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As the media continues
to portray images of American and British soldiers in gas
masks to protect themselves from potential chemical weapons
attack in the Iraq war, evidence continues to mount that miniscule
amounts of such chemicals can cause permanent brain damage
in susceptible people.
The evidence is
coming from Gulf war veterans who are suffering from debilitating
symptoms of Gulf war syndrome. According to repeated surveys,
Gulf war veterans are 30 percent more likely to be sick than
comparable groups who did not serve. Of the 696,000 troops
who fought in the war, the United States has paid disability
to more than 110,000.
In 2002, a medial
team in the United States identified three different syndromes
among U.S. Gulf war veterans. Syndrome 1 involves symptoms
such as sleep and memory disturbance, while people with syndrome
3 suffer from joint and muscle pain. Syndrome 2, the most
serious, involves symptoms such as confusion and dizziness.
Researchers used
magnetic resonance spectroscopy (MRS) to study veterans with
syndrome 2 and found that they had lost nerve cells in the
basal ganglia, structures involved in the brain functions
disturbed in those with the syndrome. Similarly, veterans
with other syndromes had also lost neurons in brain areas
that corresponded to their symptoms.
Researchers also
found that syndrome 2 veterans are eight times as likely as
healthy veterans to have been present when chemical weapons
alarms sounded in the Gulf. Additionally, syndrome 2 veterans
were about eight times more likely to have had an adverse
reaction to pyridostigmine, a drug given to soldiers, then
and now, to protect against nerve agents.
In troops who were
exposed to nerve agent and had adverse effects to the drug,
the risk of long-term side effects was five times higher than
the risk from each factor separately.
According to researchers,
both chemical weapons and the drug that protects against them,
affect the same physiological pathway. Nerve gas blocks an
enzyme that destroys acetylcholine, the neurotransmitter that
makes muscles contract, causing muscles to fatally spasm.
The drug works by blocking the enzyme temporarily to keep
nerve agents from binding to it permanently.
However, blocking
the enzyme at all may be too much for some people. In animal
studies, exposure to enzyme blockers at levels too low to
produce acute toxic effects can change brain activity and
influence the animals’ long-term behavior.
Additionally, low
doses of nerve agents affected regions in rats’ brains
used for memory and cognition--functions that are disturbed
in Gulf war veterans. The effects were more severe among stressed
animals, which may explain why soldiers who saw combat display
more severe symptoms.
Some soldiers may
also be more vulnerable to nerve agents because of low levels
of an enzyme. Researchers fond that syndrome 2 veterans have
very low levels of paraoxonase, an enzyme that is most effective
in destroying nerve agents.
A national survey
of Gulf veterans is being planned based on the three defined
syndromes and more powerful techniques to observe brain damage
are being developed. Researchers hope that the research will
lead to treatments for those already sick and prevent future
troops from getting sick. However, the progress will not come
in time to help the soldiers exposed to chemical weapons in
the conflict in Iraq.
New
Scientist March 26, 2003
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