Biomedical Engineering Reference
In-Depth Information
lack of immediate effects, the contaminated person
is often unaware of the exposure. Ocular and respi-
ratory routes of entry are also important, as is
parenteral absorption in casualties with conven-
tional wounds. Still, late decontamination may
prevent further damage, absorption, or spread of
the agent [22].
The lethal Ct
50
of sulfur mustard dispersed as a
vapor is 1500mgmin m
−
3
in an unprotected group
and 10,000mgmin m
−
3
in a group with respira-
tory protection. This demonstrates that sufficient
concentrations of vapor and sufficient exposure
times render mustard vapor lethal, even in masked
individuals. The LD
50
of liquid mustard on the skin
is 100mg/kg. Thus, administration of 7 g, about
a teaspoon, of liquid mustard to each member
of a group of individuals weighing 70 kg would
be expected to cause the death of half of those
exposed.
Table 6.10
Clinical effects from mustard exposure
Organ
Severity
Effects
Onset of
t effect
Eyes
Mild
Tearing
4-12 hours
Itching
Burning
Gritty sensation
Moderate Above effects plus
3-6 hours
Reddening
Lid edema
Moderate pain
Severe
Marked lid edema
1-2 hours
Possible corneal damage
Sever pain
Airways Mild
Rhinorrhea
6-24 hours
Sneezing
Epistaxis
Hoarseness
Hacking cough
Severe
Above effects plus
2-6 hours
Productive cough
Mild-to-severe dyspnea
Skin
Mild
Erythema
2-24 hours
6.4.4 Signs, Symptoms and Severity of
Exposure
Signs and symptoms may appear as early as 2 hours
after a high-dose exposure, whereas following a
low-dose vapor exposure, the latent or asymp-
tomatic period may extend to 48 hours. There are
several reports of individuals exposed to very large
amounts who died within hours; this type of occur-
rence is extremely rare. The typical onset time
is between four and eight hours. Topical effects
of mustard occur in the eye, airways, and skin
(Table 6.10). Systemically absorbed mustard may
produce effects in the bone marrow, GI tract, and
CNS. Direct injury to the GI tract may also occur
following ingestion of the compound. The concen-
tration (C) of the mustard vapor, time (t) of expo-
sure, ambient weather, and body site exposed are
factors in the onset time. Combined data from the
United States forces in World War I and Iranians
in the Iraq-Iran conflict suggest a high incidence
of eye, airway, and skin involvement (25% and
40% for each) [23]. However, there were higher
incidences of eye and lung damage in Iranian casu-
alties than in World War I casualties, probably
because of the larger amount of evaporation of the
agent in the hot climate.
Severe
Vesication
6.4.4.1 Eyes
The eyes are the organs most sensitive to mustard
vapor injury. The latent period is shorter for eye
injury than for skin injury. After low-dose vapor
exposure reddening of the eyes may be the only
effect. As the dose increases, the spectrum of injury
includes progressively more severe conjunctivitis,
photophobia, blepharospasm, pain, and corneal
damage. Miosis noted after mustard exposure in
both humans and experimental animals is probably
from the cholinomimetic activity of mustard [24].
Blisters do not normally form in the eyes.
Instead, swelling and loosening of corneal
epithelial cells lead to corneal edema and clouding
with leukocytes with decreased visual acuity.
Corneal vascularization with secondary edema may
last for weeks. Scarring between the iris and lens
may follow severe effects; this scarring may restrict
pupillary movements and may predispose victims
to glaucoma. The most severe damage is caused
by liquid mustard from airborne droplets or by
self-contamination. After extensive eye exposure,
