14 Ocak 2016 Perşembe

THE HELL FIRE HAPPY NEW HIJRI YEAR OF 1438 The "Hell Fire Battalion" is going "over there" within a short time. To-day they are preparing for the trip. Full equipment has been issued, and they expect to see action as soon as they arrive. There will be no long period in training camps for the "Hell Fire Boys." They will go immediately to the front, where they will train under actual war conditions with French and British "gassers." Thousands of dollars have been spent in research work for the "Hell Fire THE DAYS OF THE HELL FIRE ARE BACK ....THE TWO THOUSAND WAYS OF DESTROYING AMERICA FASTER THAN OBAMA OR THE CHINESE - TWO POUNDS OF PHOSGENE IN THE NY SUBWAY TWO SPOON'S OF TABUN VX OR SOMAN IN SOME WALL STREET OFFICE OR BANK AND THE DOWN JONES GOT DOW'N FASTER THAN THE CHINESE AND TRUMP HAVE PLENTY OF HUSSEINS TO DO THAT FOR HIM Soman, or GD (systematic name: O-Pinacolyl methylphosphonofluoridate), is an extremely toxic chemical substance. It is a nerve agent, interfering with normal functioning of the mammalian nervous system by inhibiting the cholinesterase enzyme. It is an inhibitor of both acetylcholinesterase and butyrylcholinesterase The LCt50 for soman is 70 mg·min/m3 in humans. It is both more lethal and more persistent than sarin or tabun, but less so than cyclosarin Soman is synthesized by reacting pinacolyl alcohol with methylphosphonyl difluoride. The result of this reaction is the forming of soman (3,3-dimethylbutan-2-yl methylphosphonofluoridate) which is described as “colorless liquid with a somewhat fruity odor.” The low vapor pressure of soman will also produce the volatile gas form of soman. Also, the acid hydrogen fluoride will form due to the elimination of fluoride and a proton. This acid is indirectly dangerous to humans. Skin contact with hydrogen fluoride will cause an immediate reaction with water which produces hydrofluoric acid. Tabun was made on an industrial scale by Germany during World War II, based on a process developed by Gerhard Schrader. In the chemical agent factory in Dyhernfurth an der Oder, codenamed "Hochwerk", at least 12,000 metric tons of this agent were manufactured between 1942 and 1945. The manufacturing process consisted of two steps, the first being reaction of gaseous dimethylamine (1) with an excess of phosphoryl chloride (2), yielding dimethylamidophosphoric dichloride (3, codenamed "Produkt 39" or "D 4") and dimethylammonium chloride (4). The dimethylamidophosphoric dichloride thus obtained was purified by vacuum distillation and thereafter transferred to the main Tabun production line. Here it was reacted with an excess of sodium cyanide (5), dispersed in dry chlorobenzene, yielding the intermediate dimethylamidophosphoric dicyanide (not depicted in the scheme) and sodium chloride (8); then, absolute ethanol (6) was added, reacting with the dimethylamidophosphoric dicyanide to yield tabun (7) and hydrogen cyanide (9). After the reaction, the mixture (consisting of about 75% chlorobenzene and 25% tabun, along with insoluble salts and the rest of the hydrogen cyanide) was filtered to remove the insoluble salts and vacuum-distilled to remove hydrogen cyanide and excess chlorobenzene, so yielding the technical product, consisting either of 95% tabun with 5% chlorobenzene (Tabun A) or (later in the war) of 80% tabun with 20% chlorobenzene (Tabun B) Like its predecessor sarin, cyclosarin is a liquid organophosphate nerve agent. Its physical characteristics are, however, quite different from sarin. At room temperature, cyclosarin is a colorless liquid whose odor has been variously described as sweet and musty, or resembling peaches or shellac. Unlike sarin, cyclosarin is a persistent liquid, meaning that it has a low vapor pressure and therefore evaporates relatively slowly, about 69 times slower than sarin and 20 times slower than water. Also unlike sarin, cyclosarin is flammable, with a flash point of 94 °C (201 °F). Cyclosarin (GF) also demonstrates greater toxicity than sarin (GB) in humans. Sarin has a median lethal dose (LD50) of 5 mg (for a 70 kg human), while GF has an LD50 of 1.2 mg. The median lethal concentration and time (LCt50) of cyclosarin is 50 mg⋅min/m3, which is half that of GB. Like other nerve agents, cyclosarin can be shipped in binary munitions. A cyclosarin binary weapon would most likely contain methylphosphonyl difluoride in one capsule, with the other capsule containing either cyclohexanol or a mixture of cyclohexylamine and cyclohexanol

cyclosarin, a product of commercial

 insecticide laboratories prior to 1939





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 

(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. 


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 


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.