INSECTICIDES USED

  The following chemical categories were used in the Gulf War.

(1)  Organophosphates, OPs, eg malathion, fenitrothion, azamethiphos, chlorpyrifos, diazonon, and Carbamates, CBs (eg aldicarb, carbaryl, bendiocarb, propoxur);

(2)  Pyrethroids eg permethrin. Usually formulated as sprays;

(3)  Organochlorine insecticides, eg lindane.

  These were formulated in a number of ways, as powders/dusts for delousing prisoners, as wettable powders and aerosols for spraying. The added components of the formulations may also have unquantifiable toxic effects since some, eg piperonyl butoxide, are incoroporated to increase, synergistically, the insecticidal properties of the major component. Some were also incorporated in flea collars and used to impregnate clothing, bedding, and tentage. There are reports of some personnel spraying inside their NBC suits.

INSECT REPELLENT

  DEET a well-known and widely used insect repellant was supplied in large quantities. Chemically it is N,N-Diethyl-3-methylbenzamide and represents a further chemical category of compounds. It may be sprayed or rubbed directly on to the skin, or clothing, and was supplied as a lotion or stick for personal use.

  Fungicides and Rodenticides were also widely used adding to the over all load of toxic chemicals associated with the troops. These included pentachlorophenol, potent anticoagulants, and phosphorus.

HOW DO THEY ACT?

(1)  OPs and CBs are bind to the same target enzyme, AchE, as PB and the nerve agents. They act, like the latter, as potent irreversible inhibitors, Figure 7. They also affect many other enzymes even at very low doses. There are obvious similarities between the chemical exposures of the GWVs and OP poisoned farmers and other workers involved with these agents.

  Needle fat biopsies of one GWV has shown a surprisingly high level of two OP insecticides. This requires further study to rule out any confounding exposures after the Gulf War.

  Of particular note, is their action on Neuropathy Target Esterase, NTE, which plays an important role in the development of chronic neurological damage. Such damage is now recognised and has been extensively investigated, and reported on, in a number of major reports, most recently by the Institute of Medicine and the COTS. Haley et al, 1997b, following a blinded clinical study, concluded that there was "generalised injury to the central, peripheral, and autonomic nervous systems".

  Another important enzyme is paraoxonase which has a major role in protecting against damage to the cardiovascular system. Mackness et al, 1999, 1998, 1997. A recent paper describes significant long-term damage to this enzyme which may be associated with a particular sub-group of GWVs who have a particular genotype for one form of this enzyme, Haley et al, 1999. Such an observation provides evidence of long term changes in a crucial enzyme system which is associated with protection against cardiac disease, arterial disease and strokes.

  The Gulf Veterans' Association has commissioned research in this area which is almost ready for publication. It adds considerably to the preliminary observations of Haley and co-workers. The recently presented study by Haley and Fleckenstein, 1999, on magnetic resonance spectroscopy of the brain is consistent with the possible consequences of reduced paraoxonase function. Reduced blood flow to certain parts of the brain would result from paraoxonase-associated arterial occlusion.

  However, any serine esterase, eg butyryl cholinesterase, or protease could potentially be inhibited by OPs and CBs. These classes of enzymes play important roles in the detoxification of foreign compounds, blood coagulation, the immune response, control of some neuropeptides, digestion in the gut etc. Many of these effects remain to be properly evaluated and no mention was made of these possibilities in the COTS report, 1999.

  It is also of great significance that some OP insecticides "induce psychopathologies which are reminiscent of PTSD", (Kaufer et al, 1998; Rosenstock et al, 1991; Wickelgr, 1998)

(2)  Haley et al, 1997a showed that there was an association with DEET usage and his Syndrome 3, arthro-myo-neuropathy (joints-muscle-and nerve damage). The reported synergy between DEET, OPs and pyrethroids and PB resulted in an order of magnitude enhancement of the toxic effect from these compounds (Abou-Donia et al, 1996; McCain 1997);

(3)  Pyrethroids (permethrin) and related compounds act by blocking nerve conduction by disrupting sodium channels in nerves. They are generally regarded as less toxic to humans than organophosphates since they are more rapidly broken down by enzymes in the blood. However these enzymes are powerfully inhibited by OPs and nerve agents, such as sarin, soman, tabun, and VX. The result is a significant and synergistic increase in the neurotoxicity of these compounds;

(4)  An independent laboratory has found high serum levels of lindane and pentachlorophenol in some Gulf Veterans. OCs have biological half-lives of the order of 50 years and are now widely dispersed in our environment. Lindane continues to be used in storing carrots and other vegetables. We all, therefore, have several organochlorine pesticides in our sera but the levels of these compounds in the GWVs often place them in the top 5-10 per cent of the population investigated.

  Lindane is known to be a nerve poison causing convulsions and also affecting the lungs (pulmonary oedema, heart (increased myocardial sensitivity), blood dyscrasias, kidney and liver damage. Goth 1988.

THE CONTROL OF INSECTICIDE USAGE

  The assertion has been made (Lee, 1999a) that the UK forces use of insecticides was carried out in accordance with Health and Safety regulations by trained operatives and that no excessive exposure to insecticides, therefore, occurred during the Gulf conflict.

  Nothing could be further from the truth. There is written testimony, with photographs, from a trained leader of a Hygiene Team that many containers were leaking, that no protective clothing was provided despite repeatedly drawing the attention of Senior Officers to this lack. Local supplies of insecticides were buried because of their aggressive side-effects. All this from a Senior NCO who was commended for his skill, judgement and efficiency by his Commanding Officer (Worthington/Reece-Russell 1991).

  The OPPIT report carries testimony of the use of unapproved malathion dust to delouse prisoners which lead to excessive exposure of operatives over a long period inside closed tents (Studham, 1996).

  From other troops it is clear that spraying took place as many as four times daily, that troops slept in insecticide impregnated tents which were tightly sealed and heated. Bedding was routinely sprayed whilst troops were out of their tents. This meant for many that the spray was applied to the inside of their bedding! Some troops also found themselves in accommodation that was actively being fumigated during the time they slept there. Some personnel are reported to have sprayed the inside of their NBC suits! (Thomas, 1998).

MOD DENIALS

  The habitual climate of denial, deception and disregard for the truth and the health of GWVs is well illustrated by initial vociferous denials by Mr Soames that no OPs were used in the Gulf War. This was followed by the gradual admission of a greater use of these insecticides under conditions where no protective clothing was available and excessive exposure of operatives and troops occurred. Professor Lee's comments are in line with the traditional attitudes of the MOD.

CONCLUSIONS

  It is undeniable that excessive exposure to many insecticides occurred during the Gulf conflict and that such exposures can give rise to profound neurological damage. The primary evidence of the troops themselves is much more reliable than that offered by Parliament, MOD, and MAP which has been shown to be corrupt.

CHEMICAL WEAPONS USED

(1)  Nerve Agents—these include, soman, sarin, tabun, VX. The use of PB was driven by the fear that Russia might have supplied Iraq with soman which some troops knew as Russian nerve agent, Thomas, 1998;

(2)  Mustard gases/agents—these are commonly regarded as blister agents which will irritate the skin and eyes. They were used in the first World War, WW1. They are organic alkylating agents whose biological and chemical properties are extensive; there is no known antidote!—see below;

(3)  Lewisite is another WW1 blister agent with extensive chemical and biological properties. It is an organo-arsenical compound;

(4)  Hydrogen cyanide, phosgene and its derivatives are blood agents many of them were first used in WW1.

HOW DO THEY ACT

(1)  Nerve agents, bind to the key enzyme AchE, like PB, OPs and CBs. They are potent irreversible inhibitors of this enzyme, Figure 7. Chemically they are organophosphonates, closely related to, but not identical with, organophosphates. They have been designed to have very high toxicity in humans and to be inhaled or absorbed through the skin and mucous membranes.

Together with the OP insecticides and PB they constitute the Cholinergic Triple Whammy. When the interactions and synergisms between these compounds and others, particularly DEET, are considered the assault on the cholinergic system is overwhelming.

The following catalogue of effects has been listed, headaches, miosis, rhinorrhea (runny nose), sweating, eye pain, excessive lacrimation, tightness of the chest, bronchospasm, all gradually increasing severity followed by severe weakness, involuntary micturation and defaecation, paralysis, convulsions, and finally respiratory failure and death. These are all central and peripheral cholinergic effects, both muscarinic and nicotinic (Maynard, 1992).

They will also inhibit irreversibly many serine esterases and proteases which have key roles in many essential biological processes affecting the lungs, blood, immune system, endocrine system. They penetrate the central nervous system and cause extensive central effects.

(2)  Mustard agents (H, HN1, HN2, HN3) are commonly described as blister agents or vesicants. Chemically they are aggressive alkylating agents containing chloroethyl groups attached to either sulphur or nitrogen. They produce excessive irritation to the skin and the eyes which is rapidly disabling. The mechanisms underlying this are still unclear. Although the short term effects are of battlefield importance the long term effects of their well established mutagenic and carcinogenic actions are of great significance to those who survive. There are no known treatments for this group of compounds.

(3)  Lewisite is also a vesicant with a long history. It acts principally by binding to lipoic acid a co-enzyme associated with several enzyme systems but particularly with mitochondrial energy production. Lewisite has a greater systemic toxicity than the mustard agents.

(4)  Hydrogen cyanide is the well known poison which affects oxygen metabolism and is rapidly fatal although sub-lethal doses are disabling. It is a gas which is lighter than air so in battlefield conditions is usually rapidly dispersed.

(5)  Phosgene and phosgene oxime cause extensive pulmonary oedema which is fatal. These agents generate hydrochloric acid on contact with water but this may only explain part of their activity.

ANTIDOTES AND TREATMENT

(1)  Nerve agents. PB was used as a prophylactic to provide protection against soman which rapidly "ages" AchE- see introduction and section above on PB. In addition the UK troops were provided with "combopens" which contained 2-pyridine aldoxime methanesulphonate, P2S, atropine, and avizafone.

The aldoximes are a group of compounds specifically designed to displace irreversibly bound organophosphates and nerve agents from their binding site on AchE and rescue this enzyme. P2S is an old drug (patent 1957) which like PB is a quaternary salt. It is therefore very unlikely to penetrate the CNS.

The MOD insists that PB, also a quaternary salt, does not penetrate the CNS which leaves the CNS unprotected by this prophylactic agent. P2S, similarly, will not penetrate the CNS making it impossible to rescue the inhibited AchE in the CNS. All nerve agents are known to enter the CNS. Death will follow when the central cholinergic mechanisms are overwhelmed. I do not believe that this strategy offers any real protection against nerve agent poisoning. It is fatally flawed.

Furthermore, the side-effects of P2S include headaches, disturbances of vision and muscular weakness. Distinguishing these from cholinergic poisoning is very difficult (Maynard 1992).

Atropine is the classic anti-muscarinic agent which would counteract the extensive muscarinic effects arising from inhibition of AchE. It does penetrate the CNS and would provide protection there but only at muscarinic sites.

Avizafone is a pro-drug of diazepam which requires enzymic activation. The most important enzymes for this are probably trypsin-like enzymes with a serine active-site. Such enzymes would almost certainly be inhibited by nerve agents. This casts serious doubt about the protective properties of this drug under battlefield conditions. Diazepam is a potent and proven anti-convulsant.

Mustard agents—there are no specific treatments for such exposures. The crucial long term genotoxic effects are well known but difficult to evaluate and cannot be protected against. Dr Christine Gosden believes that these agents are, in large part, responsible for the increased cancers and birth defects found among the Kurds of Northern Iraq (Gosden 1999).

Lewisite has a specific anti-dote, British Anti-Lewisite, BAL, dimercaprol, developed after WW1. I have no information about BAL being supplied to the Gulf but there is some evidence of it being detected.

Hydrogen cyanide has a specific antidote but administering it on the battlefield would be very difficult.

Phosgene and derivatives have no specific antidote and treatment on the battlefield is not a realistic option—oxygen therapy and rest are important.

EXPOSURES, DENIALS AND DETECTIONS

  The Pentagon, DOD, and VA in the States and the MoD in the UK have continuously denied and rejected any suggestions that there was any exposure to CWs by any Coalition troops. Many alarms were switched off on instructions from Senior Officers and some were disabled by removing their batteries.

  All accounts of such exposures have been attacked and a variety of explanations offered for the triggering of chemical alarms during the Gulf War. One favoured by the MoD is that of a plane flying over the area with a leaking fuel tank!

  The latest describes a massive failure in training, use, supply, and provision of the equipment. It clearly shows that there was no effective detection facilities available to the UK troops in the Gulf. In parts the descriptions are "Pythonesque", see para 59 and 60. (MoD web site accessible at http://www.mod.uk/policy/gulfwar/).

  Several major Senate and House of Representatives investigations (Reigle, 1994, Rockefeller, 1994, Shays, 1997 and Burton, 1997), testimony from GWVs, and some outstanding investigative journalism (Thomas, 1998) make such denials increasingly risible and incredible and make the disabling of alarms and their switching off acts of folly and gross negligence.

  Whilst Senator Reigle first comprehensively exposed the lies and deceits of the Pentagon and associated official bodies the Burton report comprehensively assembled overwhelming evidence of chemical detections; . . . "each of the nearly 14,000 alarms went off on average 2 to 3 times a day". Major Herbert reported chemical mines which detonated releasing sarin, mustard gas, and lewisite. Sgt Steven Wood identified visually a shell containing Russian nerve agent, soman.

  FOX vehicles were the ultimate for unequivocally identifying chemical exposures. A Gy/Sgt Grass reported speaking to every FOX vehicle commander since returning from the Gulf, everyone confirmed that they had detected chemical agents.

  "a US Marine Corps survey of 1,600 chemical defense specialists . . . who served in the Gulf War . . . [in] a declassified report stated that 221 respondents (about 13 per cent) reported some contact with or detection of Iraqi chemical weapons during the ground war."

  One particularly important example for this committee concerns Sabahiyah High School for Girls where a tank (800 to 1,000 litre capacity) suspected of containing a liquid chemical agent was discovered. Major Michael Johnson led the investigation of the tank with two FOX vehicles . . . "The mass spectrometer showed the presence of H-agent [sulphur mustard] in the soil . . . the dismounted team deployed detection paper and the chemical agent monitor . . . the detection paper registered H-agent and the CAM registered H-agent . . . these are facts and not speculation of what actions we took . . . I know that my unit . . . did in fact detect and confirm the presence of toxic chemical warfare agents in Kuwait".

  Despite one British soldier receiving chemical burns at Sabahiyah, the MoD insists that the tank contained inhibited fuming nitric acid, INFA, used as a fuel in SCUD missiles. The explanation does not fit the basic facts of the case. (Thomas, 1998).

  Chemical fallout appears to have come from three sources—

(a)  "Aerial bombardment of Iraqi field munitions depots, production and storage sites.

(b)  Explosive demolition of munitions bunkers by ground forces eg Khamisiyah.

(c)  Sporadic and unco-ordinated Iraqi use of chemical weapons, eg SCUD and Frog missiles.

  Dr Tucker in evidence identified over 55 specific chemical weapons detections or exposure incidents and their locations, from January 13 to March 26 1991".

  The Pentagon have now conceded that the Czech detections were valid and credible. Not so the MoD who still insists that there were no chemical exposures.

  SCUD missiles were explained as sonic booms but alarms still went off. (Thomas)

CONCLUSIONS

(1)  There is clear evidence of low level exposure to chemical war agents, including nerve agents, mustards, lewisite, benzyl chloride/bromide from American and Czech detections;

(2)  The UK chemical detections failed miserably for a variety of reasons involving troops of all ranks and in charge of storage, supply, training and use;

(3)  The exposures derived largely from bombing and demolition by Coalition forces;

(4)  SCUD missiles carrying chemical weapons were delivered by Iraq and contributed to these exposures;

(5)  The use of PB as a prophylactic treatment for possible nerve agents exposure, and, of P2S as post exposure treatment is fatally flawed. Neither compound will cross the blood-brain barrier leaving the brain unprotected against nerve agents;

(6)  It is questionable whether avizafone would be enzymically transformed into diazepam under battlefield conditions when exposure to nerve agent occurred.