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Volume XIV

Books and Documents

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)