Memorandum submitted by Professor Malcolm
Hooper, Scientific Advisor to the Gulf Veterans' Association
THERE WERE NO DETECTION DEVICES AVAILABLE
FOR THE RAPID DETECTION OF ANY BIOLOGICAL WEAPONS
It is therefore impossible to know that BWS'
exposures, if any, occurred during the Gulf War. There were many
reports of dead animals in the desert and one where anthrax was
identified (Thomas 1998).
Small light aircraft equipped with biological
spraying facilities were found after the war. These had originally
been supplied by Italy but it is not known if or how they had
been used. There have been suggestions that Iraq laid "biological
minefields" but there is no evidence to form a judgment on
such claims.
CONCLUSIONS
Iraq was well equipped with a variety of biological
weapons which defied detection by battlefield equipment.
It is impossible to be certain that biological
weapons were not used.
Any exposure with long-term consequences, eg
to aflatoxin a potent liver carcinogen will take time to
emerge.
It is ironic that the vaccines used to protect
against some of these biological weapons may themselves have caused
the greater injury.
OIL, SMOKE, FUELS, SOLVENTS
THE MAJOR
HAZARDS
(1) Oil from the Oil Wells. When the oil
wells were fired oil was released under pressure and crude oil
as well as smoke from the fires provided extensive pollution over
much of the area;
In total 730 wells were detonated of which 656
ignited and burned till extinguished. The remaining 74 gushed
oil forming burning lakes of crude oil. The first 94 wells were
destroyed by Coalition bombing as well as Iraqi detonation.
Some troops were drenched in oil for several
days, others drove through the area without protection against
inhaling the fine droplets or exposing their skin to oil mist.
Oil was released into the sea and contaminated
the beaches, the water supply from desalination plants, and destroyed
much wild life (Stead 1999).
(2) Smoke from the Oil Fires. This formed
a massive pall over the whole region the products of partial combustion
of the oil, often in very small particles, that could be inhaled
and enter deep into the lungs, remained suspended in the air of
Kuwait city for some two years (Anon 1994). Deposits from the
smoke were found in South America and the Himalayas;
(3) Chemical Solvents were present in the
CARC (Chemical Agent Resistant Coat) paints used to paint vehicles
without any protective clothing or masks. The solvents are potent
ozone depleting chemicals; and
(4) Leaded Fuels were used in many of the
heavy vehicles.
WHAT ARE
THE EFFECTS
OF THESE
EXPOSURES
Petroleum exposure is associated with:
Inhalation of fine oil droplets gives rise to
lipoidal pneumonias which lead to haemorrhage, necrosis and fibrosis.
Evidence of such lipoidal damage was found in sheep from the region
when they were slaughtered.
Crude oil painted on to mice resulted in 38
per cent developing cancers.
Smoke particulates are known carcinogens (Stead
1999).
Particulate levels up to nine times those causing
significant harm were found by the WHO and other investigators
(Stead, 1999).
WHAT LEVELS
OF EXPOSURE
OCCURRED
A telephone study of 10,051 ill GWVs found that
of those reporting breathing or enveloped in oilfire smoke, 96
per cent were within clear visual area of the oil fires, 90 per
cent worked or lived in, or made travel through the burning oilfields,
72 per cent; washed in water with an oily sheen, 68 per cent;
having an oily taste to their food, 66 per cent; oily taste to
drinking water, 65 per cent.
Some 85 per cent of the USA units displayed
exposure to oil well fires. The number of exposure days varied
from one to 260!
BAD SCIENCE
AND COVER
UP EXPOSED
In the course of his report, Stead 1999, identified
two studies which were put forward by the DOD and VA in support
of their conclusions that the oil well fires and smoke posed no
increased health risks to the troops. Both were very seriously
flawed.
The Friedman study on firefighters provided
no scientific data to support this conclusion. Nothing has been
published or presented for peer group assessment.
An Army monitoring study collected data outside
the period February to April when the stagnant air conditions
of those months did not exist.
CONCLUSIONS
(1) It is clear that the oil and smoke from
oil well fires provided a major health risk to the Coalition forces;
(2) This risk has not been recognised or
assessed with reference to the UK troops;
(3) Some bad science has been put forward
to suggest that there was no increased health risk to the troops;
(4) The list of damage to health by these
hazards has much in common with the adverse health effects from
other exposures; and
(5) Any examination of UK personnel must
include a full history of their movements with respect to the
oil-smoke hazard and consider the specific health threat from
these exposures.
SUMMARY OF THE BIOLOGICAL EFFECTS OF THE
DIFFERENT CHEMICAL AND BIOLOGICAL EXPOSURES
Table 4, overleaf tabulates the extensive multi-symptom,
multi-organ, multi-system effects of the chemical and biological
exposures suffered by the GWVs.
X—indicates a known adverse effect associated
with the exposure.
Table 4
KNOWN EFFECTS OF THE GULF EXPOSURES ON THE
DIFFERENT SYSTEMS OF THE BODY
|
| System | Vaccines
| PB | OPs/CBs
| Pyreth | Lind
| NA | Mus
| DU | O/S
|
|
| CNS | X |
X | X
| X | X
| X | X
| X | X
|
| PNS | X |
X | X
| X | | X
| X | |
|
| ANS | | X
| X | X
| | X | X
| | |
| CV | | X
| X | | X
| X | |
| |
| Blood | X |
X | X
| | X | X
| X | X
| X |
| Immune | X |
X | X
| | | |
| X | X
|
| GI | X | X
| X | |
| X | X
| | X |
| Mus/Skel | X
| X | X
| X | | X
| | X | X
|
| Respirat | X
| X | X
| | | X
| X | X
| X |
| Skin | X |
X | X
| X | | X
| X | X
| X |
| Renal | X |
X | X
| | X |
| | X |
|
| Liver | | |
X | | X
| | | X
| |
| Endocrine | X
| X | X
| | X | X
| | X |
|
| Genes | X |
| X |
| | | X
| X | X
|
|
CNS = Central Nervous System; PNS = Peripheral Nervous System; ANS = Autonomic Nervous System; CV = Cardio Vascular System; GI = GastroIntestinal System.
PB = Pyridostigmine Bromide; OPs = OrganoPhosphates; CBs = Carbamates; Pyreth = Pyrethroids; Lind = Lindane; NA = Nerve Agents; Mus = Mustard agents; DU = Depleted Uranium; O/S = Oil and Smoke.
|
NATURAL HAZARDS
(1) Sand—in many parts of the desert the
sand is extremely fine and was able to penetrate the weave of
the NBC suits. Anything absorbed on the sand would also be carried
into the suit and be kept in close contact with the wearer;
Sand of this nature could contribute to respiratory illness
and skin disorders particularly if it had absorbed on it micro-organisms
or toxins. El Askan disease and Muco-cutaneous Intestinal Rheumatoid
Desert Syndrome, (MIRDS)-Murray-Leisure, 1997, attempt to emphasise
this possibility. The association of GWS/I with sand is out of
favour at present.
(2) Diseases of the Region—the major concerns
were about leishmaniasis, malaria and West Nile Fever. Leishmaniasis
is carried by sandflies and some 30 cases occurred among the American
forces (Burton, 1997). Malaria and West Nile Fever are carried
by mosquitoes. Some troops were taking anti-malaria tablets but
to my knowledge no cases of either disease have been reported;
(3) Other Problems—rats and fleas and lice
were all part of the battlefield environment and had the potential
for causing disease. However, no such diseases have emerged in
those suffering GWS/I;
Some troops tell of very poor sanitary conditions which could
facilitate the spread of infectious diseases associated with enteroviruses,
cholera etc. No large outbreaks of these diseases occurred.
CONCLUSIONS
The natural hazards of the region do not appear to have contributed
significantly to GWS/I.
POST TRAUMATIC STRESS DISORDER, PTSD
This psychiatric diagnosis has caused much anger and distress
in GWVs on both sides of the Atlantic. There are some psychiatrists,
Wessley 1999, who have formed an opinion that somatisation offers
an explanation of a range of overlapping syndromes including GWS/I,
CFS-ME, fibromyalgia, MCS, PMT, and related disorders.
Dr Alun Jones who has made a life-time study of PTSD has
repeatedly said that the GWVs are not in the main suffering from
PTSD although this may contribute to the over all pattern of their
illnesses. Haley, 1997, 1997a,b, came to a similar conclusion.
The history of disease is full of psychiatric explanations
of diseases such as, diabetes, regarded as "the last strand
of neurosis caused by . . . sexual repression", Daniel, 1936;
and, Parkinsonism, where "a conflict resulting from the wish
to masturbate", was claimed to induce the characteristic
tremors of this disease, Booth, 1948. Similar claims about a variety
of other illnesses that have been made by respected clinicians
in peer-reviewed journals.
The diagnosis of PTSD and hysteria, Showalter, 1997, should
be regarded as a "last ditch" attempt to find some explanation
of chronic illnesses which require openness to new paradigms that
have a clear basis in objective medical and scientific investigations.
Furthermore the recognition that, "inhibitors of . .
. acetylcholinesterases may induce psychopathologies that are
reminiscent of PTSD", Kaufer, 1998, and the conclusion that
PB challenge causes increased cholinergic responsivity in patients
with panic disorder, Cooney, 1997, are both in accordance with
the massive cholinergic insults suffered by the GWVs.
CONCLUSIONS
There are sound grounds for rejecting the diagnosis of PTSD
in most GWVs who suffered a massive assault on the cholinergic
system.
DIAGNOSIS AND TREATMENT
Many authors have drawn comparisons between Chronic Fatigue
Syndrome—Myalgic Encephalomyelitis, CFS-ME, (Nicolson, 1997,
has made the most comprehensive identification) and related, overlapping,
syndromes, eg fibromyalgia syndrome, FM, multiple chemical sensitivity
syndrome, MCS. From this difficult and controversial area a number
of useful diagnostic and treatment possibilties are beginning
to emerge. Because of the extensive disturbances of mood and behaviour
others have seen some affinity with work carried out in autism.
Some GWVs have had batteries of tests done which have been
found helpful in insecticide poisoned farmers and others.
1. INFECTION BY
MYCOPLASMA
Nicholson, 1997, 1998, 1999, has identifed Mycoplasma
fermentens incognitus by gene-tracking techniques in 45 per
cent of a cohort of GWVS examined. This work has been replicated
and validated. The DOD has now initiated a study involving 1,000
GWVs following the diagnostic and treatment procedures proposed
by Nicholson.
Other workers have identified persistent and common infection
by other organisms, particularly Rickettsiae, in CFS-ME (Jadin,
1999).
TREATMENT
This involves repeat cycles of treatment with antibiotics
together with supporting therapies to support gut function and
control candida overgrowth, Nicholson 1999.
2. AUTISM, CFS-ME, AND
THE GASTROINTESTINAL
TRACT
The following offer new unconsidered possibilities.
Indolylacroyglycine, IAG
Shattock and co-workers, 1991, 1997, unpublished data, have
for some time been using a urinary marker molecule, indol-3-ylacroylglycine,
IAG, in the diagnosis of autism spectrum disorders. Some 80 per
cent of autistic children and adults have elevated levels of IAG
in their urine. Surprisingly, the same marker molecule is also
present at high levels in organophosphate damaged farmers, Gulf
War Veterans 34 out of 35 examined, some vaccine damaged babies,
and some CFS/ME patients.
There are other, larger, urinary peptides associated with
IAG in the urine which are also indicative of autism and related
disorders, these are being studied but remain to be fully characterised.
Autism is also associated with extensive malfunctions in
digestion, absorption and permeability in the gut. The opioid
hypothesis, convincingly relates these gastro-intestinal changes
to neuroendocrineimmune changes which offer a new understanding
of autism—see also the PB section.
The permeability of the blood-brain barrier also increases
with biological and psycholgical stress and would allow access
of these opioid compounds to the brain. Dietary changes to reduce
the opioid precursors in food, especially gluten and casein, have
proved successful in alleviating the major symptoms of autism.
Naltrexone is currently being used, in very low doses, to
treat autism. One immune-based name for CFS/ME is "naloxone-reversible
monocyte dysfunction syndrome".
The loss of pancreatic function associated with some gastro-intestinal
disorders would result in big reductions in cholecystokinin production.
Cholecystokinin is a major neuroactive peptide with extensive
CNS activity.
The current use of secretin to treat autism indicates that
pancreatic secretions may well have a big role in the normal functioning
of the gut and CNS.
Serum cysteine/sulphate ratios
Rosemary Waring, 1993, has identified very low cysteine/sulphate
ratios in autistic children, which are also found in organophosphate
poisoning, CFS/ME, and Gulf Veterans. The integrity of many membranes,
including the mucosa of the gut, is preserved by extensive sulphation
of the mucopolysaccharides in these membranes. Low sulphate levels
could reflect a loss of integrity of these membranes which would
be consistent with major changes in gut structure, and function.
Sulphation is also important in the actions of some hormones eg
dehydroepiandrosterone, cholecystokinin, gastrin. Low molecular
weight sulphated heparins have been used to treat CFS/ME.
Gut Colonoscopy
Wakefield et al, 1998, have found extensive lymphoid
hyperplasia in vaccine damaged babies with autistic developmental
changes.
Testing and Treatment
This work suggests a battery of tests for diagnosis and possible
ways of treatment.
(a) Gut permeability and uptake studies;
(b) Colonoscopy looking lymphoid hyperplasia, Wakefield
1998;
(c) Dietary changes as a method of treatment;
(d) Possible use of low dose naloxone;
(e) Possible use of secretin;
(f) Magnesium sulphate baths.
One UK GWV has found a gluten free diet very helpful in enabling
him to function at a more normal level, when he came off the diet
his symptoms reappeared, Shattock, unpublished data.
2. IMMUNOLOGICAL STUDIES
These are suggested by the Rook Zumla paper and the case
considerably strengthened by the work of Nancy Klimas, 1999 and
others in the field of CFS-ME. Studies should be carried out on
sick veterans as proposed earlier.
Meryl Nass, 1999, has suggested using a battery of tests
to screen for autoimmune antibodies which are associated with
vaccine induced damage.
Urnovitz, 1992, 1998, and LeBleu, 1999, and Suhadolnik, 1999
have investigated unusual RNA molecules in chronic diseases and
found unusual features in GWVs and CFS-ME patients.
Treatment
Klimas, 1999, offers novel and effective treatment procedures
which reverse the Th2 shift found in many CFS-ME patients involving
ex vivo challenge of the host cells and their reintroduction
by an autologous infusion. A preliminary study has demonstrated
the efficacy of this procedure.
Ampligen and isoprinosine have both been used effectively
in the treatment of CFS-ME but not tried with GWVs. They act by
modulating the immune system.
Vaccines which shift the immune system towards an improved
Th1 status may be helpful eg BCG,M Vaccae.
Endocrine changes
Richardson, 1997, has shown a correlation between the buspirone-prolactin
test and reduced cerebral blood flow measured by SPECT scans in
CFS-ME patients but this procedure has not been used to investigate
GWVs.
Treatment of insecticide poisoning
Richardson, 1999, has found choline citrate and ascorbic
acid effective in lowering the levels of organochlorine insecticides
probably by facilitating their release from lipid stores.
Detoxification procedures
Rea, internet download, has developed a number of procedures
which he uses following a thorough and detailed individual clinical
assessment. These include desensitisation techniques, toxin removal,
a regime of toxin free food and environment, depuration with saunas,
baths with sulphate and hydrogen peroxide etc.
One GWV went out to California in a wheelchair and returned
walking. He is now at university as far as we know.
In this country, Dr Jean Monro has developed similar treatments.
She has successfully treated a number of OP poisoned patients
and some GWVs. One GWV improved dramatically and quickly.
Studies with established drug regimens
Baumzweiger, 1999, regards GWS/I as an inflammatory condition
primarily affecting the brainstem. He has successfully treated
some 200 GWVs with calcium blocking drugs, human immunoglobulins
and anti-inflammatory agents.
We need to hear and learn from anyone who has established
any successful treatment of any GWVs.
CONCLUSIONS
(1) Preliminary studies in CFS-ME and autism have indicated
novel ways for the diagnosis and treatment of GWVs. These should
be further investigated as a matter of urgency.
(2) New methods of diagnosis and treatment are suggested
from the investigation of syndromes which overlap with GWS/I.
These should be investigated.
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