Transcript Acute chemical intoxications –systemically toxic chemicals

Acute chemical intoxications –
systemically toxic chemicals
Paide 4.11.03 Tiina Santonen

Chemical asphyxiants
– Carbon monoxide
– Cyanides
– Hydrogen sulphide
– Methaemoglobinemia –inducing
substances
Anticholinesterase inhibitors
 Organic solvents
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Carbon monoxide
the most common cause of chemical
intoxication in industry
 mechanism of action: binds to
haemoglobin at 200-300 higher
affinity than oxygen and forms
carboxyhaemoglobin, but it also
enters the tissues and attacts the
cytochrome system
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Adapted from Rom W.N.: Environmental and Occupational Medicine, 3rd ed.,
Philadelphia, 1998.

smoking causes 3-8 % COHb

Finnish OEL 30 ppm => 4 % COHb

IDLH 1200 ppm /30 min
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The amount of carboxyhaemoglobin is
highly dependent on the physical activity
of the exposed individual
 % COHb=[CO]air x K x T
K=constant for physical activity, at rest
K=0.018, in light work K=0.048
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If the air concentration of CO is 1%
(=10000 ppm), 50% COHb level will be
reached at rest in 16 min, in light work in 6
min
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Individual susceptibility: people
suffering from heart and lung
diseases at highest risk
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Pregnancy!

methylene chloride forms carbon
monoxide in the body
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Carbon monoxide poisoning treatment

diagnosis: anamnesis, status, blood
carboxyhaemoglobin content (does not
necessary correlate with the severity of symptoms!)

monitoring of ECG, electrolytes and
arterial blood gases

treatment:
100 % oxygen
hyperbaric oxygen (in
special cases)
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Hydrogen cyanide and
Cyanide salts

Cyanides are used e.g. in the metal
finishing operations, HCN is formed also
in fires
Cyanide ion (CN- ) inhibits the cellular
respiration by binding to mitochondrial
cytochrome oxidases
 affects all organs, however, the organs
with high oxygen demand most
susceptible
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Hydrogen cyanide: bitter almond-like
odor
 Finnish OEL 10 ppm / 15 min
 IDLH for hydrogen cyanide 50 ppm /
30 min
 symptoms of cyanide poisoning are
due to the decreased tissue oxygen
utilisation and became evident mainly
as CNS symptoms like weakness,
dizziness, nausea, headache,
confusion, convulsions and
unconsciousness
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Note: cyanide salts like KCl, NaCl, Ca(CN)2
are well absorbed through the skin
 Treatment of cyanide poisoning:
– First aid: administration of 100 % oxygen, amyl
nitrite inhalation
– Hydroxycobalamin 5 g i.v. during the 30
minutes
– (sodium nitrite or 4-dimethylaminophenol [4DMAP])
– sodium tiosulfate 25% 50 ml
– (dicobalt edetate in severe cases)
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Education of the workers for safe
handling!
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Nitriles
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Nitriles like acrylonitrile deliberate cyanide
in the body
acrylonitrile is used e.g. in the
manufacture of acrylic fibers, ABSplastics, latexes and nitrile rubber
acrylonitrile IDLH 85 ppm, well absorbed
through the skin, high vapour pressure
symptoms of poisoning are equivalent to
those of cyanides
treatment of poisoning is equivalent to
that of cyanide poisoning
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Hydrogen sulfide
formed during the decomposition of
organic materials; exposure to H2S
may occur e.g. in sewage treatment
plants, cellulose industry)
 odor of rotten eggs at low
concentrations (odor threshold 0.008
ppm), however, at high
concentrations the sense of smell is
paralyzed

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highly toxic, inhibits cellular
respiration like cyanide
 Finnish OEL 10 ppm / 15 min
 IDLH 100 ppm /30 min
 symptoms of poisoning resemble
those of cyanide poisoning
 treatment: 100 % oxygen
(amyl nitrite, sodium
nitrite, 4-DMAP)
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Methaemoglobinemia –
inducing agents

methaemoglobinemia = oxidation of
haemoglobin Fe2+ to Fe3+ => inability of
haemoglobin to carry oxygen

many aromatic amino and nitro
compounds (e.g. aniline, nitrobenzenes),
and nitrites and nitric oxide may induce
methaemoglobinemia
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Physical properties of the compound
determine the possible routes of
exposure
– For example sodium and potassium
nitrites are solid compounds, which do
not evaporise at normal conditions, but
amyl and isobutylnitrites are liquids with
a vapour pressure and may evaporise.
Aniline and nitrobenzenes are liquids
which may evaporate and be absorbed
through the skin (good fat-solubility)
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Symptoms of methaemoglobinemia:
– cyanosis (15-25 % methamoglobin), more severe
cyanosis and CNS symptoms at 40 % level of
methaemoglobinemia
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treatment of methaemoglobinemia:
– 100 % oxygen
– Monitoring of the methaemoglobin levels
– 1-2 mg/kg 1 % methylene blue i.v. in
severe poisoning cases (usually caused
by ingestion)
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Anticholinesterase inhibitors
-organophosphorus pesticides and nerve agents
like sarin and tabun
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Organophosphorus pesticides

e.g. azinphos-methyl, dichlorvos,
dimethoate, fenitrothion, azamethiphos,
isophenphos, chlorpyriphos
 used as insecticides
 depending on the use, the main route of
exposure to organophosphates is the
skin, but also inhalation exposure may
occur
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Organophosphorus pesticides

irreversible inactivation of
acetylcholinesterase => increase in
acetylcholine levels in nerve endings
=> Cholinergic symptoms which include
salivation, sweeting, lachrymation, miosis,
bradycardia, hypotension (muscarinic
effects), muscle spasms, convulsions and
finally paralysis (nicotinic effects)
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Organophosphorus pesticides
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treatment of poisoning:
- the patient should be kept at rest
-supportive care: oxygen, ventilation
-treatment of convulsions with diazepam
-antidote: atropine 2 mg every 5-10 min
-obidoxime 250 mg i.v. reactivates
acetylcholinesterase

biological monitoring: measurement of
blood acetylcholinesterase activity
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Organic solvents

aliphatic and aromatic hydrocarbons,
halogenated hydrocarbons, alcohols,
ketones, ethers, esters
 toxicity varies
 generally may cause CNS depressant
effects, some of them may sensitize
cardiac muscle for catecholamines and
cause arrhytmias
 Lipid solubility affects the toxicity
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Abusers!
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