The document discusses various toxic substances including chemical and biological weapons, with a focus on chlorine gas and cyanide, detailing their properties, mechanisms of action, epidemiology, and health effects. It highlights historical instances of chemical weapon use during World War I, medical responses to toxic exposures, and the challenges in treating poisoning from these agents. Additionally, it covers preventive measures in chemical exposure scenarios and the use of antidotes for cyanide poisoning.

1. Toxic Gases
KS Chew
School of Medical Sciences
Universiti Sains Malaysia

2. Overview
 Chemical Weapons  Radiation
 Nerve Agents – G series (GA,  α radiation
GB, GD), V series  β radiation
 Blood Agents - cyanides  γ radiation
 Blistering Agents  Nuclear
 Biological Weapons  A bomb (Atomic)
 Biological Agents – viruses (e.g  H bomb (Hydrogen)
Ebola), bacteria (Yersenia
pestis, anthrax)  Explosives
 Biological Toxins – botulism,  Large scale - Incendiary
ricin, Staphylococcal bombs, Napalm-B, Mark 77
Enterotoxin B  Smaller scale - Molotov
Cocktail (Poor man’s hand
grenades)

3. Chlorine Gas

4. Introduction
 Chlorine gas is a pulmonary irritant with
intermediate water solubility that causes acute
damage in the upper and lower respiratory tract.
 Was first used as a chemical weapon at Ypres,
France, in 1915. Of the 70,552 American
soldiers poisoned with various gases in World
War I, 1843 were exposed to chlorine gas.

5. Chemical Weapon During Second
Battle of Ypres 1915
 Was the first time Germany
utilized poison gas on a
large scale
 At around 5:00 pm on April
22, 1915, the German Army The Second Battle of Ypres by
released one hundred and Richard Jack, 146 x 234½ in., at
the Canadian War Museum.
sixty eight tons of chlorine
gas on the Allies troop

6. Chemical Weapon During Second
Battle of Ypres 1915
 Approx 6,000 French and
colonial troops died within
ten minutes at Ypres,
primarily from asphyxiation
and subsequent tissue Ruins of Ypres market
square
damage in the lungs.
 Many more were blinded.

7. Chemical Weapon During Second
Battle of Ypres 1915
 Chlorine gas forms hydrochloric
(muriatic) acid when combined
with water, destroying moist
tissues such as lungs and eyes.
 The chlorine gas, being denser
Ruins of Ypres market
than air, quickly filled the square
trenches, forcing the troops to
climb out into heavy enemy fire.

8. Chemical Weapon During Second
Battle of Ypres 1915
 Although not a historical first, it
came as a tactical surprise to the
Allies.
 After Second Ypres, both sides
developed more sophisticated gas
Ruins of Ypres market
weapons, and countermeasures, square
and never again was the use of
gas either a surprise, nor
especially effective.

9. Pathophysiology
 Chlorine is a greenish-yellow, noncombustible gas at
room temperature and atmospheric pressure.
 The water solubility of chlorine accounts for its effect
on the upper airway and the lower respiratory tract.
 Exposure to chlorine gas may be prolonged because its
moderate water solubility may not cause upper airway
symptoms for several minutes.
 In addition, the density of the gas is greater than that of
air, causing it to remain near ground level and
increasing exposure time.

10. Pathophysiology
 Chlorine is moderately soluble in water and
reacts in combination to form hypochlorous
(HOCl) and hydrochloric (HCl) acids. Elemental
chlorine and its derivatives, hydrochloric and
hypochlorous acids, may cause biological injury.
The chemical reactions of chlorine combining
with water and the subsequent derivative
reactions with HOCl and HCl are as follows:

11. Pathophysiology
 Cl2 + H2O  HCl (hydrochloric acid) + HOCL
(hypochlorous acid) or
 Cl2 + H2O  2 HCl + [O-] (nascent oxygen)
 HOCl  HCl + [O-]
 Elemental chlorine and its derivatives,
hydrochloric and hypochlorous acids, can cause
biological injury.

12. Mechanism of Action
 Mechanisms of the above biological activity are
poorly understood
 The predominant anatomic site of injury may
vary, depending on the chemical species
produced.
 Because of its intermediate water solubility and
deeper penetration, elemental chlorine
frequently causes acute damage throughout the
respiratory tract.

13. Mechanism of Action
 Cellular injury is believed to result from the
oxidation of functional groups in cell
components, from reactions with tissue water to
form hypochlorous and hydrochloric acid, and
from the generation of free oxygen radicals.

14. Mechanism of Action
 Hydrochloric acid and hypochlorous acid is highly
soluble in water.
 The immediate and predominant targets of the acid are
the epithelia of the ocular conjunctivae and upper
respiratory mucus membranes.
 Irritation of the airway mucosa leads to local edema
secondary to active arterial and capillary hyperemia.
Plasma exudation results in filling the alveoli with
edema fluid, resulting in pulmonary congestion.

15. Mechanism of Action
 Although the eye seldom is damaged severely by
chlorine gas toxicity; burns and corneal
abrasions have occurred.
 Acids formed by the chlorine gas reaction with
the conjunctival mucous membranes are
buffered, by the tear film and the proteins
present in tears resulting in epithelial and
basement membrane damage but rarely damage
deep endothelial cells

16. Epidermiology
 Chlorine gas is one of the most common single,
irritant, inhalation exposures, occupationally and
environmentally.
 In a recent study of 323 cases of inhalation
exposures reported to poison control centers,
the largest single source of exposure (21%) was
caused by mixing bleach with other products.

17. Epidermiology
 Internationally, chlorine gas
accounts for the largest single
cause of major toxic release
incidents.
 Use of chlorine internationally
is parallel to use by the US in
chemical, paper, and textile
industries and in sewage
treatment.

18. Uses of Chlorine
 To disinfect water
 For sanitation process for sewage and industrial waste.
 As a bleaching agent the production of paper and cloth.
 Used in cleaning products, including household bleach
which is chlorine dissolved in water.
 Used in the preparation of chlorides, chlorinated
solvents, pesticides, polymers, synthetic rubbers, and
refrigerants.

19. Water Park Owner To Pay Medical Expenses
(The Star, 29 November 1996)
Petaling Jaya (Selangor) Malaysia - `Sunway Lagoon', Malaysia's popular
water park says it will settle the medical expenses incurred by the five
children who were hospitalised after inhaling chlorine fumes at its theme
park here on Monday.
The incident occurred when a maintenance staff unscrewed a t-point to
clear a clogged supply pipeline which channels chlorine into the pool.
According to the National Poison Centre at Universiti Sains Malaysia in
Penang, large amount of chlorine gas absorbed by a person over a long
period is fatal. If the exposure is brief, the victim experiences dizziness and
nausea. Chlorine is a chemical used to kill bacteria and ammonia
compounds like sweat and hair-care products and to destroy algae. Chlorine
gas can be released when chemicals become 'mixed' during pool
maintenance.

20. Ref: http://www.eurochlor.org/tree

21. Pre-Hospital Care
 Prehospital care providers
should take necessary
precautions to prevent
contamination.
 The use of a self-contained
breathing apparatus with
full face mask should
protect against the effects
of chlorine gas.
Ref:
http://english.peopledaily.com.cn/200704/16/eng
20070416_366864.html

22. Pre-Hospital Care
 Remove the individual from the toxic environment.
 Bring container, if applicable, so medical personnel can
identify toxic agent.
 Commence primary decontamination of the eye and
skin, if necessary.
 Chlorine gas is denser than air and accumulates close to
the ground. Therefore, during chlorine-related
accidents, people should be instructed to seek higher
altitudes to avoid excessive exposure.

23. First World War poison gas treatment. Soldier being cleaned in a poison gas decontamination
room in France during the First World War (1914-1918). The medical staff are wearing protective
clothing and masks to prevent being contaminated. The First World War saw the first large-scale use
of chemical weapons, with a chlorine gas attack by German forces on French positions at the Second
Battle of Ypres on 22 April 1915. Around 85,000 soldiers died due to the use of chemical weapons
over the remaining years of the war. This is the American Evacuation Hospital Number 2, at Baccarat,
France. The US entered the war on 6 April 1917, playing a crucial role in helping Britain and France to
defeat Germany and its allies. Photographed on 8 June 1918.
Reference from SciencePhoto Library: http://www.sciencephoto.com/images/download_lo_res.html?id=788000137

24. Decontamination
 Eye and skin exposures require copious irrigation with
saline. In cases of suspected ocular injury, determine
initial pH using a reagent strip. Continue irrigation with
0.9% saline until the pH returns to 7.4.
 Topical anesthetics help limit pain and improve patient
cooperation.
 Following irrigation, perform slit lamp examination,
including fluorescein staining.
 Measure ocular pressures.
 Treat corneal abrasions with antibiotic ointment.

25. Cyanide Poisoning

26. Introduction
 Cyanide is generally considered to be a rare
source of poisoning; however, cyanide exposure
occurs relatively frequently in patients with
smoke inhalation from residential or industrial
fires.
 Cyanide poisoning also may occur in industry,
particularly in the metal trades, mining,
electroplating, jewelry manufacturing, and x-ray
film recovery.

27. The Use of Cyanide
 In manufacturing, cyanide is used to
make paper, textiles, and plastics.
 Present in the chemicals used to
develop photographs.
 Cyanide salts are used in metallurgy
for electroplating, and removing gold
from its ore (gold and silver mining)
 Cyanide gas is used to exterminate
pests and vermin in ships and
buildings.
Cyanide is used for the mining of gold and silver because it helps dissolve these metals and their
ores.

28. Bukit Koman folk stage protest
By SIMON KHOO
RAUB: A group of residents in Bukit Koman
renewed their protest against the move by a local
joint-venture company to extract gold from the
mines here using cyanide.
The spokesman for the group Wong Kin Hoong
said some 3,000 residents in Bukit Koman would
be directly affected as their houses were located
about 300m from the mining site….
“The old method is not harmful to humans and
the environment but will bring out about 20% of
yields as compared to some 80% using cyanide,”
he elaborated.
Raub is synonymous with gold mining activities
and has a history dating back some 200 years.
Reference:
The STAR
http://thestar.com.my/news/story.asp?file=/2007/2/13/southneast/168
40736&sec=southneast

29. Historical Cases of Cyanide
Poisoning
Ronald Clark O'Bryan (October 19, 1944
The infamous lime green gas chamber at San – March 31, 1984) was a murderer from
Quentin, where all of California's death sentences Deer Park, Texas (near Houston), who
are carried out. The prisoner is strapped to a chair was convicted of killing his eight-year-old
inside a sealed gas chamber. The executioner son Timothy on Halloween, 1974 with
(standing outside of the chamber) pulls a lever cyanide-laced candy in order to claim life
dropping potassium cyanide pellets into a vat of insurance money.
sulfuric acid, flooding the chamber with lethal
hydrogen cyanide gas.

30. Historical Cases of Cyanide
Poisoning
A can of Zyklon B with The containers above hold Zyklon-B pellets
adsorbent granules and (hydrogen cyanide) that vaporize when exposed to air.
original signed documents Originally intended for commercial use as a
detailing ordering of Zyklon
disinfectant and an insecticide, the Nazis discovered
B as "materials for Jewish
resettlement" (display at
through experimentation the gas could be used to kill
Auschwitz I museum) humans.

31. Historical Cases of Cyanide
Poisoning
The Chicago Tylenol
murders occurred when
seven people died after
taking pain-relief
capsules that had been
poisoned. The
poisonings, code-named
TYMURS by the FBI,
took place in the autumn
of 1982 in the Chicago
area of the United States.
These poisonings
involved Extra-Strength
James Warren "Jim" Jones (May 13, 1931 – Tylenol medicine capsules
November 18, 1978) was the founder and leader of which had been laced
the Peoples Temple, which is best known for the with potassium cyanide.
November 18, 1978 mass murder of more than 900
Temple members in Jonestown, Guyana along with
the killings of five other people at a nearby airstrip.

32. The Use of Cyanide
 Cyanide is released from natural substances in some
foods and in certain plants such as cassava. Cyanide is
contained in cigarette smoke and the combustion
products of synthetic materials such as plastics.
Combustion products are substances given off when
things burn.
 In manufacturing, cyanide is used to make paper,
textiles, and plastics. It is present in the chemicals used
to develop photographs. Cyanide salts are used in
metallurgy for electroplating, metal cleaning, and
removing gold from its ore. Cyanide gas is used to
exterminate pests and vermin in ships and buildings.

33. Pathophysiology
 Its principal toxicity results from inactivation of
cytochrome oxidase (at cytochrome a3), thus
uncoupling mitochondrial oxidative
phosphorylation and inhibiting cellular
respiration, even in the presence of adequate
oxygen stores.

34. Pathophysiology
 Cellular metabolism shifts from aerobic to
anaerobic, with the consequent production of
lactic acid.
 Consequently, the tissues with the highest
oxygen requirements (brain and heart) are the
most profoundly affected by acute cyanide
poisoning.

35. Cyanide Antidote Kit
 Cyanide Antidote Kit (CAK) contains amyl
nitrite pearls, sodium nitrite, and sodium
thiosulfate.
 Amyl and sodium nitrites induce
methemoglobin in red blood cells, which
combines with cyanide, thus releasing
cytochrome oxidase enzyme.

36. Cyanide Antidote Kit
 Inhaling crushed amyl nitrite pearls is a
temporizing measure before intravenous
administration of sodium nitrite.
 Sodium thiosulfate enhances the conversion of
cyanide to thiocyanate , which is renally
excreted. Thiosulfate has a somewhat delayed
effect and thus is typically used with sodium
nitrite for faster antidote action.

37. Cyanide Antidote Kit
 Avoid the sodium nitrite portion of the cyanide
kit in patients with smoke inhalation unless
carboxyhemoglobin concentration is very low
(<10%).
 The induction of methemoglobinemia from the
nitrites in addition to present
carboxyhemoglobinemia significantly reduces
the oxygen-carrying capacity of blood.

38. Cyanide Antidote Kit
 Vasodilatation leading to hypotension is another
adverse effect of CAK.
 Appropriate dosing of sodium nitrite has not
been established in children, who may develop
excessive methemoglobinemia and/or
hypotension.

39. Hydroxocobalamin
 Hydroxocobalamin combines with cyanide to
form cyanocobalamin (vitamin B-12), which is
renally cleared.
 Hydroxocobalamin administration resulted in
faster improvement in mean arterial pressure but
similar mortality and serum acidosis as
compared to sodium nitrite in animals.

40. Hydroxocobalamin
 Co-administration of sodium thiosulfate
(through a separate line or sequentially) has been
suggested to have a synergic effect on
detoxification.

41. Hydroxocobalamin
Adverse effects include
 transient hypertension (a benefit in hypotensive
patients)
 reddish brown skin, mucous membrane and
urine discoloration, and
 rare anaphylaxis and anaphylactoid reactions.

42. Carbon Monoxide
Poisoning

43. Introduction
 Carbon monoxide poisoning occurs after the
inhalation of carbon monoxide gas.
 Carbon monoxide (CO) is a product of
combustion of organic matter under conditions
of restricted oxygen supply, which prevents
complete oxidation to carbon dioxide.

44. Mechanisms of Action
 Not fully understood, but hemoglobin,
myoglobin, and mitochondrial cytochrome
oxidase are thought to be compromised.
 Treatment largely consists of administering
100% oxygen or hyperbaric oxygen therapy,
although the optimum treatment remains
controversial.

45. Introduction
Carbon monoxide is
 colorless
 odorless
 tasteless and
 non-irritating
* making it difficult for people to detect.

46. Sources
Common sources of CO:
 house fires
 furnaces or heaters
 wood-burning stoves
 motor vehicle exhaust and
 propane-fueled equipment such as portable
camping stoves, ice resurfacers, forklifts, and
engine-driven generators.

48. Suicide-Related
 Suicide was also often committed by inhaling
exhaust fumes of running car engines.
 In the past, motor car exhaust may have
contained up to 25% carbon monoxide.
 Newer cars have catalytic converters, which can
eliminate over 99% of carbon monoxide
produced.

49. Suicide-Related
 However, even cars with catalytic converters can
produce substantial carbon monoxide if an
idling car is left in an enclosed space (due to
reduced oxygen availability, and therefore, less
efficient combustion).

50. Clinical Features
 The earliest symptoms, especially from low level
exposures, are often non-specific and readily
confused with other illnesses, typically flu-like
viral syndromes, depression, chronic fatigue
syndrome, and migraine or other headaches
(often makes the diagnosis of carbon monoxide
poisoning difficult).

51.  If suspected, the diagnosis can be confirmed by
measurement of blood carboxyhemoglobin.
 The main manifestations of poisoning develop
in the organ systems most dependent on oxygen
use
 the central nervous system
 the heart.

52.  tachycardia
 hypertension
 central nervous system symptoms such as
headache, dizziness, confusion, convulsions, and
unconsciousness.
 CO poisoning may also produce myocardial
ischemia, atrial fibrillation, pneumonia,
pulmonary edema, hyperglycemia, muscle
necrosis, acute renal failure, skin lesions, visual
and auditory problems, and respiratory arrest.

53.  One of the major concerns following CO
poisoning is the severe neurological
manifestations that may occur days or even
weeks after an acute poisoning.
 Common problems encountered are difficulty
with higher intellectual functions and short-term
memory, dementia, irritability, gait disturbance,
speech disturbances, parkinson-like syndromes,
cortical blindness, and depression (depression
can occur in those accidentally exposed).

54.  Chronic
 Long term, repeated exposures present a greater
risk to persons with coronary heart disease and
in pregnant patients.
 Chronic exposure may increase the incidence of
cardiovascular symptoms in some workers, such
as motor vehicle examiners, firefighters, and
welders.
 Patients often complain of persistent headaches,
lightheadedness, depression, confusion, and

55. Characteristic Red Colour

56. Toxicity
 Toxicity is increased by several factors, including:
- increased activity and rate of ventilation,
- pre-existing cerebral or cardiovascular disease,
- reduced cardiac output, anemia or other hematological disorders,
- decreased barometric pressure, and
- high metabolic rate.
 Carbon monoxide is life-threatening to humans and other forms of air-
breathing life, as inhaling even relatively small amounts of it can lead to
hypoxic injury, neurological damage, and possibly death.
 A concentration of as little as 0.04% (400 parts per million) carbon monoxide
in the air can be fatal.
 First aid for a victim of carbon monoxide poisoning requires access to fresh
air; administration of artificial respiration and, if available, oxygen; and, as
soon as possible, medical attention.

57. Mechanism of Toxicity
 When carbon monoxide is inhaled, it takes the place of
oxygen in hemoglobin, the red blood pigment that
normally carries oxygen to all parts of the body.
 Because carbon monoxide binds to hemoglobin 230 –
270 times more strongly than oxygen, its effects are
cumulative and long-lasting, causing oxygen starvation
throughout the body.
 Prolonged exposure to fresh air (or pure oxygen) is
required for the CO-tainted hemoglobin
(carboxyhemoglobin) to clear.

58. Carbon Monoxide Binding to
Hemoglobin

59. Toxicity
The effects of carbon monoxide in parts per million Symptoms
35 ppm (0.0035%) Headache and dizziness within six to eight hours of
constant exposure
100 ppm (0.01%) Slight headache in two to three hours
200 ppm (0.02%) Slight headache within two to three hours
400 ppm (0.04%) Frontal headache within one to two hours
800 ppm (0.08%) Dizziness, nausea, and convulsions within 45
minutes. Insensible within two hours.
1,600 ppm (0.16%) Headache, dizziness, and nausea within 20 minutes.
Death in less than two hours.
3,200 ppm (0.32%) Headache, dizziness and nausea in five to ten
minutes. Death within 30 minutes.
6,400 ppm (0.64%) Headache and dizziness in one to two minutes.
Death in less than 20 minutes.
12,800 ppm (1.28%) Death in less than three minutes.

60. Carboxyhemoglobin
 Levels of carbon monoxide bound in the blood can be
determined by measuring carboxyhemoglobin, which is
a stable complex of carbon monoxide and hemoglobin
that forms in red blood cells.
 Normal carboxyhemoglobin levels in an average person
are less than 5%, whereas cigarette smokers (two
packs/day) may have levels up to 9%.
 Serious toxicity is often associated with
carboxyhemoglobin levels above 25%, and the risk of
fatality is high with levels over 70%.

61. Toxic mechanism
 The precise mechanisms by which toxic effects
are induced by CO are not fully understood.
 Carbon monoxide binds to:
1) hemoglobin (reducing oxygen transportation)
2) myoglobin (decreasing its oxygen storage
capacity)
3) mitochondrial cytochrome oxidase (inhibiting
cellular respiration).

62. Hemoglobin
 Carbon monoxide has a significant affinity to the iron (or
copper) sites in hemoglobin, the principal oxygen-carrying
compound in blood.
 CO binds to hemoglobin, producing carboxyhemoglobin
(COHb) – which decreases the oxygen-carrying capacity of the
blood.
 Inhibits the transport, delivery, and utilization of oxygen.
 Because hemoglobin is a tetramer with four oxygen binding sites,
binding of CO at one of these sites also increases the oxygen
affinity of the remaining 3 sites, which interferes with normal
release of oxygen.
 This causes hemoglobin to retain oxygen that would otherwise
be delivered to the tissue.

63. Hemoglobin
 This situation is described as CO shifting the oxygen dissociation
curve to the left.
 Because all the oxygen is in the blood, none is being given to the
tissues, and this causes tissue hypoxic injury.
 A sufficient exposure to carbon monoxide can reduce the
amount of oxygen taken up by the brain to the point that the
victim becomes unconscious, and can suffer brain damage or
even death from hypoxia.
 The brain regulates breathing based upon carbon dioxide levels
in the blood, rather than oxygen levels, so a victim can succumb
to hypoxia without ever noticing anything up to the point of
collapse.
 Hemoglobin acquires a bright red color when converted to
carboxyhemoglobin, so a casualty of CO poisoning is described
in textbooks as looking pink-cheeked and healthy (However, this
"classic" cherry-red appearance is not always seen

64. Myoglobin
 Carbon monoxide also has a high affinity for
myoglobin.
 CO bound to myoglobin may impair cardiac output and
result in cerebral ischemia.
 A delayed return of symptoms has been reported and
appears to result following a recurrence of increased
carboxyhemoglobin levels; this effect may be due to late
release of CO from myoglobin, which subsequently
binds to hemoglobin.

65. Cytochrome oxidase
 A second mechanism involves co-effects on the
mitochondrial respiratory enzyme chain that is
responsible for effective tissue utilization of oxygen.
 CO does not bind to cytochrome oxidase with the same
affinity as oxygen, so it likely requires significant
intracellular hypoxia before binding.
 This binding interferes with aerobic metabolism and
efficient adenosine triphosphate (ATP) synthesis.
 Cells respond by switching to anaerobic metabolism,
causing anoxia, lactic acidosis, and eventual cell death.

66. Pregnancy
 Carbon monoxide poisoning can have significant fetal effects.
 CO causes fetal tissue hypoxia by decreasing the release of
maternal oxygen to the fetus, and by carbon monoxide crossing
the placenta and combining with fetal hemoglobin, which has a
10 to 15% higher affinity for CO than adult hemoglobin.
 Elimination of carbon monoxide is also slower in the fetus,
leading to an accumulation of CO.
 The level of fetal morbidity and mortality in acute carbon
monoxide poisoning is significant, so despite maternal wellbeing,
severe fetal poisoning can still occur.
 Due to these effects, pregnant patients are treated with normal
or hyperbaric oxygen for longer periods of time than non-
pregnant patients.

67. Treatment
 The main medical treatment for carbon monoxide
poisoning is 100% oxygen by a tight fitting oxygen
mask.
 Oxygen hastens the dissociation of carbon monoxide
from hemoglobin, improving tissue oxygenation by
reducing its biological half-life.
 Hyperbaric oxygen is also used in the treatment of CO
poisoning (also by increases carboxyhemoglobin
dissociation and does so to a greater extent than normal
oxygen).
 Hyperbaric oxygen may also facilitate the dissociation
of CO from cytochrome oxidase.

68. Treatment
 A significant controversy in the medical literature is
whether or not hyperbaric oxygen actually offers any
extra benefits over normal high flow oxygen in terms of
increased survival or improved long term outcomes.
 There have been clinical trials in which the two
treatment options have been compared;
- of the six performed, four found hyperbaric oxygen
improved outcome and two found no benefit for
hyperbaric oxygen.

69. Indications for Hyperbaric Oxygen Treatment
in Acute CO Poisoning
Definite Indication Relative Indication
Altered mental status and/or abnormal Persisting neurologic symptoms including
neurologic examination headache and dizziness after 4 H of
100% normobaric oxygen
H/o LOC or near syncope Persisting acidosis
H/o seizure Concurrent thermal or chemical burns
Coma Pregnancy with H/o CO exposure
regardless of COHb level
H/o hypotension during or shortly after
exposure
Myocardial Ischaemia
H/o prolonged exposure
Pregnancy with COHb>15%

70. Asphyxiant Gas

71. What Is An Asphyxiant Gas
 An asphyxiant gas is a non-toxic or minimally
toxic gas which dilutes or displaces the oxygen-
containing atmosphere, leading to death by
asphyxiation (suffocation) if breathed long
enough.
 Toxic gases, by contrast, cause death by other
mechanisms, such as competing with oxygen
(e.g. carbon monoxide) or directly damaging the
respiratory system (e.g. phosgene).
Source: Wikipedia. Asphyxiant Gas. URL: http://en.wikipedia.org/wiki/Asphyxiant_gas