dr. tejas chemical emergencies sikkim - compatibility modecidm.in/pdf/day2_2/9.pdf · asphyxiants...

1

Dr.Tejas Prajapati

M.D.

Diploma in Clinical Toxicology(Australia)

Consultant Toxicologist

Ahmedabad

What is Toxicology?

The traditional definition of Toxicology is "the science of poisons." As our understanding of the working of biological systems improved, a more comprehensive definition has been put forth by Society of Toxicology.

“Toxicology is the study of adverse physico-chemical effects of chemical , physical or biological agents on living organisms and the ecosystems including prevention and amelioration of such effects”

2

A Toxic agent is anything that can produce

an adverse biological effect. It may be

chemical, physical, or biological in form. For

example, toxic agents may be

chemical (such as cyanide),

physical (such as radiation) and

biological (such as snake venom).

.

A toxic substance is simply a material which has toxic properties. It may be a discrete toxic chemical or a mixture of toxic chemicals. Lead chromate, asbestos, and gasoline are all toxic substances.

Toxic chemical Lead chromate is a

discrete toxic chemical

Gasoline..It contains a mixture of many

chemicals and may not always have a

constant composition

.

3

What is a Xenobiotic?

• Xenobiotics is anything which is foreign to the organism.

• Xenobiotics include drugs, industrial chemicals, naturally occurring poisons and environmental pollutants.

Types of Toxic Effects

• Acute effects occur after limited exposure and shortly (hours, days) after exposure and may be reversible or irreversible.

• Chronic effects occur after prolonged exposure (months, years, decades) and/or persist after exposure has ceased.

Tobacco related cancers. e.g., Cancer of mouth due to tobacco chewing, cancer lung due to smoking are chronic toxic effects

4

“All substances are poisons;

there is none which is not a

poison.

The right dose differentiates a

poison from a remedy.”

Paracelsus (1493-1541)

Dose Response Relationship

Fundamental principle of Toxicology

Dose Response Relationship

% Alcohol in Blood Observed Effect

0.05 Stimulant, Social

Relaxation

> 0.1 Incoordination

0.3 Unconsciousness

0.4 Possible Death

5

Non-Traditional Weapons

5th Century B.C. use of pitch and sulfur in wars between Athens and Sparta

6

19th Century Hong Kong

1857 Arsenic laced bread sold to British patrons to induce terror at the E Sing Bakery

7

Toxin Classes

• Chemical

Warfare

• Biologicals

• Nuclear Agent

• Others

Classification of Chemical

Agents

• Blistering agents or

vesicants

• Pulmonary or

choking agents

• Cellular asphyxiants or blood agents

• Nerve Agents

• Incapacitants

8

Blistering

Agents/

Vesicants

• Lewisite

• Phosgene oxime

• Mustards of

– Sulfur

– Nitrogen

Blistering Agents

• Irritation to:

– Mucus Membranes

– Skin

– Occasionally deeper tissues

• Onset minutes to hours

• Care supportive

• Decontamination

• BAL?

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The various accidents due to these

consequences are well known and gives

prominent caution to prepare, practice and

amend the fire/Toxic Disaster Management

plans for each and every hazardous process

As per amended factory Act each chemical

industry has to prepare Disaster

Management On site and Off site and submit

plans to chief Inspector of Factories &

Boilers for their approval.

Organizations world wide have learnt the

importance of applying principles of

prevention and protection in chemical

industries in hard way.

Each chemical industry aims to achieve

totally zero accident potential.

Therefore prevention, protection and

suppression techniques have been applied to

reduce the probability of disaster.

12

Some of the worst disaster of toxic gas

releases have occurred in chemical

Industries like MIC, Ammonia, and

Chlorine etc.

Some data’s on past planning in detail

which explains the various stages of

Disaster Management plan.

Bhopal,, 1984Union Carbide had a plant in Bhopal, India, for the

production of insecticide Carbaryl. Methyl iso cyanate was

an intermediate used in the process

On the night of Dec. 2nd and 3rd, 1984, a Union Carbide plant in

Bhopal, India, began leaking.

13

Bhopal Gas Tragedy• Worst industrial disaster in history

• 2,000 people died on immediate aftermath

• Another 13,000 died in next fifteen years

• 10-15 persons dying every month

• 520,000 diagnosed chemicals in bloodcausing different health complications

• 120,000 people still suffering from

– Cancer

– Tuberculosis

– Partial or complete blindness,

– Post traumatic stress disorders,

– Menstrual irregularities

Rise in spontaneous abortion and still birth

How it happened

• December 3-4, 1984: 40 tonnes of

methyl iso-cyanate (MIC) released from

Union Carbide plant at Bhopal

• Accidental release caused by leakage of

water into MIC storage tank

• None of the safety systems worked

• Safety standards and maintenance

system ignored for months

• Complete absence of community

information and emergency procedures

• Public alarm system operated after the

gas had leaked for nearly four hours

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Most killed or injured lived in Shanty town that grew up

too close to the plant.

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Lessons learned� Reduce inventory of hazardous material (MIC)

� Keep all the safety related equipment in order

� Keep residential areas away from the plant

� Proper Management

Flixborough, UK, 1974

� Company’s name: NYPRO Ltd.

– Sudden release of 30 – 50 tonnes of cyclohaxane

– Massive explosion

– Complete plant destruction

– Casualties 28

– Injured 36

– 1821 houses damaged

– 167 shops and factories damaged half mile away

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Flixborough, the process

� 6 reactors in parallel used for cyclohexane

oxidation

� The reaction was slow and the conversion was

kept low to prevent formation of byproducts

� Each reactor has a working volume of 20 tonnes

of cyclohexane

Flixborough, the process

�One of the reactors had minor crack which was

detected on time and removed for repair.

� In order to keep the operation going, a pipe was

installed temporarily in the free space of the

removed reactor.

�No engineer involved as the site engineer had left

NYPRO.

17


Cracked

reactor

Flixborough, UK, 1974�Plant operated for about two months

�The dogleg pipe exposed to continuous stress and

tensions and started to weaken gradually.

�Eventually a slight increase in pressure twisted the

pipe and broke it at both ends.

� Huge volume of reactants and products released

and caused a massive explosion

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� The control room collapsed completely.

� 18 people died in the control room.

� Explosion shattered the windows and caused the

roof to collapse

� Some died from flying broken window glasses

and debris

� Some died from roof collapse

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MAJOR CHEMICAL DISASTERS THAT

SHAPED PUBLIC POLICY

• Triangle Factory Fire New York (USA) 1911

100 garment workers died in fire

• Minamata Mercury Disaster (Japan) 1932-68

3,000 people suffered, severe mercury poisoning symptoms, deformities or death

• Seveso Dioxin Disaster (Italy) 1976

3,000 animals died, 70,000 slaughtered to prevent dioxins entering food chain

• Bhopal Gas Disaster (India) 1984

15,000 killed, over 500,000 affected • Shri ram Oleium gas Leak (Delhi) 1986

1 Died, 1000 Injured

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• 1985 - Covenant Group found to possess 33 gallons of

cyanide Northwestern Arkansas

• 1992 - Police prevented Neo-Nazis from using cyanide in

synagogue

• 1994 - Aum Shinrikyo used sarin in Matsumoto

– 7 dead, 280 injured

• 1995 - Aum Shinrikyo uses sarin in Tokyo subway

– 12 dead, 5,500 injured

Chemical Terrorist Events

Examples of major toxic releases.Chemical Consequences Place and year

Phosgene 10 - Poza Rica, Mexico, 1950

Chlorine 7 - Wilsum, Federal Republic of

Germany, 1952

Dioxin - 193 Seveso, Italy, 1976

Ammonia 30 25 Cartagena, Colombia, 1977

Sulphur dioxide - 100 Baltimore, Maryland, United States,

1978

Hydrogen

sulphide

8 29 Chicago, Illinois, United States, 1978

Methyl

isocyanate

2,500 200,000 Bhopal, India, 1984

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Chemical involved Consequences Place and year

Death Injuries

Methane 136 77 Cleveland, Ohio,

United States, 1944

Liquefied petroleum

gas

18 90 Ferzyn, France, 1966

Liquefied natural gas 40 - Staten Island, New

York, United States,

1973

Methane 52 - Santa Cruz, Mexico,

1978

Liquefied petroleum

gas

650 2,500 Mexico City, Mexico,

1985

Examples of major fires

Examples of industrial explosionsChemical involved Consequences Place and date

Dimethyl ether 245 3,800 Ludwigshafen, Federal Republic of

Germany, 1948

Kerosene 32 16 Bitburg, Federal Republic of Germany,

1948

Isobutane 7 13 Lake Charles, Louisiana, United

States, 1967

Oil slops 2 85 Pernis, Netherlands, 1968

Propylene - 230 East Saint Louis, Illinois, United

States, 1972

Propane 7 152 Illinois, United States, 1974

Cyclohexane 28 89 Flixborough, United Kingdom, 1974

Propylene 14 107 Beek, Netherlands, 1975

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Are We

Prepared

….???

Types of Chemical Accidents

1. Industrial

2. Transportation

3. Household

4. Others

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Chemical Categories

Chemical Categories

1.1.1.1. AcidsAcidsAcidsAcids

2.2.2.2. BasesBasesBasesBases

3.3.3.3. FlammableFlammableFlammableFlammable

4.4.4.4. OxidizersOxidizersOxidizersOxidizers

5.5.5.5. Pyrophoric SubstancesPyrophoric SubstancesPyrophoric SubstancesPyrophoric Substances

6.6.6.6. LightLightLightLight----Sensitive ChemicalsSensitive ChemicalsSensitive ChemicalsSensitive Chemicals

7.7.7.7. CarcinogensCarcinogensCarcinogensCarcinogens

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Major Chemical Exposures

• Asphyxiants

• Cholinesterase inhibitors (Organophosphorus nerve agents)

• Respiratory tract irritants

• Corrosives and Vesicants

Types of Emergencies

• Onsite Emergency

• Offsite Emergency

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First Responder Requirements

• Understand What Hazardous Materials Are

• Know Risks of Hazardous Materials

• Understand Outcomes

• Recognize a Hazardous Materials Release

• Identify the Hazardous Material, If Possible

• Determine Need for Additional Resources

• Understand First Responder Roles

First Responder’s Capacity

• Recognize Signs, Symptoms, and Indicators

• Know What to Tell

• Recognize Trends

• Know Whom to Contact

• Notify Technical Responders

• Provide Safety Guidance

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Asphyxiants

These are agents which cause tissue hypoxia with

prominent neurologic and cardiovascular signs.

There are two types

- Simple Asphyxiants : e.g. methane, propane,

carbon dioxide. They physically displace oxygen

in inspired air and their inhalation results in

oxygen deficiency and hypoxemia

- Chemical Asphyxiants: e.g. carbon monoxide,

cyanide and hydrogen sulfide. They interfere with

oxygen transport and cause tissue hypoxia

Asphyxiants

Signs and Symptoms of Asphyxiant

exposure:

- Tissue hypoxia related to CVS and CNS

- Absence of respiratory tract irritation

- No increase in secretions

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Asphyxiants

Typical Presentation:Mild Symptoms:

Headache, fatigue, anxiety, irritability,

Dizziness, nausea

Moderate to Severe Symptoms:

Dyspnoea, Altered mental status, cardiac

ischemia, syncope, coma, seizure

Asphyxiants

Carbon monoxide : can be released from

combustion powered appliances e.g. generators,

smoke, burning coal in poorly ventilated areas.

CO has 250 times more affinity for hemoglobin than

oxygen

Cyanide: binds to cellular cytochrome oxidase and

blocks aerobic utilization of oxygen . Toxicity is

sudden in onset. Hallmarks of cyanide toxicity are

persistent hypotension and severe lactic acidosis

despite adequate arterial oxygenation

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Asphyxiants

Treatment:

1. Give 100% oxygen and this may be the only

treatment required for simple asphyxiants. It also

accelerates the elimination of CO.

2. Cyanide poisoning is treated with Lily antidote

kit which contains sodium nitrite and thiosulfate

3. Sodium nitrite produces methemoglobinemia

which binds free cyanide to produce

cyanmethemoglobin

4. Sodium thiosulfate converts cyanide to

thiocyanate.

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Respiratory tract irritants

Cause for release:

- in most industrial accidents, the hazardous

materials released are respiratory irritants

- Tear gas and choking agents

Factors affecting clinical effects:

- Direct tissue reactivity

- Dose

- Reflex stimulation

- Water solubility

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With high solubility: Ammonia, Sulfuric acid,

Chloramines( produced by mixing ammonia and hypo

chlorite.These agents mostly cause upper respiratory

tract irritation

Riot control agents and lacrimators:

e.g.Chloroacetophenone, are aerosolized solids which

cause intense, immediate and usually self-limiting

burning on exposed surfaces, mainly eyes

Intense or prolonged exposure to both groups can

cause bronchospasm and acute lung injury esp. in

persons with underlying lung disease.

Ammonia;

Formaldehyde;

Hydrogen chloride;

Sulfur dioxide

ChlorineChlorineChlorineChlorine

Phosgene;

Nitrogen dioxide

Toxico-dynamics of Irritant Gases

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With intermediate solubility: Chlorine in small doses

irritates the upper resp. tract and in larger doses can

lead to bronchospasm and acute lung injury

With low solubility: Phosgene is specific example of

this class. Initially the person may be asymptomatic,

but lung injury may be manifested after 15-48 hours.

Another example is Nitrogen dioxide which is

responsible for Silo-filler’s disease in agricultural

workers

Respiratory tract irritantsTreatment:

- Life support

- High flow oxygen

- Decontamination by irrigation of eyes & skin

- Brochodilators

- Corticosteroids for severe airway reactivity

For acute lung injury:

- Bed rest between exposure and onset of

symptoms

- PEEP ( Positive end expiratory pressure) to

maintain oxygenation in pulmonary oedema

- Antibiotics - ?, Diuretics - No

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Ammonia Leakage from a Tanker in Rajkot Region

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Cholinesterase Inhibitors

Most likely agent in accidental release:

Organophosphorus pesticides

Most likely agent in act of Terrorism:

Sarin and VX

Routes of Entry: These agents are absorbed by

inhalation, by ingestion and even through skin. Even

one drop of agent VX on skin can be lethal

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Two main groups:

- Organophosphorus insecticides

- Nerve gases used in warfare

On Monday 20 March 1995, five members of

Aum Shinrikyo launched a chemical attack on

the Tokyo Metro, one of the world's busiest

commuter transport systems, at the peak of the

morning rush hour . The chemical agent used,

liquid sarin, was contained in plastic bags

wrapped in newspaper. At prearranged stations,

the sarin packets were dropped and punctured

several times with the sharpened tip of the

umbrellas.

Aum Shinrikyo is the former name of a

controversial group now known as Aleph. The

prosecution said that it was an attempt to bring

down the government and install Shoko

Asahara, the group's founder, as the "emperor"

of Japan. Shoko Asahara

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Location Tokyo, Japan

Date (March 20, 1995)

7:00-8:10 a.m.

Attack type Chemical warfare

Weapon(s) Sarin

Deaths 12

Injured 1,034 (50 severe;

984 temporary

vision problems)

Perpetrator

(s)Aum Shinrikyo

Mechanism of Action

• Cholinesterase inhibitors bind and inhibit acetylcholine esterases.

• Acetylcholine esterase breaks down acetylcholine

• ACh mediates neurotransmission at

� Nicotinic receptors

o nicotinic muscular junctions,

o autonomic nicotinic synaptic junctions (sympathetic and parasympathetic), and

� Muscarinic receptors:

o end-organ synapses (GI tract, glands, bladder, pupils).

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N

Autonomic Nervous System Somatic Central

Parasympathetic Sympathetic

N N N

ACh ACh AChACh

ACh

M

M

ACh ACh

A A

Epinephrine Norepinephrine

N

ACh

Sweat Glands

Glands

Bladder

Gut

Heart

Heart

Blood Pressure Neuromuscular

Junction

Brain

Autonomic

Ganglia

End

OrganM


Ophthalmic symptoms: miosis, dim vision,

headache and eye pain.

Gastrointestinal symptoms: occur especially after

ingestion. Abdominal cramps, nausea, vomiting,

diarrhea, fecal and urinary incontinence

Nicotonic symptoms: weakness of skeletal

muscles, fasciculations and paralysis.

Cardiovascular symptoms: may be tachycardia

and hypertension due to nicotinic stimulation but

mostly bradycardia due to muscarinic effects

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Central Nervous System: range from irritability,

mild cognitive impairment to convulsions and

coma

Respiratory system: Multiple mechanisms like

hypersecretion, bronchoconstriction, paralysis of

respiratory muscles can contribute respiratory

failure.

CNS

Muscarinic (DUMBELS) Nicotinic (MTWHF)

Diarrhea Mydriasis Confusion

Urination Tachycardia Convulsions

Miosis Weakness Coma

Bradycardia, Bronchorrhea

Bronchospasm

Hypertension,

Hyperglycemia

Emesis Fasciculations

Lacrimation

Salivation, Secretion,

Sweating

Peripheral Nervous System

Signs and Symptoms of Poisoning

Caused by Cholinesterase Inhibitors

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Treatment: Supportive treatment includes oxygen,

suctioning of secretions and mechanical

ventilation

Antidotes: There are three antidotes.

Atropine works mainly at the muscarinic sites. In

adults it is given in doses of 2 mg every 5 –10

minutes and the dose is adjusted to minimize

respiratory secretions, airway resistance and dose

is adjusted by clinical judgement.


Pralidoxime: Reactivates acetyl cholinesterase and

thus works at nicotinic, muscarinic and central

nervous system receptors. The initial dose is 1 gm

administered over 20-30 minutes

Benzodiazepines: are highly effective

anticonvulsant agents. They should be administered

in all persons with severe intoxication

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Differences between Nerve agents and OP insect.

OP insecticides: They are oily, less volatile

liquids, have slower onset of toxicity, effects last

longer and require larger cumulative dose of

atropine.Ageing of bound Ops and Che is slow.

Nerve agents: They are watery and volatile, acting

rapidly and severely but their effects last a shorter

time. Ageing is quick e.g. with Soman it occurs in

minutes, with Sarin in three to five hours

Corrosives

Include

- Acids

- Bases

- Oxidizers

- White phosphorus

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Corrosives

Acids: cause coagulative necrosis which is

a thick hardened scab like surface that

somewhat limits deeper penetration of acid

Most of the acids cause local toxicity but

some like chromic acid may cause systemic

toxicity

Bases: produce liquefactive necrosis

resulting in deeper and more severe chemical

burns

Corrosives

Oxidizers: also cause chemical burns the

degree of which depends on the concentration

of the oxidizer, duration of contact, whether

skin is intact or damaged

White phosphorus: can cause serious skin

burns with significant systemic toxicity

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Corrosives

Signs and Symptoms: Acids, bases and

oxidizers are highly water soluble and therefore

primarily injure the upper airway. Coughing,

burning, laryngospasm and oedema of the upper

airway may occur. Irritation of eyes , corrosive

chemical burns of the eyes may lead to

blindness.

Corrosives can cause hypoxemia and

hypovolemia. Oxidizers can cause

methemoglobinemia. White phosphorus burns

can cause hypocalcemia

Corrosives

tTreatment: Decontamination: If the person is exposed only

to fumes, removing all clothes may be enough.

If there is contact with liquids or solids wash

with copious amounts of water for sufficient

time .Special attention should be given to skin

folds, axillae, genital areas and feet.

WP should be rapidly removed. It can be

identified in dark or with copper sulfate.

Removed WP should be placed under water to

prevent spontaneous combustion

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Corrosives

Eye decontamination: continuous irrigation

with water or sterile saline. A local anesthetic

may be needed . Continue till the

conjunctival sac pH is 7.

Antidote: If there is methemoglobinemia,

methylene blue may be given I/V

WP may cause hypocalcemia leading to

tetany, prolonged QT interval , torsades de

pointes. This may need I/V calcium

Hydrofluoric acid

Used extensively in industries like petroleum

industry, semiconductor production and

aluminium production

It is weak acid but can cause severe toxicity

It can penetrate into deep tissues even to the

bones

Fluoride ion has high affinity for Calcium and

Magnesium. This leads to hypocalcemia,

hypomagnesmia and hyperkalaemia

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Hydrofluoric acid

Electrolyte abnormalities have profound effect on

excitable tissues i.e., nervous system, skeletal

muscles, cardiac muscle and smooth muscle

manifested as

- severe neuropathic pain at the site of contact

- muscle twitching and tetany

- myocardial irritability

- prolonged QT interval and potential for torsades de

pointes

Hydrofluoric acid

Calcium is a specific antidote for HF acid burns

and toxicity

Calcium gluconate can be used topically by

making into gel ( 2.5%) or undiluted (10%)

inside a surgical glove for finger tip, thumb and

hand exposures

It may also be administered subcutaneously

Intra-arterial injection can be used for finger tip,

thumb and hand burns

For systemic fluoride poisoning, I/V calcium

gluconate titrated to control cardiac

dysrhythmias, hypocalcemia and hypo-mag

44

Hydrocarbons and halogenated

hydrocarbons

They constitute a large number chemicals. Some

contain straight carbon chains and are called

aliphatic hydrocarbons.They can be gases, liquids

or solids.

Aromatic hydrocarbons contain benzene rings

Halogenated hydrocarbons are substituted with

halides such as fluoride, chloride, bromide or

iodide


hydrocarbons

Hydrocarbons are insoluble in water.

They are highly flammable.

Gaseous hydrocarbons can serve as simple

asphyxiants.

They sensitize the myocardium to

catecholamines

They cause CNS depression and can lead coma

Halogenated hydrocarbons are mostly

hepatotoxic

45


hydrocarbons

Signs and Symptoms:

- Exposure to gases and vapors of hydrocarbons

can cause simple asphyxia

- Narcosis, respiratory depression and resp. arrest

- Chemical pneumonitis due to prolonged

exposure to long chain hydrocarbons like

gasoline. Short chain HC like methane, ethane,

propane do not cause chemical pneumonitis

- Ingestion can cause aspiration pneumonitis


hydrocarbons

Signs and Symptoms: Tachyarrhythmias, phenol

is especially likely to cause dysrhythmias and

pump failure

- Defatting dermatitis, painless burns due to

phenol

- Liver damage with raised transaminases, fatty

liver

- Renal damage

46


hydrocarbons

Treatment: - Remove from source of exposure

- Remove clothes for gases and vapors

- For liquids , wash with water

- Adequate eye decontamination

- Ensure adequate ventilation, 100% Oxygen

- Beta blocker for ventricular irritability

- Continuously reassess the patient and give

supportive treatment

Acute Methemoglobinemia

47


Clinical Presentation: Methemoglobin is an

abnormal hemoglobin in which the usual reduce

Ferrous state of the heme iron is oxicidized to

Ferric form

Patient may appear deeply cyanosed yet

completely asymptomatic at Meth-Hb conc. less

than 10-15%. At higher concentrations, signs and

symptoms of anoxia appear


Meth-Hb levels Signs and Symptoms

20-30% Headache, fatigue, nausea

30-45% Dyspnoea on exertion,

lethargy & tacchycardia

50-70% Arrhythmias, coma,

seizures, resp. distress,

lactic acidosis

>70% Cardiovascular collapse,

death

Anemic patients have symptoms at lower

Meth-Hb levels

48


Treatment:

-Supportive Tt. like O2, decontamination of skin,

- Antidote : Methylene blue is indicated if Meth-

Hb levels are more than 30% or patient is

showing s/s of anoxia

Dose: 1mg/kg body wt of 1% solution slowly

over a period of 5 minutes. Repeat after 1 hour if

patient is still symptomatic. Some chemicals may

need many doses but do not exceed 7 mg/kg

• The plant authorities should immediately contactthe local administrator in case hazard is likely tospread beyond the factory.

• The concerned Police Officers along with civicofficials should make arrangements for evacuationof the people from the vicinity to safe areas.

• The plant authorities should extend all technicalsupport in controlling the damage.

• Most importantly, it is the responsibility of theindustry management that the people do not getpanicky.

• After all the hazard is totally eliminated, people maybe brought back to their respective places ofworking and living.

MEASURES TO BE TAKEN DURING

THE EMERGENCY CONDITIONS

49

Right-to-Know

RightRightRightRight----totototo----Know laws mandate that employers:Know laws mandate that employers:Know laws mandate that employers:Know laws mandate that employers:

• Inform employees about toxic chemicals they Inform employees about toxic chemicals they Inform employees about toxic chemicals they Inform employees about toxic chemicals they

might be exposed to in their workplace.might be exposed to in their workplace.might be exposed to in their workplace.might be exposed to in their workplace.

• Provide training about safe handling practices and Provide training about safe handling practices and Provide training about safe handling practices and Provide training about safe handling practices and

emergency procedures.emergency procedures.emergency procedures.emergency procedures.

• Maintain MSDS for immediate access in the Maintain MSDS for immediate access in the Maintain MSDS for immediate access in the Maintain MSDS for immediate access in the

workplace/job site.workplace/job site.workplace/job site.workplace/job site.

Material Safety Data Sheets (MSDS)

Section 1 - Product and Company IdentificationProduct and Company IdentificationProduct and Company IdentificationProduct and Company Identification

Section 2 - Composition/Information on IngredientsComposition/Information on IngredientsComposition/Information on IngredientsComposition/Information on Ingredients

Section 3 - Hazards Identification Including Emergency OverviewHazards Identification Including Emergency OverviewHazards Identification Including Emergency OverviewHazards Identification Including Emergency Overview

Section 4 - First Aid MeasuresFirst Aid MeasuresFirst Aid MeasuresFirst Aid Measures

Section 5 - Fire Fighting MeasuresFire Fighting MeasuresFire Fighting MeasuresFire Fighting Measures

Section 6 - Accidental Release MeasuresAccidental Release MeasuresAccidental Release MeasuresAccidental Release Measures

Section 7 - Handling and StorageHandling and StorageHandling and StorageHandling and Storage

Section 8 - Exposure Controls & Personal ProtectionExposure Controls & Personal ProtectionExposure Controls & Personal ProtectionExposure Controls & Personal Protection

Section 9 - Physical & Chemical PropertiesPhysical & Chemical PropertiesPhysical & Chemical PropertiesPhysical & Chemical Properties

Section 10 - Stability & Reactivity DataStability & Reactivity DataStability & Reactivity DataStability & Reactivity Data

Section 11 - Toxicological InformationToxicological InformationToxicological InformationToxicological Information

Section 12 - Ecological InformationEcological InformationEcological InformationEcological Information

Section 13 - Disposal ConsiderationsDisposal ConsiderationsDisposal ConsiderationsDisposal Considerations

Section 14 - MSDS Transport InformationMSDS Transport InformationMSDS Transport InformationMSDS Transport Information

Section 15 - Regulatory InformationRegulatory InformationRegulatory InformationRegulatory Information

Section 16 - Other InformationOther InformationOther InformationOther Information

50

Prehospital use of antidotes

Quality of the first call medical assessment

Early lifesaving value, with little or no alternative measure

Distance and time interval to the hospital

Clinical situation: great value of toxidromes!

Probability of use,

depending on local epidemiology and industrial activities

Particular risk of mass casualties (strategic storage)

(hydroxocobalamin, atropine, pralidoxime, …)

Prehospital use of antidotes

Ease and safety of use, possible adverse effects

Storage conditions, shelf life (glucagon, fomepizole,

hydroxocobalamine, …)

Cost, including waste of unused or outdated products

(hydroxocobalamin, digoxin antibodies, viper antivenom, ..)

Qualification and skill level of the prehospital emergency

team (good knowledge of toxidromes)

51

Activated Charcoal

Pesticides ==== OP organo phosphorus

PAM(Oximes)

Atropine

52

Ethylene Glycol

Methanol

Ethylene Glycol / Methanol

Cyanide antidotes

Hydroxocobalamine +/- thiosulfate

� Expensive

� Very safe

� First choice if uncertain CN poisoningor smoke exposure: any sign of tissue hypoxia

Dicobalt Edetate (Kelocyanor®)

� Relatively cheap

� Cardiovascular side-effects

� Mass CN poisoning (industrial, terrorism) ?

53

Preparedness

55

Shelters

Basic Rules of Chemical Safety

Be Aware!

Be Alert!

Be Alive!

56


Rule #1

Don’t buy or store chemicals

you do not need.


Rule #2

Store chemicals in their

original container.

57


Rule #3

Always wear appropriate

safety gear and work in a

safe environment.


Rule #4

Always dispose of chemicals

safely.

58

Recommended Hazardous Material

Antidotes

Antidote Indications

Atropine OP pesticides

Calcium gluconate Hydrofluoric acid and fluoride

( gel and I/V)

Cyanide antidote kit Cyanide

Methylene blue Methemoglobin forming agents

Recommended Hazardous Material

Antidotes

Antidote Indications

Oxygen Carbon monoxide

Pralidoxime OP pesticides

Pyridoxine Hydrazine

59

Take Home Message

• Educate your people!

• Contact your local office of Disaster

Preparedness

• Work with your Disaster/

Emergency Medical and Nursing

staff to develop an action-plan.

• Conduct disaster drills on all shifts.

• Managers must be prepared with

manpower, supplies and staff.

Preparedness

Preparedness Is the Key to

combat Chemical disaster

• Awareness

• Training

• Equipment

• Resources

• Planning

• Exercises

60

YOU Control the

Situation...

... the situation doesn’t control you

Response and Planning Exercises

Maru Associates

Poison Help LineDr.Tejas Prajapati

M.D.

Diploma in Clinical Toxicology(Australia)

[email protected]

9825820138

24x7

dr. tejas chemical emergencies sikkim - compatibility modecidm.in/pdf/day2_2/9.pdf · asphyxiants...

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