As noted earlier in this chapter, pesticides DOD shipped for use during the
Gulf War fell into five major categories: OP pesticides, methyl carbamate
pesticides, organochlorine pesticides (lindane), pyrethroid pesticides (chiefly
permethrin), and DEET.
Several OP pesticides were used during the Gulf War, including chlorpyrifos,
diazinon, dichlorvos, and malathion. When administered in high doses, OP
pesticides cause irreversible inhibition of acetylcholinesterase, an enzyme
crucial to normal nerve and nerve/muscle function. Inhibiting
acetylcholinesterase leads to unique and highly characteristic poisoning
symptoms. Immediate symptoms of OP poisoning in humans usually develop within
four hours of exposure and include narrowing of the pupil of the eye (miosis),
headache, nausea, dizziness, anxiety, and restlessness. Severe and rapid onset
poisoning symptoms include muscle twitching, weakness, tremor, incoordination,
vomiting, abdominal cramps, diarrhea, sweating, salivation, tearing, runny
nose, and production of phlegm. Life-threatening symptoms include
unconsciousness, incontinence, convulsions, and depression of breathing
function. According to DOD, its medical monitoring and surveillance efforts
reported no cases of immediate and severe OP poisoning symptoms in U.S.
military personnel during the Gulf War.
Some individuals who recover from immediate and severe OP poisoning show
long-term (lasting more than a year), subtle, neuropsychological abnormalities
that can be detected using a battery of standardized neuropsychological tests.
In an epidemiologic study of such long-term effects, severely poisoned
individuals showed clear but subtle differences in intellectual functioning,
academic skills, abstraction and flexibility of thinking, and simple motor
skills. For example, about a five point difference in IQ was measured in
severely poisoned versus control subjects.
Neurophysiologic effects were less apparent; abnormalities were found only in
measurements of memory, abstraction, and mood and on one test of motor
reflexes.221 These effects could not be detected, however, in a subset of the
same worker population that had been exposed to doses of OP pesticides that
were too low to cause the symptoms of immediate and severe poisoning.241 Other
studies of low-level occupational exposures reinforce
the finding that these types of long-term effects present solely in the
aftermath of severe and immediate OP agent poisoning.4,241
Some OP pesticides that are no longer sold in the United States have been
associated with human cases of a second type of delayed toxic effect called
organophosphate-induced delayed neurotoxicity (OPIDN, sometimes referred to as
delayed neuropathy). Initial symptoms are muscular incoordination progressing
to numbness, tingling, fatigue or a cramp-like pain in the calf muscles, and
even moderate to severe muscular weakness and paralysis.7,117 Typically,
effects occur 7 to 14 days following recovery from immediate and severe
poisoning by the OP pesticide and involve neuropathologic lesions and
degeneration of the nerve axon and myelin nerve sheath in both the central and
peripheral nervous systems;117 these effects are easy to measure in a clinical
setting. In general, OPIDN caused by OP pesticide poisoning is associated with
immediate poisoning symptoms.
All OP pesticides sold in the United States today are routinely screened for
OPIDN toxicity with a standardized hen assay used by EPA; the hen is a
laboratory animal especially sensitive to OPIDN effects. For some OP agents,
these effects only can be observed by giving the hen extremely high doses that
would rapidly lead to death, but then keeping the hen alive through the use of
protective drugs such as atropine. Many investigators conclude any OP agent
theoretically could cause this effect at sufficiently high doses, but
that, in fact, immediate toxic effects cause death before delayed effects can
be seen.117 None of the pesticides DOD shipped to the Gulf War test positive
for OPIDN in standard EPA screens.
Methyl carbamate insecticides shipped for use
during the Gulf War included propxur (Baygon®), carbaryl (Sevin®), and
methomyl (Lannate®). These insecticides reversibly inhibit
acetylcholinesterase, which leads to poisoning effects similar to OP
poisoning. Poisoning with methyl carbamates tends to be of much shorter
duration-with a greater margin of safety between symptom-producing and lethal
doses-compared to OP pesticides, which bind permanently with
DOD shipped the pyrethroid insecticide permethrin to
the Gulf for use as an insect repellent. Permethrin is used widely in the
United States as the active ingredient in personal care products, such as
shampoos and lotions, and for treating clothes to make them insect repellent.
There are few reported poisonings of humans by permethrin, most likely because
such a large dose is required to cause poisoning. Humans rapidly detoxify and
excrete permethrin. Clinical signs of immediate permethrin poisoning following
large oral doses become evident within two hours and include incoordination,
ataxia, hyperactivity, and convulsions, followed by prostration, paralysis, and
death.171 Unlike OP pesticides, the Committee found no reports of long-term
effects from permethrin poisoning in
A National Research Council (NRC) subcommittee that reviewed possible health
problems for military personnel wearing permethrin-treated military clothing
concluded it is unlikely that soldiers using such uniforms would experience
adverse health effects at the suggested exposure levels. The subcommittee
concluded, "the weight of evidence shows that permethrin is unlikely to be a
skin irritant or skin sensitizer for military personnel who are exposed to it
dermally from wearing permethrin impregnated [uniforms]." The estimated "no
observable adverse effect level" for immediate neurotoxic effects in humans
from daily exposure is 200 milligram (mg)/kilogram, which is approximately
three million times greater than estimated dermal exposure from permethrin
treated uniforms.171 NRC's worst-case estimate of lifetime
carcinogenicity risk for humans wearing permethrin treated uniforms was less
than 2 in 1,000,000.
In laboratory animal studies, dermal absorption of permethrin is low,
although scientists observe neurotoxic effects if the substance is
injected.171,301 Most, but not all, studies have reported permethrin does not
cause damage to genetic material in a wide variety of standard measurement
systems. Permethrin is neurotoxic to laboratory animals at high oral doses.
Rats fed permethrin at 6,000 mg/kg for 14 days showed fragmented and swollen
sciatic nerve axons and myelin degeneration. However, nerve conduction studies
in 23 permethrin workers showed no evidence of nerve
impairment associated with permethrin exposure.171 Rodent bioassays of chronic
exposure to permethrin showed carcinogenic effects, such as liver and lung
adenomas and lung carcinomas in mice, but data on human carcinogenicity of
permethrin are lacking.
DOD shipped one organochlorine pesticide,
lindane, to the Gulf region. Lindane, once widely used as an agricultural
insecticide in the United States, is still available as a lotion to treat head
and body lice and scabies.283,301 Lindane is dermally absorbed, stored in body
fat, and only slowly leaves the body. Reports document that a few people who
have used large amounts of lindane on their skin have had blood disorders and
even seizures. Under conditions of extremely high exposure, lindane can cause
liver and kidney disease.
Some pregnant laboratory animals orally treated with the maximum tolerated dose
(the dose just below that causing immediate and severe toxicity) showeda
statistical increase in the number of fetuses with extra limbs, indicating that
lindane is a teratogen for this laboratory animal strain. Lindane has not been
shown to be a human carcinogen, although long-term oral exposure of
lindane to certain species and strains of laboratory rodents has been
reported to cause liver cancer.283 Hence, DHHS has determined that lindane
should be viewed as a human carcinogen.
DEET, first introduced in 1955, continues to be a widely used liquid
insect repellent in the United States, and DOD shipped approximately two 2-oz
tubes per U.S. service member during the Gulf War. According to EPA, 50 to 100
million Americans use DEET-containing insect repellents annually. Relative to
most pesticides, DEET has notably low immediate toxicity.190,301 Although
generally well tolerated when used as an insect repellent applied to human
skin, about five to nine percent is absorbed through skin, and
reports exist of tingling, mild irritation, and occasional skin peeling
following repeated application.301 Topically applied DEET is rapidly
eliminated, mostly in the urine. In the past 35 years a few reports in the
medical literature suggest rare neurotoxic effects.190 In adult humans,
ingestion of enormous doses of DEET has been associated with immediate toxic
effects, including tremors, generalized seizures, and coma, although no
long-term effects of poisoning have been reported.320 (For possible synergistic
effects, see section on PB later in this chapter.)
Rats continuously fed DEET up to the maximum tolerated dose over three
generations showed a slight increase in the high-dose animals in a single
neurological abnormality-a slight increase in exploratory locomotor
activity-and no histopathologic central nervous and peripheral nervous system
changes of significance.190 Other reports indicate that rats fed the maximum
tolerated dose of DEET can show severe and often fatal prostration accompanied
by a brain myelinopathy.320
What do we conclude about the risks of pesticides to Gulf War
According to DOD, after-action reports from in-theater medical personnel did
not reveal any U.S. troops reporting symptoms that would indicate pesticide
poisoning. Evidence from studies of humans poisoned by OP pesticides suggests
that low-level exposures that do not cause signs and symptoms of immediate and
severe poisoning will not result in long-term health effects.
Thus, the Committee concludes it is unlikely that health effects and
symptoms reported today by Gulf War veterans are the result of exposure to
pesticides during the Gulf War. Lindane is an animal liver carcinogen, but it
is too early to see an elevated liver cancer rate in Gulf War veterans.
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