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3.  Chemical warfare is the use of the toxic properties of chemical substances to kill, injure or incapacitate an enemy in warfare and associated military operations  A chemical substance intended for such use in military operations is defined as a chemical warfare agent (CWA).

4.  These have been elaborately described in ancient Chinese literature.  In 600 B.C. Helleborus roots were used successfully by the Athenians to contaminate water supplies  Spartans ignited pitch and sulfur to create toxic fumes during the Peloponnesian War in 429 B.C.  Their use reached a peak during World War I (WWI).  French were the first to use ethylbromoacetate in WWI.  CWA’swere not used on the field during WorldWar II (WWII) due to the fear that the enemy possessed more deadly CWA’s, except for by the Germans who used them in the infamous gas chambers for mass genocide of Jews.  In the Iraq–Iran war,  Acts of terrorisms as in the Japanese underground rail station attacks

6. Iran-Iraq War: 1980-88  Iraq: Chemical weapons ◦ Widespread use  Blistering agent: Lewisite  Nerve agent: Tabun ◦ Heavy Iranian casualties, deaths

7. - 1988: Iraq bombed their Kurds with mustard, nerve and cyanide gas - Over 5,000 died 75% women and children

8. T ECHNICAL C OMPLEXITY Biological Chemical Nuclear R ISK !! Chemical: low complexity, high probability LOWHIGH LOW HIGH

10. Al Qaida threat  Documents found ◦ Chemical agents ◦ Bombs  Reported attempt ◦ Jordan, 2004  US Embassy  Suicide missions ◦ Easier success

11.  The chemical weapons convention (CWC) which came into force in 1997 stated that all member countries must destroy all chemical weapons over a 10-year period, with the treaty providing a “leveling out principle” that ensures possessors destroy their stockpiles at roughly the same time.  More than 170 countries have signed the CWC and 139 have ratified it.

14.  North Atlantic Treaty Organization (NATO) has classified agents of chemical terrorism as

15.  North Atlantic Treaty Organization (NATO) has classified agents of chemical terrorism as:  Blister agents  Nerve agents  Choking agents  Asphyxiants  Behavior altering agents

17. Blister agent or vesicants are a group of chemicals that cause severe blistering when they come in contact with skin. These may also have systemic effects if absorbed These agents are not very lethal as far as causing death is concerned but can incapacitate the enemy and overload the already burdened health care services during war time.

18. These include : sulfur mustard (SM) nitrogen mustard ( NM) Lewisite ( L)

19. Sulfur mustard 1. Mahdi Balali-Mood, M. D., Ph. D. Visiting Professor of Newcastle University, UK. Professor of Medicine and Clinical Toxicology Director, Medical Toxicology Research Centre Imam Reza Hospital, Faculty of Medicine, Mashhad University of Medical Sciences, 2. Beeta Balali-Mood, M Chem, M Res, PhD candidate Department of Chemistry, Imperial College London, London, U. K. 3. Mohammad Moshiri, M.D., Ph.D. student of toxicology Department of Pharmacodynamy and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Iran

20. Definition: Sulfur mustards (SMs), commonly known as mustard gas Since these had a mustard like odor, these were called sulfur mustard or mustard gas. alkylating agents (capable of causing short and long term morbidity.)

21. History:  They were discovered accidentally In 1917  the German forces used SM for the first time in battlefield.  It accounted for about 70% of the million-plus gas related casualties in WWI.

22. Properties:

23.  Sulfur mustard is not a gas but a pale yellow, oily liquid : of specific gravity of 1.27 vaporizes at 25 ◦C decomposes at 217.5 ◦C. Hence it is a liquid in cold and damp environments and easily vaporizes in warm dry environments  It is heavier than air with a density 5.6 times that of air  impure form  odor of mustard  pure form  colorless and odorless  It is sparingly soluble in water and soluble in fat, fat solvents, and other common organic solvents  It penetrates ordinary clothes easily in the vaporized form

24. Uses: It has no industrial use at present

25. Mechanism of human toxicity ☼ SM’s are alkylating agents ☼ They damage all exposed epithelial surfaces, both in aerosol and liquid form ☼ These effects appear within 2–12 h after exposure, depending on the exposure dose ☼ The exact mechanism of its toxicity is yet to be elucidated : (Most) It dissolves aqueous media, such as sweat, rapidly forming extremely reactive cyclic ethylene sulfonium ions. These reactive ions react with deoxyribonucleic acid (DNA) in rapidly dividing cells leading to cellular death and inflammatory reactions (alternative theory) It depletes the cell of Glutathione which leads to oxidative damage and cell death

26. Clinical features: Exposure to SM results in high morbidity and psychological impact but low mortality. The mortality rate with sulfur mustard is estimated to be 2– 5%.

27. Clinical features: Most often exposed surfaces i.e. skin, airways, and eyes suffer the brunt of the damage. ΘEyes Θ Conjunctivitis Θ Photophobia Θ Blepharospasm Θ Pain Θ Corneal damage( can lead to perforation ) Θ Glaucoma may develop later as a result of scarring.

28. Clinical features:  Dermatological manifestations are :  second degree burns  Steven–Johnsons syndrome or toxic epidermal necrosis.  painful erythema  vesicles or bullae containing a transudative straw colored  As the fluid is a transudate it does lead to as much protein loss as would be expected with burns of a similar nature

29. Clinical features:  Inhalation of SM leads to :  irritation of the nose  epistaxisis  pharyngeal pain  laryngitis  voice changes  Cough  Dyspnea  Terminally, There may be necrosis of airways with hemorrhagic edema, pseudomembrane formation and obstruction of the bronchi. Pseudomembrane formation and laryngospasm are the major cause of death in the first 24 h. Secondary bacterial pneumonia may cause mortality between the third and fifth days

30. Clinical features: Systemic absorption from ingestion : gastrointestinal tract ( nausea and vomiting lasting up to 24 h) central nervous system (seizures, behavioral abnormalities and psychological problems) bone marrow suppression.  Late complications :  ulcerative keratitis  Chronic bronchitis  pulmonary fibrosis  hypo or hyperpigmentation of skin  psychological problems.  In a study involving 500 soldiers who were exposed to SM during the Iran– Iraq war (1983–1988) showed that all of them developed either pulmonary or ocular complications 15 years after the war

31. Iraqi Warheads Armed with Sulfur Mustard UN Weapons Inspector Team

32. Treatment: ®There is no specific antidote. ®Supportive treatment remains the mainstay.

33. Treatment: ®Removal of exposed persons by well protected rescuers is of prime importance.  Thereafter removal of all clothing  giving a through bath.  Clothing removed should be packed in plastic bags.

34. Treatment: ® skin : ® Larger bullae require unroofing with saline irrigation and application of antibiotics (silver sulfadiazine or modified Dakins solution) over denuded areas. ® Management of large areas of skin involvement is similar to burns patient requiring supportive measures but with special regard to fluids as these patients are prone to pulmonary edema. ® Eye : ® Irrigation ® topical antibiotic

35. Treatment: ® Respiratory : ® Chemical pneumonitis, characterized by productive cough, dyspnea and fever, occurs within 12–24 h of inhalation ® Infection generally occurs on the third to fifth day, signaled by an increased fever, pulmonary infiltrates, and an increase in sputum production with a change in color. ® Bronchodilators and glucocorticoids are of benefit for bronchospasm. ® Recent research has shown some beneficial effects of vanilloid compounds and N-acetylcysteine in animal trials ® Bone marrow : ® Bone marrow suppression beginning on the 3rd day and peaking at 7–14 days requires granulocyte colony- stimulating factor, transfusion support or even bone marrow transplants

36. Definition: Nitroge nmustard’s (NM’s) are alkylating agents nitrogen analogues of SM’s HN-3HN-2HN-1 (tris(2-chloroethyl) amine(bis(2- chloroethyl) methylamine (bis(2-chloroethyl) ethylamine C6H12Cl3NC5H11Cl2NC6H13Cl2Nformula It is odorless when pure but has been reported to have a bitter almond odor fruity odor at high concentrations and a soapy odor at low concentrations faint, fishy or mustyodor It has a much lower vapor pressure than HN-1 or HN- 2 and is insoluble in water. It is sparingly soluble in water but miscible with acetone and other organic solvents solublity at temperatures greater than 256 ◦C at temperatures greater than 194 ◦C decomposes

37. Uses: HN-1 was originally used for treatment of warts HN-1, 2 and 3 have no utility except as a CWA.

38. Mechanism of human toxicity ☼ These are alkylating agents ☼ damage the DNA in dividing cells like the SM’s

39. Clinical features: Typically, signs and symptoms of NM exposure do not occur immediately. The onset of symptoms may be up to several hours after exposure to the agent ( dose dependent )

40. Clinical features: These agents, like SM’s, affect the skin, eyes, respiratory tract and gastrointestinal tract Like SM’s, systemic absorption can lead to bone marrow suppression and central nervous system effects.

41. Treatment: ® As no specific antidote exists for NM exposure, management is supportive and on similar lines as that of SM’s.

42. Definition: Though it has never been used in warfare, it is classified as a potential CWA. Properties:

43. Mechanism of human toxicity ☼ It can easily penetrate ordinary clothing and even rubber. ☼ It is a powerful blistering agent and damages the surfaces it comes in contact with ☼ Since it also contains arsenic, some features of arsenic toxicity can also develop.

44. Clinical features: Signs and symptoms are similar to other blistering agent. refractory hypotension known as Lewisite shock, can develop in persons exposed to L. Bone marrow suppression is not a feature of toxicity.

45. Treatment: ®Removal of casualties by well protected staff from area of contamination is most important followed by :  removal of clothing  A liberal bath. ®supportive treatment ®Specific antidote :  British anti-Lewisite (dimercaprol, BAL) is used for systemic or severe toxicity.  Sodium 2,3-dimercaptopropane 1-sulfonate (DMPS)  meso 2,3 dimercaptosuccinic acid (DMSA)

47. Nerve agents are organophosphate compounds, similar to organophosphate pesticides, but a group (lethal agents) of chemical warfare agents These are the deadliest of CWA’s Overview These agents have both chemical names as well as 2-letter NATO codes. G series agents: representing “Germany”  GA (Tabun)  GB (Sarin)  GD (Soman)  GF  V Series agents: denoting “Venomous”.  VE  VG  VM  VX

48. Nerve agents are an excellent weapon for terrorist purposes  are synthesized easily  are synthesized cheaply  are easily dispersed  are difficult to detect  feared by public opinion  are highly lethal, Overview

49. The earliest recorded use of cholinesterase inhibitors was by native tribesmen of Western Africa They used Calabar bean as an “ordeal poison” in witchcraft. An extract of Calabar bean was later used for various medicinal purposes and the active principle “physostigmine” was isolated in 1864 History

50. Wurtz in 1854 synthesized the first organophosphate compound, tetraethyl pyrophosphate (TEPP) In 1937 Gerhard Schrader developed the general formula for all organophosphorus compounds and manufactured GB and GA. History

51. In 1995, the Japanese cult Aum Shinrikyo used GB in terrorist attacks in Tokyo resulting in 12 deaths History The nerve agents GA and GB were first used on the battlefield by Iraq against Iran during the first Persian Gulf war and again against the Kurdish

52. As a result, they tend to remain close to the ground and pose a risk particularly to the people in low areas and below ground shelters. Properties GB All nerve agents are liquid at standard temperature and pressure. Nerve agents are four to six times denser than air.

53. VX spreads slowly and remains in the place for weeks or longer after exposure and thus called a persistent nerve agent. VX does not pose a major inhalation hazard under usual circumstances, but it is well absorbed through the skin Properties VX

54. The relative lethality as determined in animal studies is VX > Soman > Sarin > Tabun Properties

55. Delivery systems of nerve agents are bombs, missiles, cluster spray and spray tanks. Properties BLU-80/B Bigeye binary chemical munition dispenser would have carried 180 pounds of VX nerve agent

56. Mechanism of human toxicity

57. Acetylcholinesterase Hydrolyses acetylcholine (ACh) Is mainly associated to nerves and muscles Being typically found on the synapse Is a specific enzyme for the diagnosis of OP poisoning is called true cholinesterase usually estimated in red blood cells (RBC) [ RBC ChE ] Mechanism of human toxicity

58. Butyrylcholinesterase  known as plasma cholinesterase or pseudocholinesterase  Hydrolyses butyrylcholine  Is synthesized by the liver  being found in large amounts in the serum [plasma ChE]  Is less specific but more sensitive than AChE Mechanism of human toxicity

59. the active site of AChE can be divided in: (i)an esteratic subsite, where the serine and the histidine of the catalytic triad are located, which binds to the acyl group of ACh; (ii) an anionic subsite, constituted by negative charges that interact with the quaternary ammonium group of Ach (iii) a hydrophobic region, contiguous or close to the esteratic and anionic subsites, which is important for the binding of arylic substrates

60. Mechanism of human toxicity

61. NameSynonymAging T1/2 SarinGB~5 hours SomanGD~2 min TabunGA>40 hours VXNone>40 hours

62. N ERVE AGENTS Clinical features

63. N ERVE AGENTS Clinical features  Exposure of a person to nerve agent vapor :  Eye : miosis due to papillary muscle contraction “the world going black” In terrorist or battlefield cenarios, most victims are effected via vapor route. The pupillary muscles are the most accessible cholinergic synapses. Thus miosis may be the first symptom in these patients

64. N ERVE AGENTS Clinical features  Exposure of a person to nerve agent vapor :  Secretory gland : Increase in secretions from various glands (manifesting as rhinorrhea, salivation, bronchorrhea)  Respiratory : contraction of bronchial smooth muscle resulting in bronchospasm and impaired ventilation of the lungs leading to hypoxia and death “The patient drowning in his own “ “secretions.”

65. N ERVE AGENTS Clinical features  Exposure of a person to nerve agent vapor :  Gastrointestinal tract: abdominal cramping and pain nausea& vomiting & diarrhea  heart Increased or decreased heart rate Hypo or Hypertension the blood pressure and heart rate are relatively unpredictable in exposed patients

66. N ERVE AGENTS Clinical features  Exposure of a person to nerve agent vapor :  Muscles Fasciculation ( movie) twitching paralysis  When adenosine triphosphate (ATP) is depleted late in the course, flaccid paralysis follows  in botulinium intoxication flaccid paralysis occurs earlier in the course due to presynaptic inhibition of ACh release by the toxin

67. N ERVE AGENTS Clinical features  Exposure of a person to nerve agent vapor : brain loss of consciousness Multifocal seizures Central apnea Difficult in concentrating Restlessness

68. N ERVE AGENTS Clinical features  Death is due to respiratory failure due to a combination of  Bronchorrhea  Bronchospasm  Respiratory muscle paralysis  Central apnea.

69. N ERVE AGENTS Clinical features  Neuropsychiatric sequelae in non-dose dependant fashion have been described  This syndrome overlaps with post- traumatic stress disorder (PTSD) and in some patients it may actually be a true PTSD  It may due to hypoxic encephalopathy

70. N ERVE AGENTS Clinical features  Other delayed manifestations that have been observed include  organophosphorus induced neuropathy ( not seen with VX )  intermediate syndrome It is characterized by : o muscular weakness and occurs after apparent recovery from the acute cholinergic syndrome and reflects prolonged action of acetylcholine on nicotinic receptors.  delayed neurobehavioural syndrome has been described in a small proportion of nerve agent survivors.

71. Directions for Using Auto-Injectors Mark I kit 71 Atropin 2-PAM The dose (2 mg) of atropine available in auto injector is not adequate for the moderate to severe exposure to nerve agents

72. Priorities:  protect themselves from contamination:  personal protective equipment  or by thoroughly decontaminating the patient.  rescuers should wear : a protective mask (or mask containing a charcoal filter for a SCBA device, not a surgical or similar mask) heavy rubber gloves (surgical gloves offer negligible protection) Avoid skin contact with victims until decontamination has been carried out Treatment

73. Decontamination Skin decontamination :  large amounts of a chlorine-liberated solution such as 5.0% hypochlorite solution (household bleach) followed by copious water rinsing.(alkaline PH)  alkaline soap and water followed by a water rinse. (gently & without rubbing)  Generous amounts of water alone Care should be taken to clear under the nails, intertriginous areas, axillae, groin, and hair Treatment

74. Decontamination  A skin decontamination kit approved by FDA containing activated charcoal impregnated with ion exchange resins (Ambergard™ XE-555 ) is also available Treatment

75. ABC:  Oxygen administration and assisted ventilation should be undertaken as soon as possible in those with respiratory distress.  Airway resistance may be very high initially, causing some mechanical ventilators to malfunction, but it will return toward normal after atropine administration.  Supplemental oxygen through an endotracheal tube with positive end-expiratory pressure is indicated for severely hypoxic patients.  It is important to improve tissue oxygenation before atropine administration to minimize he risk of ventricular fibrillation  Frequent airway suctioning may be required for copious bronchial secretions. Treatment

76. Antidotes: Atropine Titrated with the goal of the therapy being drying secretions and resolution of bronchoconstriction and bradycardia In fact, atropine should be given intravenously in doses to produce mild to moderate atropinisation : dryness of tongue, pharyngeal and bronchial tree Tachycardia Mydriasis Treatment

77. Oximes Several oximes are employed for reactivation of AChE inhibited by OPCs, provided that the phosphylated enzyme is not aged yet. They are especially useful in the treatment of OPCs nicotinic effects. All of them have three great deficiencies: (i) the utilized oximes are generally quaternary ammonium ions and, as hydrophilic compounds, have many difficulties to cross the blood-brain barrier: ( 1 to 10% of their plasma levels) As a consequence, they can reactivate only a small fraction of the inhibited AChE in the CNS; (ii) oximes do not reactivate aged phosphyl-enzymes; and (iii) unlike atropine, oximes are not effective against all OPCs, having different activities for each one of them. Treatment

78. Oximes The choice of oximes presently based on :  Protection against lethality  Cost  Availability  Side effects ( Obidoxime = more toxic ) Treatment HLo7>HI6>obidoxime>pralidoxime

79. Diazepam Anticonvulsant Cholinergic GABAergic Midazolam is the fastest acting and most effective Treatment

82. Overview Asphyxiants are substances that cause tissue hypoxia These are classified : simple & chemical

83. simple chemical Methane and Nitrogen physically displace oxygen in inspired air, resulting in oxygen deficiency and hypoxemia. Cyanides interfere with oxygen transport at cellular level causing tissue hypoxia, anaerobic metabolism and lactic acidosis The important chemical asphyxiants used as CWA’s include : cyanogen chloride (CK), hydrogen cyanide (HCN), arsine (SA).

84. Cyanogen chloride, also known as chlorine cyanide, chlorocyan, or cyanochloride It was used during WWI by the French Two properties made it an effective CWA: A. CK could penetrate the masks of that time. The “mask breaking” properties of cyanogen chloride lead to its mass production (around 11,000 tons) by the US. B. it was not inflammable and therefore did not burn up during the “burster” charge. Cyanogen chloride (CK)

85. Uses: Cyanogen chloride is used in industry for synthesis of herbicides, ore refining, and as a metal cleaner Cyanogen chloride (CK)

86. Mechanism of human toxicity:  Cyanide interferes with aerobic respiration at a cellular level by forming a reversible complex with the cytochrome oxidase enzyme system (This enzyme is responsible for oxygen utilization and cell respiration)  The resultant inhibition of cytrochrome oxidase enzyme results in inability to utilize oxygen and accumulation of lactic acid and cell death from tissue anoxia

87. Clinical features:  Onset is usually rapid with deaths occurring in less than 10 min Cyanogen chloride (CK) Inhalation in low concentration breathlessness, Headache Dizziness Anxiety Palpitations Mydriasis blurring of vision nausea Exposure to high concentrations hyperventilation, followed by : loss of consciousness, Convulsions fixed and dilated pupils

88. Clinical features:  Despite hypoxia, there is no cyanosis  Instead the color of skin turns cherry red Cyanogen chloride (CK)

89. Treatment: supportive management, three specific antidotes are available and include nitrites, dicobalt edentate and hydroxycobalamine/thiosulfate A. Ten milliliters of 3% sodium nitrite is given intravenously over 5–20 min  Amyl nitrite (one 0.2 ml ampoule inhaled over 0.5–1 min) can be used in case intravenous access is a problem B. followed by sodium thiosulfate which is given as 25 ml of a 50% solution intravenous over 10 min Cyanogen chloride (CK)

90. Treatment: Cyanogen chloride (CK) Nitrites convert hemoglobin to methhemoglobin Methhemoglobin binds to cyanides more avidly as compared to cytochrome oxidase and thus preventing the toxicity Sodium thiosulfate removes cyanide from methhemoglobin by forming sodium thiocyanate which is removed from the body and methhemoglobin is converted back to hemoglobin.

91. Treatment: Hydroxycobalamine/thiosulfate is emerging as the  drug of choice as it has minimal adverse effects  It has been recently approved by the FDA There is no head to head comparison between the three antidotes, but considering the safety profile and overall efficacy, hydroxycobalamine is the drug of choice Cyanogen chloride (CK)

92. HCN is also known as hydrocyanic acid or prussic acid Liquid hydrocyanic acid was first produced by Scheele in 1782 However, under the brand name Zyklon-B it was perhaps most infamously employed by the Nazi regime inmid-20 th century as a method of mass extermination in 1980 s in the Iran–Iraq war against the Kurds It is highly toxic and in sufficient concentrations it rapidly leads to death Hydrogen cyanide (HCN)

93. Uses: HCN is a precursor to many chemical compounds ranging from polymers to plastics. It is used in the pharmaceutical industry and also for fumigation of ships and buildings. Hydrogen cyanide (HCN)

94. Mechanism of human toxicity:  Is same as that of CK. Clinical features:  The most important route of poisoning is through inhalation,  Though they can be absorbed through the skin.  Signs and symptoms are similar to those seen after exposure to CK Hydrogen cyanide (HCN)

95. Treatment: Is on the same lines as for CK. Hydrogen cyanide (HCN)

96. Arsine (arsenic hydride, arsenic trihydride, arseniuretted hydrogen, arsenous hydride, hydrogen arsenide) is the most toxic form of arsenic Although arsine itself has not been used as a CWA, several arsine-derived organoarsenic compounds have been developed and used as CWAs, including lewisite (beta- chlorovinyldichloroarsine), adamsite (diphenylaminearsine) Clark I (diphenylchlorarsine) Clark II (diphenylcyanoarsine).

97. Mechanism of human toxicity:  Inhaled arsine gas causes rapid destruction of red blood cells leading to hypoxia and renal failure  Mechanism is believed to be nonspecific disruption of ion gradients, leading to cell membrane instability and lysis of red blood cells

98. Clinical features:  It has delayed onset of action with a latent period up to 24 h  The symptoms are due to rapid destruction of red blood cells (hemolysis)  abdominal pain  Hematuria (red urine)  Jaundice  Discoloration of conjunctivae (red, orange, brown, or brassy) and jaundice is seen.  In severe cases patient may be passing red or cola colored urine and may develop acute renal failure or acute respiratory distress syndrome

99. Treatment: Properly protected personnel should remove the victim from continued exposure to arsine There is no specific antidote Victims should be administered a) high flow oxygen b) Exchange transfusion should be used in cases of severe hemolysis c) Forced alkaline diuresis may prevent development of renal failure d) In patients with established renal failure, hemodialysis should be instituted

102.  Lung toxicants are the general class of gases that are toxic to the human lung when inhaled  Resulting in an inflammatory response.  This manifests as :  Pulmonary edema  Reduced pulmonary compliance  Altered gas exchange  The CWA’s under this category include : chlorine chloropicrin (PS) phosgene (CG) diphosgenenitrogen oxides.

103.  Chlorine was discovered in 1774  Chlorine was given its current name in 1810  Germany used chlorine as a CWA during WWI without much success,

104. Properties : » It is heavier than air, there by tending to accumulate in low lying areas

105. Uses : ∆ Chlorine is most commonly used as a bleaching agent in the paper and cloth industry ∆ Detergents وایتکس ∆ It is also used to make pesticides, rubber and solvents ∆ Amongst the household uses it is used as a disinfectant in drinking water and in the swimming pool. ∆ It is also used to treat industrial waste and sewage

106. Mechanism of human toxicity: When chlorine gas comes into contact with moist tissues such as the eyes, throat, and lungs, hydrochloric and hypochlorous acid is produced. Hypochloro us acid degenerates into hydrochloric acid And nascent oxygen. Both hydrochloric acid and nascent oxygen damages the lung tissue resulting in an inflammatory response that damages the alveolar- capillary membrane of the human lung. This manifests as pulmonary edema, reduced pulmonary compliance, and altered gas exchange.

107. Clinical features : ⥁ These depend upon site of exposure and concentration of gas ⥁ Immediately after exposure patients complains of ⥁ chest tightness ⥁ burning sensation in the nose, throat and eyes ⥁ redness and blisters on the skin similar to frostbite ⥁ Within 2–4 h of exposure ⥁ Breathlessness ⥁ acute lung injury (ARDS)

108. Treatment:  Removing the causalities from the site by well protected personnel  There is no specific antidote.  Measures include removal of all clothing and providing supportive medical care.  Most available research evaluates parenterally administered corticosteroids, although animal models demonstrate a beneficial effect of nebulized beclomethasone and nebulized budesonide following acute chlorine poisoning

109. Mechanism of human toxicity: Is the same as that of chlorine

110. Clinical features : Because of its relative inertness and the small size of its molecule, chloropicrin penetrates gas mask filters causing vomiting This makes the victim remove the gasmask. For this reason, it is often mixed with other chemical weapons

111. Treatment:  Is along the same lines as following exposure to chlorine

112. Uses : ∆ Since WWII, CG has found extensive industrial uses. ∆ It is widely used in chemical industries such as pharmaceuticals, dyes, pesticides and polyurethane for foam rubber products

113. Mechanism of human toxicity: Is same as that of chlorine.

114. Clinical features : ⥁ Following exposure:  coughing,  burning sensation in the throat and eyes,  choking  breathlessness. ⥁ This is followed by a symptom free period which varies from 2 to 48 h ⥁ followed by acute lung injury  Acute lung injury is precipitated by exercise as was frequently reported in the WWI.  In persons who remain asymptomatic and whose lungs appear clear on chest films obtained 8 h after exposure acute lung injury is unlikely to develop

115. CXR Progression

116. Treatment:  Removing the casualties from the site by well protected personnel.  Removal of clothing and liberal bath in soap water helps to decontaminate.  Exposure to CG may cause acute lung injury as late as 48 h.  There is no antidote.  Treatment is symptomatic and supportive.  The role of steroids is not proven (Diller, 1985).  Exposed people should be observed for up to 48 h.  If the patient survives for more than 48 h, the prognosis is excellent  In experimental studies, N-acetylcysteine and Ibuprofen has shown promising results in phosgene induced lung injury.e.

118. Behavioural agents/incapacitating agents  Following WWII, the US military investigated a wide range of possible nonlethal, psychobehavioural chemical incapacitating agents. These included : lysergic acid diethylamide (LSD-25) Ketamine fentanyl carfentanil glycolate anticholinergics.

119. Behavioural agents/incapacitating agents  The only agent classified as CWA is 3-quinuclidinyl benzilate, an anticholinergic compound.  It is codenamed as BZ by NATO.  It is alleged that BZ was stockpiled by Iraq in large quantities, code named Agent 15.  It is also believed that BZ was the chemical warfare agent used to subdue terrorists in Moscowon 26 October 2002,  The exact nature of the gas still remains unknown