Biomedical Engineering Reference
In-Depth Information
antidotal activity of atropine after the miosis caused
by accidental exposure to vaporized Tabun [3].
While many countries developed and
weaponized nerve agents it was not until March
1984 when Iraq used tabun filled aerial bombs
against Iranian soldiers in the Iran-Iraq War. The
Iraqis continued to use tabun in addition to sarin
until the end of the war in August 1988. In addition
to the use of nerve agents against Iranian soldiers,
in March of 1988 Iraq soldiers killed hundreds
of Iraqi Kurds in the town of Halabja (population
80,000) during aerial bombing raids a day after
troops from the Kurdish Patriotic Union of
Kurdistan (PUK) entered the town. These attacks
involved multiple chemical agents—including
mustard gas, and the nerve agents SARIN,
TABUN and VX, and possibly cyanide [4].
In June 1994, members of Aum Shinrikyo,
a Japanese cult, released sarin in an apartment
complex in Matsumoto, Japan. In this attack there
were almost 300 casualties, including 7 dead [5].
This cult followed with another attack in March
1995 when five two-man teams released nerve
gas in Tokyo's subway cars by puncturing liquid
sarin-filled plastic bags (30% full strength). This
resulted in over 5500 “casualties” seeking medical
attention of which 984 were moderately poisoned
and held for observation or treatment. Fifty-four
were severely poisoned; of which 12 died [6].
While much attention is given to nerve agents the
potential enormity of the chemical threat to civilian
population was fully displayed in the 1984 indus-
trial accident that released methylisocyanate and
chlorine gas over Indian city of Bhopal. Of the
estimated 38,000 immediate inhalation casualties,
some 8000 eventually died [7].
While industrial terrorism remains a reality, the
pragmatic choice for small-unit terrorist action for
chemical weapon deployment is the highly vapor-
izable G-series of nerve agents.
6.2.2 Physical Characteristics
The three G agents, GA (tabun), GB (sarin), and
GD (soman), are moderately volatile liquids at
normal temperatures (Table 6.1). Though all the
nerve agents can be absorbed through the skin,
because the G agents are volatile they require
larger topical doses for toxicity. Thus, the primary
risk of these agents is by inhaling the vapor
or aerosol. While vapor or aerosol effects occur
within minutes the risk of injury after dermal expo-
sure is prolonged because, even if skin decontami-
nation occurs, continued absorption from the inner
layers of the skin can result in a delayed onset of
symptoms for as long as 18 hours.
The highly volatile G-agent (sarin) stands out
as a terrorist weapon because of it is the most
volatile at room temperature and the toxicity of the
resultant vapor is quite high. Because of the small
amount required for toxic effects it can be trans-
ported covertly as clear liquid sealed in a container
that can be vaporized when exposed to air. In addi-
tion, because of the volatility a small amount of sarin
Table 6.1
Nerve agent toxicological and physical properties
Agent
Volatility
a
Boiling
point
C
Vapor
density
b
Vapor toxicity
Skin toxicity
Ct
50
mg min m
−
3
c
Death
Aging
Miosis
Death
LD
50
mg
d
Tabun (GA)
610
240
56
2-3
400
1000
Hours
Sarin (GB)
22,000
158
47
3-5
100
1700
Hours
Soman (GD)
3900
198
63
2-3
70
350
2min
VX
10.5
298
92
50
10
Hours
Information consolidated from text and tables in unclassified military and civilian sources
a
Volatility is the amount (mg) of agent in 1m
3
at 25
C.
b
Vapor Density is compared to air.
c
Ct
50
—the product of concentration [C] of the nerve agent over time t[t] o produce effects in 50% of those exposed to vapor or
aerosol.
d
LD
50
—Dose of liquid nerve gas placed on the skin that will cause death in one half of exposed subjects.
