration. Lung. Low-power drawing through      bronchiectatic cavity.      Peribronchial      and periarterial fibrosis  
   39. Case 106.    Mustard-gas burn, 512 months'    duration. Lung, showing marked peribronchial and perivascular fibrosis,      interstitial fibrosis, organizing pneumonia, chronic edema, bronchiectasis 
   40. Case 106. Lung.    Section a. Edema of    alveoli and interlobular septum 
   41. Case 106. Lung.    Section b, through cavity    in the upper lobe 
   42. Case 106. Lung.    Section c. Taken from    opaque whitish tissue in anterior portion of upper lobe. Lung structures      over      large areas obliterated by poorly vascularized granulation tissue, densely      infiltrated with plasma cells
   43. Case 106. Lung.    Section d,    through thickened bronchi at hilum of lower lobe 
   44. Case 107. Late    stricture of trachea    following mustard-gas inhalation 
   45. Superimposed    outlines of three X-ray    photographs taken at intervals during phosgene poisoning to show changes in      shape      of the heart. The solid line indicates the normal. The dotted line      shows      the right-sided dilatation 39 
      minutes after gassing. The broken line      is      from a photograph taken 11 hours and 53 minutes after exposure to the      gas. The      heart had then become pendular in shape and        much reduced in        size 
   46. Diagram of dog's    respiratory tract viewed    from behind. The interlobular fissures and the accessory caudate lobe are      well      shown  
   47. Diagram of    bronchial tree of dog showing    bronchi of first, second, and third order (A, B, C) and infundibula (D) 
   48. Normal bronchus.    Bronchiolar termination    in a dog's lung, showing transition from high ciliated epithelium of bronchi      to      the flattened epithielium of the infundibular  
   49. Bronchus plugged    with sloughs of "cooked"    epithelial lining. The cytoplasm of the cells is quite homogeneous and      hyalinized  
   50. Higher    magnification of necrotic lining    shown in Figure 49 
   51. Multiple areas of    focal necrosis in lung    of dog dying 20 hours after chlorine gassing 
   52. Higher    magnification of an area of focal    necrosis such as is shown in Figure 51. Death occurred 6 hours after gassing.      The      alveolar walls about an atrium are completely hyalinized and stain      deeply      with eosin 
   53. Marked    perivascular edema in acute death    from chlorine. The lymphatic channels of the adventitia are widely      distended with      fluid 
   54.    The cells of the    exudate are chiefly    polynuclears which accumulated in and about      an atrium 
   55. Organizing    bronchiolitis 5 days after    chlorine gassing. Lumen of bronchus is filled with a network of fibroblasts and      there is a similar organizing process going on in the adjacent pulmonary      alveoli. In the bronchial and      alveolar walls there is much old hyalinized      fibrin  
   56. Purulent    bronchitis in a dog dying 23    days after exposure to chlorine. The cells in the bronchi are chiefly      Polynuclears, but in the adjacent alveoli are many large mononuclear cells 
   57.    Obliterating bronchiolitis in a dog    killed 32 days after chlorine gassing. The main bronchus has a normal, probably      regenerated epithelial lining. The small tributary bronchus is occluded by      an      organized mass of tissue adherent       to the wall in places 
   58. Chronic    bronchitis and patchy emphysema    in a dog dying 58 days after chlorine gassing 
   59. Bronchiectatic    cavities in lung of dog    dying 39 days after chlorine gassing. The lung tissue supplied by these      bronchi is      completely atelectatic  
   60. Sloughing of    bronchial epithelium in dog    killed 3 hours after exposure to chlorine
   61. Acute necrotizing bronchitis 10    hours    after chlorine gassing. There is complete sloughing of mucosa and a diffuse    inflammatory reaction throughout the bronchial wall. Note the marked edema of    tissue surrounding a large peribronchial    vessel
   62. Regeneration of bronchial epithelium    4    days after chlorine gassing. One mitotic figure is      seen 
   63. Low magnification    of lung of dog dying 2    months after exposure to chlorine. Chronic bronchitis and bronchiectasis      with      atelectasis and occasional patches of        emphysema  
    64. Higher magnification    of one of the    bronchi shown in Figure 63. Bronchus is moderately dilated. Adjacent lung tissue      is      atelectatic  
   65. Higher    magnification of two bronchi shown    in Figure 63. Lumina are filled with a cellular inflammatory exudate. There      is      also a chronic peribronchial reaction 
   66. Lung of dog dying    2 days after exposure    to phosgene. Fibrin stain shows a heavy deposit along the alveolar walls,      outlining      them everywhere quite distinctly  
   67. Higher    magnification of an area shown in    Figure 66. In places the fibrin strands extend across the septa  
   68. Early    inflammatory reaction about    bronchiole 18 hours after phosgene gassing. Cells are chiefly polynuclears. There is      a      generalized edema of the lung tissue  
   69. Broncho pneumonia    causing death 7 days    after exposure to phosgene. The bronchial wall is necrotic and there is      considerable hemorrhage in the pneumonic        exudate. Lung is moderately        edematous  
   70. Early stage of    organization of pulmonary    exudate 4 days after phosgene gassing  
   71. Higher    magnification of bronchial wall    shown in Figure 70. Fibroblasts are seen extending in a loose growth from the      submucosa. One mitotic figure is present
   72. Organizing    bronchiolitis in a dog killed    14 days after phosgene gassing. The lung grossly showed irregular patches of      emphysema and atelectasis, and tuberclelike nodules were felt      throughout the      lung  
   73. Higher    magnification of two bronchi shown    in Figure 72. The peribronchial thickening and the polypoid growths in      the      lumina are well shown  
   74. Necrosis of    bronchial epithelium and    subepithelial edema in acute death from chloropicrin      gassing  
   75. Widespread edema    of lung associated with    acute death from chloropicrin. Note occasional clear spaces (air bubbles) in      some      of the alveoli  
   76. Acute bronchitis    and bronchopneumonia    causing death 3 days after exposure to chloropicrin. The lung tissue      separating      the pneumonic patches is markedly edematous  
   77. Lung of  "recovered" dog killed 4 days    after chloropicrin gassing. In alveoli surrounding the bronchioles there are      structures resembling giant cells. As shown in Figure 78, the structures are      composed of fused mononuclear cells 
      inclosing hits of old fibrin and      degenerated      red cells  
   78. Higher    magnification of an alveolus from    Figure 77, showing the structure of phagocytic giant cells. Note their      resemblance to capillaries  
   79. Organizing    bronchiolitis in a dog killed    2 months after exposure to cyanogen bromide. The character of the cells      taking      part in the organization is well shown. The bronchiole has been partially      relined by an epithelium of irregular form but    mostly of the flattened type 
   80. Widespread edema    of lung in acute death    from dichlorethylarsine. The clear round spaces indicate the presence of      air      bubbles  
   81. Necrotization of    the bronchial lining    associated with acute death from dichlorethylarsine. A few air bubbles are seen      in      the exudate filling the lumen  
   82. Marked    perivascular edema and dilatation    of lymphatics in acute dichlorethylarsine      gassing  
   83. Ulceration of    cornea following exposure    to dichmlorethylarsine. Perforation of the cornea has taken place, with      infection of      the anterior chamber
   84.    Blister formation in    epiglottis in a clog    dying acutely from exposure to dichlorethylarsine. The epidermis is severely      damaged and there is a widespread inflammatory        reaction in the tissues        beneath  
   85. A higher    magnification of one of the    blisters shown in Figure 84. The fluid of the bleb is rich in fibrin, which stains      deeply  
   86. Complete necrosis    of the mucosa of a    large bronchus, resulting from dichlorethylarsine gassing. There is a marked      inflammatory reaction throughout the wall of        the bronchus  
   87. Thick layer of    fibrin along the alveolar    wall 7 days after phosgene poisoning 
   88. Hemorrhage into a    perivascular sheath of    a pulmonary vessel in a dog dying 10 days after phosgene gassing  
   89. Necrosis of    bronchial epithelium with    acute inflammatory reaction 24 hours after chlorine gassing  
   90. Wall of small    bronchus showing    mucosa entirely destroyed by phosgene and a large bronchus of same animal with      uninjured      mucosa  
   91. A comparison of    the injury to the    tracheal mucosa by chloropicrin, phosgene, and chlorine. A, Chloropicrin, with damaged      but      intact epithelium; B, chloropicrin with sloughing of superficial epithelial      layer; C, phosgene, with undamaged mucosa; D,        chlorine, with killed and        exfoliated        mucosa  
   92. Mustard-gas    lesion at 1 hour  
   93. Mustard-gas    lesion at 3 hours  
   94. Mustard-gas    lesion at 18 hours  
   95. Mustard-gas    lesion at 22 hours  
   96. Mustard-gas    lesion at 46 hours 
   97. Mustard-gas    lesion at 72 hours 
   98. Mustard-gas    lesion at 4 days 
   99. Mustard-gas    lesion at 9    days  
   100. Mustard-gas    lesion at 18 days  
   101. Mustard-gas    lesion at 20 days 
   102. Mustard-gas    lesion at 49 days  
   103. Typical    mustard-gas vesicle about 20    hours after application 
   104. Lesion of human    skin one-half hour after    application of mustard gas 
   105. Human skin, 18    hours after application    of mustard gas, Transition between slightly damaged epitheliurn and      epithelium      showing hydropic degeneration. Early        blister formation  
   106. Human skin 18    hours after application of    mustard gas. Early vesicle formation 
   107. Human skin 18    hours after application of    mustard gas. High-power view of hydropic change, with early vesicle      formation  
   108. Human skin 18    hours after application of    mustard gas. High-power view of small      vesicle. Separation of epidermis      from      papillary layer  
   109. Human skin 36    hours after application of    mustard gas. Vesicle formation in epidermis and leucocyte infiltration of      papillae  
   110. Human skin 36    hours after application of    mustard gas. High-power view at border of lesion showing changes in      epidermis      and leucocyte infiltration and edema of papillary layer  
   111. Droplet lesion    of mustard gas on human    skin 7 days after application. Low- power view showing area of necrosis of      epidermis and upper portion of corium, with intense hyperemia of the      surrounding      vessels. Moderate edema and very little small-celled infiltration 
   112. Rabbit.    Application of mustard gas at    11.30 a. m. Droplet used was slightly larger than the standard. Marked      subcutaneous      edema as seen at 4 p. m. on the same day 
   113. Rabbit. Skin of    belly shows results of    four applications of standard drops of mustard gas. Above two areas of typical      edema; the one on the rabbit's right untreated, the one to the left washed      off in      5 minutes by water. The latter is more diffuse, larger in area, but less        intense. Below, on the rabbit's right, an area washed after 5 minutes with soap        containing an excess of free alkali. This area shows the least reaction. On the        lower        left is an area treated, after 5 minutes, with potassinm permanganate. The        reaction here is most marked 
   114. Rabbit. Two areas of    mustard-gas    application. Advanced eschar formation.  
   115. Rabbit.    Low-power view of mustard-gas    lesion in rabbit 2 hours after application. Extreme      subcutaneous edema.      Epidermis      but slightly changed. 
   116. Guinea pig.    Low-power view of    mustard-gas lesion 5 ½ hours after application. Extreme subcutaneous edema. Epidermis      necrosed in center of lesion 
   117. Rabbit. Border    of lesion 2 hours after    application of mustard gas. To the right of the middle, the epidermis is still      living;      to the left nearly completely necrosed, necrosis extending into the      upper      portion of the corium. Early edema
   118. Rabbit. Two    hours after application of    mustard gas. Changes in epidermis and corium. Marked vascular change, with      beginning migration of leucocytes.Small hemorrhages by diapedesis. Early      edema  
   119. Guinea pig 5    ½hours after application    of mustard gas to skin of abdomen. Deep      subcutaneous edema  
   120. Rabbit. Six days    after application of    mustard gas. Treatment with zinc oxide paste 5 minutes after use of      mustard      gas. Center of lesion, complete necrosis of epidermis, hair follicles,      and      upper portion of corium, extending  even to the sweat glands. No reaction  
   121. Rabbit. Six days    after application of    mustard gas. Treatment with zinc ointment 5 minutes after application.      There      was no edema stage. Epidermis is dead, and there is a moderate      inflammatory      reaction in the corium. Reaction much less intense than in control  
   122. Rabbit. Six days    after application of    mustard gas. Treatment after 5 minutes with 2 percent solution of silver      nitrate      and 5 percent lead acetate. Primary edema was nearly completely controlled,      but      necrosis, 6 days later, is marked, extending        deep into the corium, with        more        rapid separation of the slough  
   123. Rabbit.    Periphery of same lesion as    Figure 122. Area of less damage 
   124. Rabbit. Six days    after application of      mustard gas, untreated. Border of lesion. Necrosis less marked. Beginning        repair  
   125. Rabbit. Six days    after application of    mustard gas, untreated. Intermediate zone. Separation of necrotic epidermis      and      papillary layer, with infiltration of leucocytes into the necrotic tissue.      Fibroblastic proliferation in lower part of       dermis, with regeneration of hair      follicles.      Intense congestion of subcutaneous vessels 
   126. Rabbit. Six days    after application,    untreated. Adherent slough, representing the necrotic epidermis and upper portion      of      the corium, involving the hair follicles 
   127. Section of skin    of penis, 8 days after    exposure to strong concentration of mustard-gas      vapor. Intense hyperemia 
   128. Section of skin    of scrotum, from same    individual as in Figure 127. Necrosis of epidermis; intense hyperemia 
   129. Human skin 1    week after exposure to    strong concentration of mustard-gas vapor. Microscopically, the changes      consist      of increased cornification, pycnosis of the cells of the epidermis,      and      necrosis of the papillary layer of the       corium. The only living cells in the      upper      portion of the corium are pigmented chromatophores 
   130. Human skin 1    week after exposure to    strong concentration of mustard-gas vapor. Edge of large vesicle showing the      necrosis of the upper portion of the corium, congestion of vessels, and      separation      of the epidermis 
   131. Section    of skin from same case as Figure      130. Area of collapsed vesicles; necrosis of epidermis and corium;        congestion        of vessels  
   132. Skin from axilla    of same patient as    Figure 130. Necrosis of skin to the depth of the large sweat glands. These show      also      partial necrosis, with some early regeneration 
   133 Infected    gangrenous area from skin of    back  
   134. Section of    corium from skin of same    patient as Figure 130, showing dlilated lymphatics filled with fibrin thrombi,      in the      lower portion of the corium.Some of these lymphatics contain      partially      hemolyzed red blood cells in small numbers 
   135. Microscopic    section of eschar 4 weeks    after exposure. Areas of regenerating epithelium from the sweat glands  
   136. Microscopic    appearance mustard-gas    decubitus 4 weeks after exposure. Destruction of tissue too great for      regeneration.      Necrosis extends below the level of the sweat glands 
   137. Photomicrograph    of regenerating    epidermis under the wet Dakin and saline method of treatment, 4 weeks after      injury.      Note the regeneration of the epithelium from the remains of the hair      follicles and sweat glands 
   138. Completely    healed mustard-gas lesion 4    weeks after injury treated 12 days with grease method, with increasing infection      and      gangrene. Under the wet Dakin and saline method infection was checked      promptly and healing begun. Regeneration of epidermis from hair      follicles      and sweat glands 
   139. Photograph taken    1 week after 40    minutes' exposure to strong concentration of mustard-gas vapor. Treated with grease      method      during this time, with increasing infection and gangrene of      epidermis.      Change of treatment to the wet Dakin saline method effected prompt      healing  
   140. Diffuse erythema    of the skin due to    exposure for 10 to 12 minutes to strong concentration of mustard gas. Treated 1      week      by the grease method, with increasing infection of the dead skin,      particularly around the genitals and       anus. Change of treatment to the wet      Dakin      and saline methods resulted in prompt healing 
   141. Rear view of    same patient shown in    Figure 140  
   142. Acute urethritis    and phimosis due to    mustard gas. One week after exposure
   143. Buttocks of same    patient as Figure 142
   144. Photograph 1    week after one-half hour    exposure to strong concentration of mustard gas. During this time treated by      the      grease method. Photograph shows very well the protection afforded      by      the tight belt. The more marked       lesions in the axillae, bends of the      elbows,      and genitals, and the large flaky character of the primary desquamation      and the      pigmentation are well shown 
   145. Back of patient    shown in Figure 144 
   146. Diagram    illustrating the distribution of    mustard-gas eschars, 4 weeks after exposure to strong concentration of      mustard      gas. The hatched areas represent the lesions  
   147. Mustard-gas    lesions of back at 1 week 
   148. Skin lesions of    mustard gassing 1 week    after exposure 
   149. Twenty-four    hours after direct    application of standard droplet of dichlorethylsulphide to cornea of right eye. Marked      edema      of lids and surrounding subcutaneous        tissue  
   150. Twenty-four    hours after direct    application of standard droplet of dichlorethysulphide to cornea. Marked edema of      lids,      flecks of purulent exudate. The marked congestion of the conjunctival      vessels      is best seen in the bulging edematous mass of the superior palpebral      conjunctiva  
   151. Twenty-four    hours after direct    application of standard droplet of crude mustard-gas liquid to the cornea. Extreme edema      of      conjunctiva, especially marked in upper lid and nictitating membrane.      Seropurulent exudate 
   152. One week after    direct application of    standard droplet of dichlorethylsulphide to the cornea. Lids still somewhat      edematous.      They were sealed by a marked purulent exudate which adheres along the      lid      margins and to the adjacent hair. A marked purulent rhinitis,      referable      to involvement of the mucosa through the nasolacrymal duct, is evident  
   153. Two weeks after    direct application of    standard droplet of dichlorethylsulphide to the cornea. Marked reduction of      edema.      Much less purulent exudate. Indurated lids exhibit the      characteristic  "ruffling" and partial entropion of the upper lid in the later stage and the      smooth ectropion of the lower lid. The lower half of the cornea shows a marked      clouding  
   154. Two weeks after    direct application of    standard droplet of dichlorethylsulphide to the cornea. Marked depilation about      the      eye. Characteristic "ruffling' and entropion of upper lid and marked      ectropion of lower lid. The corneal cloudiness and lack of luster are very      apparent, likewise the staphyloma in the lower half of the anterior quadrant 
   155. Two weeks after    direct application of    standard droplet of dichlorethylsulphide to cornea. Specimen obtained by excision      of      lids and orbital evisceration. Marked depilation especially at the      inner      canthus. Characteristic "ruffling" and entropion of upper lid. Corneal      cloudiness  
   156. Three weeks    after direct application of    standard droplet of dichlorethylsulplhide to center of cornea. Same rabbit as      Figure      154. Marked ectropion of lower lid. Porcelainlike cloudiness of the      cornea      most marked in the lower half 
   157. Three weeks    after direct application of    standard droplet of dichlorethylsulphide to cornea. Specimen obtained by excision      of      lids and evisceration of orbit. Anterior segment of globe in profile to      show      apparent staphyloma of cornea toward the inner canthus. The corneal      cloudiness is well shown  
   158. Rabbit's eye at    4 weeks after direct    application of standard droplet of dichlorethylsulphide to cornea 
   159. Six weeks after    direct application of    standard droplet of dichlorethylsulphlide to cornea. Combined ectropion and entropion      of upper lid with resulting "ruffling" of lid margin. Ectropion of      lower      lid. Organization of the necrotic cornea with extensive arborizations of      newly      formed blood vessels, best seen in the upper half of the cornea. Even in      the      photographs these can be traced from the sclera across the superior arc      of      the limbus to the central portion of the cornea. The same eye is shown in      Figures      160 and 161  
   160. Enlargement of    Figure 159, to show    details of changes  
   161. Seven weeks    after direct application of    standard droplet of dichlorethylsulphide to cornea. Same eye as in Figure 159.      Here      given in profile to show marked irregularity of covered surface. Note      especially the prominent apparent staphyloma in the selera toward the      inner      canthus  
   162. Five weeks after    direct application of    dichlorethylsulphide to cornea. Dosage about twice the size of the standard      droplet.      Lids not separated. Eye untreated. Resulting panophthalmitis,      with      collapse of eyeball  
   163. Cornea 2 hours    after application of    standard droplet of dichlorethylsulphide. First stage of necrosis of corneal      epithelium      and of the cells of the interstitial substance. Marked pycnosis of the      corneal      epithelium, the cells of the lowest layer alone being barely      distinguishable. The      nuclei of the interstitial substance and of the endothelial lining of      the      anterior chamber are also pycnotic. Section taken at corneal vertex 
   164. Section of    cornea at vertex 5 hours    after direct application of standard droplet of dichlorethylsulphide. Desquamation of      necrotic epithelium in center of vertex. Pycnosis of remaining epithelium      and      of cells of the interstitial substance.        Complete necrosis of endothelial        cells of anterior chamber 
   165. Section of    palpebral conjuntiva 8 hours    after application of standard droplet of dichlorethylsulphide. Complete necrosis      of      epithelium. Marked congestion. Minute hemorrhages. Polynuclear      infiltration 
   166. Palpebral    conjunctiva 26 hours after    application of standard droplet of dichlorethylsulphide, showing advancing      necrosis,      more marked infiltration, congestion, minute hemorrhages, and edema 
   167. Cornea 30 hours    after exposure to vapor    of dichlorethylsulphide. Complete necrosis of cornea 
   168. Palpebral    conjunctiva 34 hours after    application of standard droplet of dichlorethylsulphide. Section at fornix of upper      lid, showing the complete loss of the necrotic surface, extreme edema, and      polynuclear infiltration 
   169. Section from the    same region as in    Figure 168, but taken deeper down, showing the extreme edema and liquefaction      necrosis,      below the narrow band of the sphincter orbicularis 
   170. Cornea 42 hours    after application of    standard droplet of dichlorethylsulphide. Membrane of Descemet appears as a bright      hyaline line staining red with eosin  
   171. Cornea 3 ½ days    after application of    standard droplet of dichlorethylsulphide. Complete necrosis of corneal tissue;      ulceration of surface; beginning infiltration with polynuclear leucocytes and      collection of      polynuclear leucocytes along the line of the necrotic endothelium  
   172. Section of    sclerocorneal junction 3½    days after application of standard droplet of dichlorethylsulphide. Infiltration of      leucocytes, beginning fibroblastic and angioblastic proliferation 
   173. Section of upper    lid at palpebral margin    4 days after direct application of standard droplet of      dichlorethylsulphide.      Advanced ulceration, beginning repair  
   174. Section of same    lid, near fornix.    Regeneration of the conjunctival epithelium. Disappearance of the edema and advancing      cicatrization of the subconjunctival      tissues  
   175. Section of    corneal vertex 7 days after    application of standard droplet of dichlorethylsulphide. Ulcerated surface.      Infiltration of necrotic cornea with polynuclears and scattered fibroblasts.      Beginning regeneration of endothelium 
   176. Section of    corneal vertex 4 weeks after    application of standard droplet of dichlorethylsulphide, showing the marked      irregularities in the corneal surface; regeneration of corneal epithelium and      endothelium of anterior chamber;       edema of the interstitial substance with      some      fibroblastic repair 
   177. Sclerocorneal    junction of same eye as in    Figure 176, 4 weeks after application of standard droplet of      dichlorethylsulphide,      showing vascularization and repair proceeding from the sclera 
   178. Section of    corneal limbus 4 weeks after    application of standard droplet of dichlorethylsulphide. Advancing repair into the      cornea from the sclerocorneal junction 
   179. Section from the    inferior portion of the    cornea 7 weeks after application of the standard droplet of      dichlorethylsulphide.      Persistent ulcer; marked polynuclear infiltration of the cornea, and      repair.      Blood vessels have reached the 
      center of the cornea 
   180. Section from the    inferior portion of    corneal limbus, 7 weeks after application of standard droplet of      dichlorethylsulphide.      Partial regeneration of corneal epithelium. Marked polynuclear      infiltration      and advanced vascularization and repair of the substantia propria.        Regeneration of the endothelium of the anterior        chamber 
   181. Section from the    superior half of the    corneal vertex 7 weeks after application of standard droplet of      dichlorethylsulphide,      showing the greater degree of cicatrization usually found in this portion 
   182. Section of    corneal limbus from same eye    as Figure 181, showing advanced cicatrization 
   183. Ciliary body    from eye of rabbit exposed    12 hours in gassing chamber to a concentration of 1 to 50,000      dichlorethylsulphide      vapor. Animal died 92 hours later. Marked collection of polynuclear      leucocytes in anterior chamber, in the ciliary body, and in the iris of the      left      eye, which had received no treatment with the dichloramine-T solution  
   184. Iris of same eye    in Figure 183 showing congestion, edema, and polynuclear infiltration.    Marked polynuclear exudate in    the anterior chamber 
   185. Congestion of    the conjunctival vessels    persisting to a marked degree, 4 weeks after exposure to dichlorethlysulphide      vapor 
   186. Persistent    congestion 4 weeks after    exposure to dichlorethylsulphide vapor. Acute symptoms were very severe and the      patient still complained of dimness of vision when he left the hospital      after 5      weeks 
   187. Marked    conjunctival congestion and    hordeolum of left upper lid in a case of severe mustard-gas conjunctivitis, 4      weeks      after exposure. The hordeolum is a part of the general staphylococcus      furunculosis which may characterize the later stages of the severe skin burns 
   188.    Dichlorethylsulphide conjunctivitis 4    weeks after exposure to vapor. In the acute stage there was extreme      photophobia,      lacrymation, pain, edema, and purulent exudation. The residual      congestion      and seropurulent exudation are still evident 
   189.    Dichlorethylsulphide conjunctivitis 4    weeks after exposure to vapor. The severity of the original process is indicated by      the      severe skin changes. The persistent congestion is the sole evidence of the      severe      conjunctivitis that was present 
   190. Experimental    gassing apparatus.    Pathological laboratory, University of Michigan. A, washer containing sulphuric      acid; B, gas container; C, gassing box; D and E, degassing bottles; F,      standard      gas meter; G, suction pump  
   191. Rabbit. Exposed    40 minutes to a I to    110,000 concentration of dichlorethylsulphide vapor. Killed 12 hours after      removal      from gassing chamber. Section of lung. Marked congestion, edema,      and      areas of partial atelectasis alternating with those of emphysema 
   192. Exposed 20    minutes to a concentration of    1 to 15,000 dichlorethylsulphide vapor. Killed 36 hours after gassing. Section      of      trachea showing acute catarrhal desquamative tracheitis; marked mucoid      degeneration of the epithelium; congestion and edema of the submucosa.      Lumen      filled with mucous containing many desquamated cells 
   193. Rabbit. Exposed    30 minutes to a    concentration of 1 to 15,000 dichlorethylsulphide vapor. Killed 4 ¼ days after      gassing.      Section of larger bronchus, showing lumen filled with edema fluid.      Bronchial epithelium shows marked       mucoid and hydropic degeneration 
   194. Lung of same    rabbit as Figure 193. Acute    congestion and edema 
   195. Section of    laryngeal mucosa of rabbit.    Exposed 35 minutes to a concentration of 1 to 30,000 dichlorethylsulphide      vapor.      Killed 30 hours after gassing. Pycnosis and mucoid degeneration of the      epithelium. Marked congestion and- edema of the submucosa  
   196. Section of    tracheal wall of same rabbit    as Figure 195. Similar changes in epithelium and submucosa  
   197. Exposed 6 hours    to a concentration of 1    to 50,000 dichlorethylsulphide vapor. Died 60 hours after gassing. Section of      large      bronchus showing purulent necrotic        bronchitis  
   198. Section of lung    from same case as Figure    197. Area of purulent bronchopneumonia, with colony of cocci in the      center of      the field 
   199. Rabbit. Exposed    for 6 hours to a    concentration of 1 to 50,000 dichlorethylsulphide vapor. Died 7 days after      gassing.      Eschar from upper portion of larynx  
   200. Same rabbit as    in Figure 199. Section of    larynx showing diphtheritic ulcer
   201. Mustard-gas    lesions of tongue, pharynx,    larynx, and trachea, in fatal human case. Dorsum of tongue shows      diphtheritic      eschars. Diphtheritic necrosis of pharynx, mucosa of larynx, and      trachea.      Marked edema, with diphtheritic       necrosis of the arytenoepiglottidean fold 
   202. Case I. Private    Ha. Mustard-gas lesion    of dorsum of tongue. Base of ulcer from which the diphtheritic membrane has      become detached 
   203. Case I. Private    Ha. Section of    diphtheritic lesion on vocal cord. Epithelium of mucosa completely destroyed and a      mucofibrinous membrane partly detached from the surface. Extreme      hyperemia of      the vessels. Some small-celled    infiltration 
   204. Case I. Private    Ha. Section of main    division of bronchus. Picture of catarrhal bronchitis. Marked mucoid      degeneration and vacuolation of the bronchial epithelium. Congestion,      small-celled infiltration, and edema of       the bronchial      wall 
   205. Case I. Private    Ha. Section of upper    lobe of lung. Congestion and edema. Acute emphysema 
   206. Case I. Private    Ha. Section of lower    lobe of lung. More intense congestion. Minute hemorrhages by diapedesis. Areas      of      partial atelectasis, alternating with emphysematous areas. Edema 
   207. Dog. Received 4    minims of    dichlorethylsulphide on meat. Died 5 days afterwards. Small mustard-gas eschar in      stomach      mucosa. Early fibroblastic proliferation 
   208. Dog. Received    0.06 c. c. of    dichlorethylsulphide in capsule. Died 12 days later. Portion of base of very large      eschar      of stomach wall, extending nearly to the serosa. Marked leucocyte      infiltration 
   209. Rabbit. Exposed    12 hours to a    concentration of 1 to 50,000. Died 92 hours after gassing. Mustard-gas eschar on      tongue 
   210. Rabbit. Eschar    resulting from    subcutaneous injection of 0.03 c. c. of dichlorethylsulphide, 18 days after      injection 
   211. Rabbit. Eschar    resulting from    subcutaneous injection of 0.06 c. c. of dichlorethylsulphide, 11 days after    injection 
   212. Rabbit. Received    subcutaneous injection    of 0.045 c. c. of dichlorethylsulphlide. Died on third day during mild diarrhea.      General mucoid degeneration 
   213. Rabbit. Received    subcutaneous injection    of 0.18 c. c. of dichlorethylsulphide. Began to have diarrhea 7 days after      injection      and died 4 days later. Section of upper portion of small intestine      showing      acute catarrhal enteritis 
   214. Same rabbit as    in Figure 213. Extreme    mucoid degeneration. Catarrhalenteritis. Mucous diarrhea 
   215. Section of cecal    wall from same rabbit    as in Figure 213. Marked catarrhal inflammation.      Mucous      diarrhea-
   216. Rabbit. Received    subcutaneous injection    of 12 c. c. of dichlorethylsulphide. Diarrhea began on second day, the animal      dying 3 days later. Extreme mucoid degeneration of the entire      intestinal      epithelium. Mucous diarrhea 
   217. Dog. Received    subcutaneous injection of    0.24 c. c. of dichlorethylsulphide. Died in 4 days, with a very severe      diarrhea.      Extreme catarrhal desquamative enteritis.        Mucoid degeneration and        necrosis        of the glandular epithelium  
   218. Same dog as in    Figure 217. Middle    portion of small intestine showing desquamation of the superficial epithelium and      necrosis of the epithelium of the gland of Lieberkuehn.        Severe enteritis 
   219. Rabbit. Received    subcutaneous injection    of 0.06 c. c. of dichlorethylsulphide. Severe diarrhea from fourth to ninth      day.      Killed 15 days after injection. Mucosa of intestines intensely congested      and      edematous. Marked mucoid degeneration with cystic glands.      Regeneration of superficial epithelium 
   220. Rabbit. Received    subcutaneous injection    of 0.06 c. c. of dichlorethylsulphide. Very severe diarrhea on fifth to seventh      day      afterwards. Apparent recovery. Killed on the thirty-second day after      injection. Mucosa shows excessive        mucous formation 
   221. Rabbit. Received    subcutaneous injection    of 0.03 c. c. of dichlorethylsulphide. Very severe diarrhea on fourth to eighth      day.      Died on twelfth day after injection. Intestines showed severe      catarrhal      enteritis. Section of spleen showing    the great number of pigmented    phagocytes in the blood sinuses 
   222. Rabbit.    Sloughing lesion produced by    subcutaneous injection of 0.60 c. c. of hydrochloric acid, 24 hours after      injection 
   223. Detrimental    effects of water (Vapor    tests). Dichlorethylsulphide vapor was applied to the skin; 62, bare skin; 63,.      skin      coated with water; 64, skin coated with sodium bicarbonate water paste; 65,      skin      coated with soap; 66, skin coated with kaolin water paste. The photograph      was      taken 7 days after the application.        (The figures in parenthesis refer        to        experiments) 
   224. Protective    action of petrolatum when    dichlorethylsulphide is applied as "splash," and when applied through fabric. In      experiments No. 10 and No. 11 the alcoholic dichlorethylsulphide was      applied      directly to the skin; No. 11 was       previously vaselined. The protective      value of      the petrolatum in No. 11 is apparent. In No. 12 and No. 13 the      alcoholic      dichlorethylsulphide was dropped on a small square of cloth and      this      was applied to the skin; No. 13 was first oiled with      petrolatum. Note that      the two lesions are practically alike. The photograph was taken 19 days      after      the application 
   225. Value of    protective oiling. In No. 8 the    dichlorethylsulphide was applied to the bare skin, in No. 9 to oiled skin. Both      were      washed with oil, after 15 minutes. Observe the much greater effect on      the      unprotected skin in No. 8. The    photograph was taken 24 days after    the    application 
   226. Comparison of    oils. Observe the degree    of effect. Each area received 0.01 c. c. of 3 percent solution of      dichlorethylsulphide in the oil, spread over a surface of about one-half inch diameter.      The      photograph was taken 2 days       after application. The solvent oils were      as      follows: 110, liquid petrolatum; 111, raw linseed oil; 112, boiled      linseed      oil; 113, olive oil; 114, castor oil; 115, cod-liver        oil. (The figures refer to        experiments) 
   227. Protective value    of dichloramine-T.    Pieces of filter paper about 5 min. square, and containing about 0.001 c. c. of 95      per      cent dichlorethylsulphide were applied to the center of a square of      skin,      covered with the protectives. The       coatings were as follows: 117, raw      linseed      oil; 118, linseed oil and kaolin, 1 to 3; 119, same, with 3 per cent of soft      soap;      120, petrolatum kaolin, 1 to 1; 121, dichloramine-T, 10 percent in      chlorcosane; 122, solid paraffin. The photographs were made 1 day after the      application. Note that the reaction is less in 121 than in the others; 26 and      30 are      recrudescences of lesions 25 days old. (The figures refer to      experiments) 
   228. Efficiency of    dry powders.    Dichlorethylsulphide vapor was applied. Note the normal lesion in the bare skin (26); the      slight protection afforded 1b zinc stearate (30); and the complete      protection      from kaolin, fuller's earth, and       charcoal, indicated by the absence of      lesions      in a straight line drawn from (26) to (30). The photograph was taken 3 days      after the application. (The numbers in parenthesis refer to      experiments) 
   229. Rabbit No. 9,    serial No. 41. Death 2 1/2    hours after second injection of dichlorethylsulphide. Lung: Edema (oe) in part      fibrinous. Stasis of leucocytes (Lc) in capillaries. Coagulum in      bronchus (B)      and distension of peribronchial lymphatic vessel (L) 
   230. Rabbit No.    13, serial No. 55.    Died in less than 18 hours after intravenous injection of dichlorethylsulphide, 0.01 g.      per      kilo. Spleen, showing caryorrhexis of cells of follicles, with phagocytosis      of      chromatin fragments  
   231. Rabbit No. 20,    serial No. 96. Died 4    days after injection of 0.1 gin. per kilo intravenously. Small intestine: Complete      hemorrhagic necrosis of mucosa (AM); extreme fibrinous edema of submucosa (Oe) 
   232. Normal rabbit.    Bone marrow of femur.    Megacaryocyte (M) 
   233. Rabbit No. 24,    serial No. 104. Died 3    days after second injection of dichlorethylsulphide, 0.005 gm. per kilo      intravenously. Bone marrow of femur, showing extreme aplasia. The sinuses (B)      are      wide and congested. In the edematous pulp (oe) are many fat cells      (F).      Myelocytes, polymorphonuclears, and megacaryocytes are absent.      There      are few islands of normoblasts (N). The pale nuclei (R) are those of      the      reticular cells. (Somewhat lower magnification than Figure 232 
   234.    Dichlorethylsulphide, 11 hours after    exposure. Collagen fibers (C) separated by granular coagulum (oe). Distended      lymphatic vessel (L). Emigrated leucocytes (1c) 
   235.    Dichlorethylsulphide, 98 hours after    exposure. Superficial pustules (p) at margin of lesion. Increased pigmentation      (pq)      in adjacent epithelium. Leucocvtic infiltration of corium 
    236. Dichlorethylsulphide, 98 hours    after    exposure. Thinning of epithelium (E), infiltration of corium (C) with    leucocytes    showing caryorrhexis. Degenerated hair follicles (H) 
   237.    Dichlorethylsulphide, 7 days after    exposure. Beginning sequestration of necrotic epithelium (El) and superficial      corium (C) by ingrowth of regenerating epithelium        (E2). Proliferation of cells        of        sheaths of hair follicles (H1H2)  
   238.    Dichlorethylsulphide, 14 days after    exposure. The sequestration of the dead epidermis (El) and the underlying      necrotic      tissue (C,) by ingrowth of regenerating        epithelium (E2). Desquamated keratin        (K)  
   239.    Dichlorethylsulphide, 14 days after    exposure. Same designations as Figure 238
   240.    Dichlorethylsulphide, 11 days after exposure. Hypertrophic cells at    margin of hair follicles 
   241. Lewisite No. 1,    24 hours after exposure.    Edema, leucocytes in corium (L). congestion of superficial capillaries      (B),      early degenerative changes and thinning of epidermis (E) 
   242. Lewisite No. 1,    48 hours after exposure.    Transition between living epidermis (El) and dead epidermis (E2). Leucocytic      infiltration at margin of lesion (Ic), edema of deeper layers (oe) 


