1. . Chemical warfare is the use of the toxic properties of chemical substances to kill, injure or incapacitate an enemy in warfare and associated

1

Chemical warfare agents

.

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).

Difinition

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

History

.

Chemical Warfare: Iran-Iraq War

Iran-Iraq War: 1980-88 Iraq: Chemical weapons

◦ Widespread use Blistering agent:

Lewisite Nerve agent: Tabun

◦ Heavy Iranian casualties, deaths

Chemical Terrorism: Iraqi Kurds

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

TECHNICAL COMPLEXITY

Biological ChemicalNuclear

RISK!!

Chemical: low complexity, high probability

LOW HIGH

LOWHIGH

Present Chemical Terrorist Threats

Al Qaida threat Documents found

◦ Chemical agents◦ Bombs

Reported attempt◦ Jordan, 2004

US Embassy Suicide missions

◦ Easier success

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.

The chemical weapons convention (CWC)

Major Iraqi Sites Suspected of Housing Chemical Weapons

For Comparison…United States Stockpiles of CW (June, 2000)

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

classification

North Atlantic Treaty Organization (NATO) has classified agents of chemical terrorism as:

Blister agents Nerve agents Choking agents Asphyxiants Behavior altering agents

classification

Blister agents

Blister agentsDefinition :

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 absorbedThese 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.

Blister agentsDefinition :

These include :sulfur mustard (SM)

nitrogen mustard ( NM)

Lewisite ( L)

Sulfur mustard 1. Mahdi Balali-Mood, M. D., Ph. D. Visiting Professor of Newcastle University, UK. Professor of Medicine and Clinical ToxicologyDirector, Medical Toxicology Research CentreImam Reza Hospital, Faculty of Medicine, Mashhad University of Medical Sciences,

2. Beeta Balali-Mood, M Chem, M Res, PhD candidateDepartment 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

Blister agentsSULFUR MUSTARD (SM)

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

long term morbidity.)


History:They were discovered accidentally

In 1917the German forces used SM for the

first time in battlefield.It accounted for about 70% of the

million-plus gas related casualties in WWI.


Properties:


Properties: 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


Uses:It has no industrial use at

present


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


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%.


Clinical features:Most often exposed surfaces i.e. skin, airways, and eyes suffer the brunt of the damage.

ΘEyes Θ ConjunctivitisΘ PhotophobiaΘ BlepharospasmΘ PainΘ Corneal damage(can lead to perforation)Θ Glaucoma may develop later as a result of

scarring.


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


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


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.

Þ Late complications :Þ ulcerative keratitisÞ Chronic bronchitisÞ pulmonary fibrosisÞ hypo or hyperpigmentation of skinÞ psychological problems.Þ 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

Iraqi WarheadsArmed with

Sulfur Mustard

UN Weapons Inspector Team


Treatment:®There is no specific antidote.®Supportive treatment

remains the mainstay.


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.


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


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

Blister agentsNitrogen mustards (NM’s)

Definition:Nitroge nmustard’s (NM’s) are alkylating agentsnitrogen analogues of SM’s

HN-3 HN-2 HN-1

(tris(2-chloroethyl) amine

(bis(2- chloroethyl) methylamine

(bis(2-chloroethyl) ethylamine

C6H12Cl3N C5H11Cl2N C6H13Cl2N formula

It is odorless when pure but has been reportedto have a bitter almond odor

fruity odor at high concentrations and a soapy odor at low concentrations

faint, fishy or musty odor

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

Blister agents

Uses:HN-1 was originally used

for treatment of warts

HN-1, 2 and 3 have no utility except as a CWA.

Nitrogen mustards (NM’s)

Blister agents

Mechanism of human toxicity☼These are alkylating agents

☼damage the DNA in dividing cells

like the SM’s


Blister agents

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 )


Blister agents

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


Blister agents

Treatment:® As no specific antidote

exists for NM exposure, management is supportive and on similar lines as that of SM’s.


Blister agents

Definition:

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

Properties:

Lewisite (L)

Blister agents

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.

Lewisite (L)

Blister agents

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.

Lewisite (L)

Blister agents

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)

Lewisite (L)


Blister agents

Nerve agents Asphyxiants Choking agents Behavior altering agents

classification

• 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

O ve rv ie w

• 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”.VEVGVM VX

• Nerve agents are an excellent weapon for terrorist purposes

are synthesized easily are synthesized cheaply are easily dispersedare difficult to detect feared by public opinion are highly lethal,

O ve rv ie w

• 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

Hi

st or y

• 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.

Hi

st or y

• In 1995, the Japanese cult Aum Shinrikyo used GB in terrorist attacks in Tokyo resulting in 12 deaths

Hi

st or y

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

• 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.

Pr o p er ti es

GB

All nerve agents are liquid at standard temperature and pressure.

•Nerve agents are four to six times denser than air.

• 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

Pr o p er ti es

VX

• The relative lethality as determined in animal studies is

• VX > Soman > Sarin > Tabun

Pr o p er ti es

• Delivery systems of nerve agents are bombs, missiles, cluster spray and spray tanks.

Pr o p er ti es

BLU-80/B Bigeye binary chemical munition dispenser would have carried 180 pounds of VX nerve agent

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Acetylcholinesterase Hydrolyses acetylcholine (ACh) Is mainly associated to nerves and musclesBeing typically found on the synapse Is a specific enzyme for the diagnosis of OP

poisoningis called true cholinesteraseusually estimated in red blood cells (RBC)

[ RBC ChE ]

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Butyrylcholinesterase known as plasma cholinesterase or

pseudocholinesteraseHydrolyses butyrylcholine Is synthesized by the liverbeing found in large amounts in the serum

[plasma ChE]Is less specific but more sensitive than AChE

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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

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Name Synonym Aging T1/2

Sarin GB ~5 hours

Soman GD ~2 min

Tabun GA >40 hours

VX None >40 hours

NER

VE A

GEN

TS

Clinical

features

NER

VE A

GEN

TS

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 cholinergicsynapses. Thus miosis may be the first symptom in these patients

NER

VE A

GEN

TS

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.”

NER

VE A

GEN

TS

Clinical

features

Exposure of a person to nerve agent vapor :Gastrointestinal tract:

abdominal cramping and pain nausea& vomiting & diarrhea

heartIncreased or decreased heart

rateHypo or Hypertensionthe blood pressure and heart

rate are relatively unpredictable in exposed patients

NER

VE A

GEN

TS

Clinical

features


Muscles Fasciculation ( movie)twitching paralysisWhen 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

NER

VE A

GEN

TS

Clinical

features


brain loss of consciousness Multifocal seizures Central apnea Difficult in concentrating Restlessness

NER

VE A

GEN

TS

Clinical

features

Death is due to respiratory failure due to a combination of

Bronchorrhea Bronchospasm Respiratory muscle paralysis Central apnea.

NER

VE A

GEN

TS

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

NER

VE A

GEN

TS

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.

Directions for Using Auto-Injectors Mark I kit

71

Atr

opin

2-PA

M

The dose (2 mg) of atropine available in auto injector is not adequate for the moderate to severe exposure to nerve agents

• 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 outTr e at

m e nt

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

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DecontaminationA skin decontamination kit

approved by FDA containing activated charcoal impregnated with ion exchange resins (Ambergard™ XE-555 ) is also available

Tr e at

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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.

Tr e at

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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

Tr e at

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• 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 .

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• Oximes The choice of oximes presently based on :

Protection against lethality Cost Availability Side effects ( Obidoxime = more toxic )

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HLo7>HI6>obidoxime>pralidoxime

• Diazepam Anticonvulsant Cholinergic GABAergic

Midazolam is the fastest acting and most effective

Tr e at

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Blister agents Nerve agents

Asphyxiants Choking agents Behavior altering agents

classification

Asphyxiants/blood agents

Asphyxiants/blood agentsOverview

Asphyxiants are substances that cause tissue hypoxia

These are classified : simple & chemical

simple chemicalMethane 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).

Asphyxiants/blood agents

Cyanogen chloride, also known as chlorine cyanide, chlorocyan, or cyanochloride

It was used during WWI by the FrenchTwo 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.

Asphyxiants/blood agentsCyanogen chloride (CK)

Uses:

Cyanogen chloride is used in industry for synthesis of herbicides, ore refining, and as a metal cleaner



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

Clinical features: Onset is usually rapid with deaths occurring in less than 10

min


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

Clinical features: Despite hypoxia, there is no cyanosis Instead the color of skin turns cherry red


Treatment: supportive management, three specific antidotes are available and include nitrites,

dicobalt edentate and hydroxycobalamine/thiosulfateA. Ten milliliters of 3% sodium nitrite is given

intravenously over 5–20 minAmyl 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


Treatment:


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.

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


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-20th century as a method of mass extermination

in 1980s in the Iran–Iraq war against the Kurds

It is highly toxic and in sufficient concentrations it rapidly leads to death

Asphyxiants/blood agentsHydrogen cyanide (HCN)

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.


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


Treatment:Is on the same lines as for CK.


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).

Asphyxiants/blood agentsArsine

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


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


Treatment:Properly protected personnel should remove the

victim from continued exposure to arsineThere is no specific antidoteVictims should be administered

a) high flow oxygenb) Exchange transfusion should be used in cases

of severe hemolysisc) Forced alkaline diuresis may prevent

development of renal failured) In patients with established renal failure,

hemodialysis should be instituted



Blister agents Nerve agents Asphyxiants

Choking agents Behavior altering agents

classification

Choking/pulmonary damaging agents

CHOKING/PULMONARY DAMAGING AGENTS

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 edemaReduced pulmonary complianceAltered gas exchange

The CWA’s under this category include : chlorine chloropicrin (PS) phosgene (CG) diphosgenenitrogen oxides.


Chlorine was discovered in 1774 Chlorine was given its current name in

1810 Germany used chlorine as a CWA

during WWI without much success,

Chlorine (Cl)


Properties : » It is heavier than air, there by tending

to accumulate in low lying areas

Chlorine (Cl)


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

Chlorine (Cl)


Mechanism of human toxicity:

Chlorine (Cl)When

chlorine gas

comes into

contact with

moist tissues such as the eyes, throat,

and lungs,

hydrochloric and hypochlorous acid

is produced

.

Hypochlorous 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.

Thismanifests as

pulmonary

edema, reduce

d pulmon

ary compliance,and

altered gas

exchange.


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)

Chlorine (Cl)


Treatment: Removing the causalities from the site by well

protected personnelThere 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

Chlorine (Cl)


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

Chloropicrin (PS)


Clinical features :

Chloropicrin (PS)

Because of its relative inertness and the small size of its molecule, chloropicrin penetrates gas mask filters causing vomiting

This makes the victim removethe gasmask.

For this reason, it is often mixed with other chemicalweapons


Treatment: Is along the same lines as following

exposure to chlorine

Chloropicrin (PS)


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

Phosgene (CG)


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

Phosgene (CG)


Clinical features : ⥁ Following exposure:

coughing, burning sensation in the throat and eyes, choking breathlessness .

⥁ This is followed by a symptom free period which varies from2 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

Phosgene (CG)


CXR Progression

Phosgene (CG)


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.

Phosgene (CG)


Blister agents Nerve agents Asphyxiants Choking agents

Behavior altering agents

classification

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.

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