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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?
9
10
11
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
14
Most killed or injured lived in Shanty town that grew up
too close to the plant.
15
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
16
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
Flixborough, UK, 1974
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
18
Flixborough, UK, 1974
Flixborough, UK, 1974
� 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
19
Flixborough, UK, 1974
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
20
• 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
21
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
22
Are We
Prepared
….???
Types of Chemical Accidents
1. Industrial
2. Transportation
3. Household
4. Others
23
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
24
Major Chemical Exposures
• Asphyxiants
• Cholinesterase inhibitors (Organophosphorus nerve agents)
• Respiratory tract irritants
• Corrosives and Vesicants
Types of Emergencies
• Onsite Emergency
• Offsite Emergency
25
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
26
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
27
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
28
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.
29
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
30
Respiratory tract irritants
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
31
Respiratory tract irritants
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
32
Ammonia Leakage from a Tanker in Rajkot Region
33
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
34
Cholinesterase Inhibitors
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
35
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).
36
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
Cholinesterase Inhibitors
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
37
Cholinesterase Inhibitors
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
38
Cholinesterase Inhibitors
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.
Cholinesterase Inhibitors
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
39
Cholinesterase Inhibitors
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
40
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
41
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
42
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
43
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 and halogenated
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 and halogenated
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 and halogenated
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 and halogenated
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
Acute Methemoglobinemia
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
Acute Methemoglobinemia
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
Acute Methemoglobinemia
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
54
55
Shelters
Basic Rules of Chemical Safety
Be Aware!
Be Alert!
Be Alive!
56
Basic Rules of Chemical Safety
Rule #1
Don’t buy or store chemicals
you do not need.
Basic Rules of Chemical Safety
Rule #2
Store chemicals in their
original container.
57
Basic Rules of Chemical Safety
Rule #3
Always wear appropriate
safety gear and work in a
safe environment.
Basic Rules of Chemical Safety
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)
drtejasforensic@yahoo.com
9825820138
24x7
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