insecticide laboratories prior to 1939
IS JUST BY ISIS A QUESTION OF TIME
AND MONEY AND IS CHEAP THAN
THE A-BOMB FROM IRANIAN LANDS
USE ONLY IN CONFINED ENVIRONMENTS
They are Phosgene
(COCy, and Di-chlor-ethyl-sulphide, (CH4C1)^S, or ' Mustard Gas'. Phosgene is the chief of all the many gasses and liquids that are used for their effects as pulmonary irritants. Chlorine belongs to this group and was the first Poison Gas used by the Germans in April 1915, but it has long since been superseded by more effective chemical substances. The pulmonary irritants are inhaled as gasses or vapours. They may cause some water- ing of the eyes, but the chief effect noticed at once is a catching of the breath or a choking sensation so that the chest feels gripped and incapable of free respiration. Coughing and vomiting may follow, and then after a delay of time varying from a few minutes to several hours an inflammatory reaction appears in the lungs themselves, with the development of an acute oedema that may commence insidiously and yet progress so rapidly as soon to be an immediate menace to life itself. The alveoli fill with oedema fluid, which then rises into the bronchial tubes and may appear in a most abundant expectoration of thin frothy fluid. Aeration of the blood is seriously interfered with, because the air sacs are either drowned with oedema fluid or burst by the efforts of coughing. Moreover the actual circulation through the lungs is embarrassed, both by the pressure of the oedema fluid on the capillary vessels and by the local thrombosis that occurs in many places in the smaller lung vessels. The blood itself is concentrated by the loss of serum so that the count may rise to even eight or nine million red corpuscles to the cu. mm. and this change probably adds to the difficulties of the circulation. The gassed man can no longer get the oxygen that he wants, and he either dies in obvious asphyxia with progressive circulatory failure, or he collapses as the result of some muscular effort that suddenly makes a greater call for oxygen and so reveals the deficiency of the supply. Death is the result simply of this inflammatory oedema of the lung, and it occurs chiefly in the first and second day after exposure to Phosgene. A few cases may chance to develop secondary bacterial infections of the lungs and to succumb to a later broncho-pneumonia, but they are relatively rare. The main clinical features of acute Phosgene poisoning may therefore be summarized as follows : (i) Catching of the breath, choking, and coughing immediately on exposure to the gas. (ii) Inability to expand the chest in a full breath after removal from the poisoned air. (iii) Vomiting, hurried shallow respiration, and sometimes coughing with an abundant expectoration, follow. Pain is felt behind the sternum and across the lower part of the chest. Fine rales are heard in the axillae and over the back. (iv) Cyanosis next appears, in association either with a full venous congestion or with the pallid face of circulatory failure. The development of these dangerous symptoms may occur after many hours' delay, and sometimes with unexpected rapidity in an apparently slight case as the result of muscular effort. (v) Death, which may or may not be preceded by mild delirium or unconsciousness, rarely occurs after the first or second day. Di-chlor-ethyl-sulphide is spoken of as being a vesicant. It may exert its irritant action either as a vapour in low concentra- tion in the air or b}'^ direct contact from splashes of the liquid. The liquid or vapour clings to the clothing of men exposed to Yellow Cross shells, and thus slowly exerts its continuously irritant action on their bodies. No irritant effect at all is felt on first exposure, whatever the concentration may be, but after a delay of about two to six hours the skin and mucous membranes begin to react with a progressive inflammation that may result in local necrosis and desquamation of these covering membranes. There is intense conjunctivitis; the skin turns an angry red, and this erythema is soon followed by skin blistering here and there over the face and body. The passage of the vapour down the respiratory tract may cause such severe injury to the lining mucous membranes of the trachea and bronchioles that they are eventually destroyed and sloughed away. Bacterial infection then seizes upon these raw surfaces, and the patient may die from secondary septic broncho-pneumonia. Death is never the direct result of the action of the poisonous vapour. From the 2nd day onward through the first and second week severely affected men may die, but only as the result of secondary bacterial infection. This poison therefore differs entirely from the lung irritants such as Phosgene, which kill directly and speedily b}^ flooding the lungs with oedema fluid. The main features of poisoning from Mustard Gas may be resumed as follows : (i) Delay of the irritant effect for at 'least two to three hours, and then a comparatively slow development of the various inflammatory reactions. (ii) Vomiting, and a sense of burning in the eyes, with discomfort in the throat, hoarse cough, and some retro-sternal pain. (iii) Intense conjunctivitis that temporarily 'Winds' the man. (iv) Burning of the exposed skin surfaces and of the moist areas in the axillae and groin, followed by blistering, excoriation, and brown staining. (v) Inflammatory necrosis of the mucous membrane of the trachea and bronchi, with the secondary development of infec- tive bronchitis or septic broncho-pneumonia. (vi) Death is relatively uncommon : it occurs later than the first day and only as the result of septic complications. LIST OF PLATES No. I. Microscopic section of human lung from phosgene shell poisoning. Death at the nineteenth hour after gassing. II. Blue type of asphyxia from phosgene poisoning, with intense venous congestion. III. Pallid type of asphyxia from phosgene poisoning, with circulatory failure. IV. Gangrene of foot caused by vascular thrombosis from chlorine poisoning. V. Erythema of skin from general exposure to the vapour of Yellow Cross substance. VI. Blistering of buttocks by mustard gas. VII. Burning of scrotum and penis by mustard gas. VIII. Brown staining from mustard gas. IX. Ulceration of trachea by mustard gas. X. Microscopic section of human lung from mustard gas poisoning, with death at end of second day (40 hours). XI A. Severely burned eye in the acute stage. XIb. Slightly later stage of acute burning. XI I A. Stage of resolution after severe burning. XIIb. Late stage of resolution. XIIIa. Drawing of the cornea in the acute stage of severe burning. XIIIb. Drawing of cornea m the stage of resolution after severe burning. PLATE NO. 1 Microscopic section of human lung from phosgene shell poisoning. Death at the nineteenth hour after gassing. The piece of lung shown is almost entirely useless for aeration of the blood. Most of the pulmonary alveoli are filled with oedema fluid, and the walls of the air-sacs are burst asunder in many places. The rounded edges of these torn walls can be recognized both in the areas of emphysema and in the parts that are flooded with oedema fluid. The bronchus also is filled with oedema fluid, but it should be noted that its lining epithelium is intact and pus cells have not accumulated in the secretion. The blood vessels of the alveolar net- work are congested ; and intravascular thrombosis is frequently found in these smaller vessels, though it is not actually shown in the area of this section. The main changes in the lung are : Congestion, and occasional thrombosis, of the network of pul- monary blood vessels. Abundant outpouring of inflammator}' oedema fluid both into the tissues and into the air spaces of the alveoli and bronchi. Disruptive emphysema of the weakened lung tissue. The result of these changes is that the blood circulation through the lungs is impeded, and the respiratory exchange of gasses between the blood and the air in the lung is seriously diminished. The gassed man is in danger of death by asphyxia so long as his lung is drowned in oedema fluid. From the third day onwards the oedema fluid is reabsorbed or expectorated, and the lung soon resumes its functions. Broncho- pneumonic complications may develop from secondary infections, but they are not very common. The recovery of the lung, even after severe gassing appears to be functionally good. In the earlier stages of convalescence there may still be signs of persisting oxygen want, so that tachycardia with excessively rapid respiration is the result of even slight physical effort. Later these disabilities vanish. The microscopic examination of lungs in these stages of recovery has not been made.