I have put together this small collection of papers to offer a scientific explanation to the layperson, of the cause of B.S.E. For too long the British Public have been fed a tissue of lies ranging from cattle being fed human remains for the river Ganges to cattle feed with is years old. There are a few other stupid explanations but I hope that by using proven science we can uncover the truth however unpalatable that may be.

My problem is that I never saw any difference between what happened to human victims of organophosphates and what happended to the cattle diagnosed with B.S.E. This is not a theory which I wanted to prove.

I would like to pay tributed to the late Dr. Kitty Little for her work, some of which I include in this paper and also to the late Rachel Carson for her work on “Silent Spring”. The latter pretty well depicted the onset of B.S.E. with the use of organophosphates. Page 47 reads as follows:

‘Use of animal systemics has concentrated chiefly on control of the cattle grub, a damaging parasite of livestock. Extreme care must be used in order to create an insecticidal effect in the blood and tissues of the host without setting up a fatal poisoning. The balance is delicate and government veterinarians have found that repeated small doses can gradually deplete an animal supply of the protective enzyme cholinesterase, so that without warning a minute additional dose will cause poisoning.’

At my meeting with Professor Gabriel Horn of Cambridge University some years ago I asked that the autopsy papers on B.S.E. cattle be made public, or if that was not possible then that the tests should be done again! It would be a great deal easier if the British Veterinary Society made public the results of the original tests.

There has never been a case of horizontal transmission of B.S.E. so how as it managed to cross the species barrier to humans? . . . . it hasn’t!

I would like to think that I hav compiled and put together this booklet myself. . . . I didn’t, I owe a great deal to a number of people who have helped and encouraged me over the years. Without the initial help of Shirley, George and Ray my family would not have survived, the managed to make their voices heard on the dangers or organophosphates. Margaret Percival has been a tower of support and the same thanks go to Richard Bruce and Stella Masters. Certain sections of the press have been wonderful. When the Farmers Guardian get going they never seem to stop and I am grateful for the amount of space I have been given over the years. The same can be said for the Rochdale Observer and of course the Farmers Weekly. There is a special thanks to Arthur Lindon and the Lincolnshire farmers and the Lincolnshire Echo newspaper. The farmers bought and paid for my fax machine and more recently contributed financially to the publication of this missive. Thank you also to the people who bought the first of my efforts, “Cause and Effect” The Search for the Truth”. These contributions have kept the show on the road. I send my wishes to you all . . . Thank you.

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In 1992 myself and my family were diagnosed as suffering from Organophosphate sheep dip poisoning by blood tests carried out at Guys Hospital, London.

The fact that we all nearly died was seen as an irrelevance by Government departments. There was no treatment offered, or indeed any acknowledgement of our predicament. In simple terms, we were to be ignored to enable Government to cover its tracks - after all, they were responsible for licensing all veterinary products. In the face of such stonewalling, I decided to make my own enquiries, and contacted the following establishments for information - I am extremely grateful for their help:

The World Health Organisation
The Environmental Protection Agency, Washington, USA
The University of New Jersey, USA
The Pesticide Trust
The Royal Society of Chemistry, London
The Hazards Society, London

plus many private individuals. I am also extremely grateful to my lawyer for his support and advice. He has copies of all the papers in my possession.

With the help of the Royal Society of Chemistry, I obtained scientific information on all the OP compounds used as sheep dips, ie Diazinon, Propetamphos, Chlorfenvinphos, Carbophenothion; and via a third party, went on to Crufomate, which he had used as a warble fly dressing. I later explored all the OPs which had been used in the Gulf War.

What I began to find extremely worrying from this collection of information was that all OPs were cholinesterase inhibitors - the damage caused was cumulative, and research using laboratory animals showed that most were carcinogenic and also responsible for malformations in up to and including the third generation of offspring.

The destruction of the central nervous system, immune system and peripheral nervous system was also apparent with most OP compounds.

My next move was to collect as many published scientific papers as I thought were relevant. Copies of the following are enclosed:

1. Poisoning on the Farm by Dr Redhead, published in the Lancet in 1968. This paper explains the importance of the cholinesterase levels in man. It should be borne in mind that OPs were designed to attack the cholinesterase in insects, and will of course have the same effect on cattle.
2. Effects of Chronic Organophosphate Pesticide Exposure on the Central Nervous System by Richard J Korsak and Miles M Sato, published in 1977. This paper is important because it exposes the frontal lobe brain damage suffered by exposed victims.
3. Environmental Trichlorfon and Cluster of Congenital Abnormalities by Andrew E Czeizel et al, published in the Lancet in 1993. This paper is devastating in its content, and the fact that it has been ignored in the UK is unbelievable. The effect on the foetus is beyond words.

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There are many other papers in my possession, which are of course available to the Inquiry, but I hope to have painted an adequate picture of the effects of OP poisoning on the insect, human and animal species for the present. I move on ...

As mentioned above, I received an enquiry about Crufomate. The information on this compound, plus the sight of BSE-afflicted cattle on television, made me aware of the alarming similarities in both our situation and that of the cattle. To put it bluntly, the human OP victims were going off their heads and off their legs! The cattle were becoming more obvious than the shepherds (more than 900 shepherds have committed suicide since 1984). Click here to view papers on crufomate

Black's Veterinary Dictionary, 10th Edition (1973) provided quite a lot of answers where it describes the effect on cattle treated with Crufomate for warble fly. The VMD deny knowledge of Crufomate (see letter attached) but the British Veterinary Association should still have the results of all the testing done on cattle before they gave their blessing to its usage. I have persistently called for the testing of cholinesterase levels in cattle before and after treatment for warble fly. This is unnecessary - it has been done, and the results should be made available to the Inquiry by the BVA as a matter of urgency. The maternal transmission is explained in the following paper:

Reproduction and Growth of Progeny of Female Mice mated after treatment with Crufomate - author M A Khan - Research Station Lethbridge, Alberta, Canada; published in the Journal of Scientific Health in 1981. It is interesting to observe that when the first damning scientific papers on a product are published, the chemical companies react in a somewhat vigorous manner - by withdrawing the offending compound and substituting it with something considerably worse!

I consider that I have proved the link between OPs and BSE. What I could never see was a link between BSE and nv CJD, unless nv CJD was some other form of chemical poisoning. Had these two conditions been the same, there would not have been any OP victims left alive to tell the tale. In any case, the Department of Social Security have been paying out Industrial Injury Benefit to OP victims in industry for decades.

There are very few, if any, recorded deaths from chemical poisoning in the UK, but there are numerous reported deaths from "glue sniffing", "inhalation of lighter fuel", etc. Autopsies on all these deaths would presumably show frontal lobe brain damage, plus failure of the respiratory tract - but I digress. The nearest I have come to identifying nv CJD as a form of chemical poisoning is a version of Pyrethroid poisoning, the symptoms of which are identical to those exhibited by nv CJD victims (see enclosed literature).

I have requested Mr Rutter of the VMD to forward my findings to SEAC. He has intimated that he has done this, although I have had no response from SEAC. I also passed my findings to Mr Frank Dobson, the Minister for Health, on 23rd February 1998, without receiving any reply to date. I have also sent to the Inquiry, prior to this paper, such scant information on Pyrethroids as is available, in the hope that it may be of assistance to any further victims diagnosed with nv CJD.

Finally, the chemical companies should be invited to submit all research papers to the Inquiry - I am sure they have much more than I do, and some effort should be made immediately to help the thousands of suffering shepherds. It is also of extreme importance that every scrap of information relating to Pyrethroid poisoning be made available to the general public as a matter of urgency. The fact that these compounds are being used as a head lice treatment for children is appalling.

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Annex 1: Warble fly outbreaks and the use of organophosphates
Introduction
Eradication campaigns
Treatment and dosage for warble fly

1 This Annex describes how the Government responded to the incidence of warble fly infestations in the 1970s and 1980s. Warble fly was a significant cattle pest in the 1970s and 1980s throughout England and Wales in particular, the greater incidence being in the southern half of the country. Surveys had shown that the average incidence of cattle affected by warble fly passing through livestock markets was over 40 per cent in England and Wales and about 20 per cent in Scotland.

2 The larvae of the warble fly live within the body of the cow. Their presence may cause distress to the animal and can have severe economic consequences. The meat may be damaged, and heavily infected hides can be useless for leather. Furthermore, milk yield can be reduced by as much as 25 per cent.

Eradication campaigns

3 In 1978 it was estimated that 38 per cent of cattle in Great Britain were infected with warble fly. The eradication campaign began with the Warble Fly (England and Wales) Order 1978 (SI 1197), 3 which relied on compulsory treatment of affected animals in spring with recommendations for voluntary treatment of all susceptible cattle in the autumn. ⁴ 4 On 15 March 1982 the Warble Fly (England and Wales) Order (SI 234) ('the 1982 Order') 5 came into force. This made warble fly infestation in cattle a notifiable disease, 6 gave MAFF veterinary inspectors power to serve compulsory treatment notices on farmers whose herds were found to be affected by warble fly, and allowed inspectors to restrict the movement of cattle until the treatment was carried out. 7 The 1982 Order required infected cattle to be treated in spring, with a follow-up treatment in autumn. ⁸ The eradication schemes also provided for veterinary inspection of the treatment on farm, and the exemption of cattle from treatment under the authority of a veterinary inspector, if the inspector was satisfied that it was impracticable or inexpedient to treat the animal in question.

5 By 1983 only localised areas of low incidence remained, and the Warble Fly (England and Wales) (Infected Areas) Order 1983 (SI No 1382) ('the 1983 Order') was introduced. 9 This allowed the Minister of Agriculture, Fisheries and Food to declare an area to be an 'infected area' if he or she believed or suspected that warble fly existed in that area, and to require treatment of cattle there. ¹⁰

6 Infected areas were declared at various times, notably after the hot dry summers of 1983 and 1984. After the 1983 Order came into force, Anglesey was declared an 'infected area'. 11 In 1984 infected areas were declared in six localities; Anglesey, the Lleyn Peninsula in Gwynedd, east Cornwall, parts of Dorset and Wiltshire, parts of north Somerset and south Avon, and parts of the Dumfries and Galloway region. 12 Further orders were made in 1985 covering west Cornwall, east Cornwall, much of south Devon, Dorset and parts of neighbouring counties including most of south Avon, and the Isle of Anglesey and the Lleyn Peninsula. 13 In 1986 the areas subject to orders were west Dorset, neighbouring parts of Somerset, and south-west Devon including Dartmoor.

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7 By January 1985, the incidence of affected cattle had declined from the 1978 figure of 38 per cent to less than 0.01 per cent.

8 In 1993 warble fly re-entered the UK in imported cattle, which resulted inthe Agriculture Departments increasing serological checks on imported cattle.In England and Wales, 39 areas were subject to 'infected area treatment' in the autumn. From 1994, animals found to be infested were sent back to the countryof origin. 15 The Animals (Post-Import Control) Order 1995 required all imported bovines (other than those from Northern Ireland or those for immediate slaughter) to be treated with an approved warble fly treatment within 24 hours of arrival at premises of destination.

9 MAFF continues to run a comprehensive control programme under the legislation in force. Whenever infestation is found or suspected, either the individual animals or the herd, and in some cases all animals within three kilometres of the affected herd, are required to be treated, and movement restrictions apply. Blood testing is available where practicable, allowing treatment to be restrictedto infested animals only. Regular publicity campaigns are run, and importers are reminded of their obligation to treat imported cattle.

Treatment and dosage for warble fly

10 Under the 1978 Order, farmers were required to treat their cattle with either Phosmet, Famphur or Fenthion - pour-on types of organophosphate (OP) insecticide - or Derris, a contact insecticide. This Order and the subsequent Orders required these products to be applied according to manufacturers' instructions.

11 Pour-on OPs are effective because of the systemic nature of their action, which ensures the death of a high percentage of larvae before they complete their migration. Non-systemic or contact insecticides remain on the surface of the treated animal. 19 Pour-on OPs were applied to cattle along the back of the head and the entire length of the spinal column.

12 The 1982 Order discontinued the use of Derris as an alternative to OPs, because the activity of Derris meant that it was only effective in destroying larvae as they emerged from the animal. The Government therefore considered it to be ineffective in helping to eliminate warble fly on a national basis.

13 Ivomec (active ingredient ivermectin), an injectible parasiticide for cattle, was introduced to the market in 1981 and provision for its use to treat warble fly was made in the 1982 Order. If Ivomec was used on dairy cows, milk could not be used from those cows for a period of 28 days, in contrast to a six-hour withdrawal period if OPs were used. Accordingly, Ivomec was more commonly used on beef cows and other cattle, as the financial penalties for dairy farmers were severe.

14 It has been estimated that the peak level of OP usage was around 1979-80, with a reduction in the following years as the infection became less common and the use of Ivomec increased.

15 However, Mr Mark Purdey, an organic farmer, suggests that OPs were used more extensively in the 1980s, and had a significant impact on the BSE story - see vol. 2: Science for further discussion of his theories.

6

CRUFOMATE.
AN ORGANOPHOSPHATE USED AS TREATMENT FOR WARBLE FLY.

There has long been a belief in the farming community that the treatment of animals with chemicals has been the root cause of BSE but to believe something and to prove it are two quite different things. I am now confident that we have proved the theory.

My interest in the organophosphate group of chemicals and the danger they represent, goes back ten years to 1992, when myself and my family were devastated by the compulsory use of organophosphate sheep dips. To learn more I had to make enquiries overseas and I owe a great deal to the E.P.A. Washington who were very generous with their help and information.

I have never seen any difference between what happened to the cattle with BSE and what happened to the poisoned shepherds. When you can’t walk between two gates in a field without falling over, you know you have a problem and when you begin to lose the power of speech and reasoning then you become absolutely sure. The sight of afflicted cattle on T.V. filled many of us with dread.

My scientific background is none existent but it seemed a good idea to start with the Health and Safety Data sheets of all the products relating to sheep dip. The information was astounding and explained why the farmers and the shepherds had never had sight of them until 1993. I then began to collect data on the compounds used for treatment of warble fly infestations in cattle; Crufomate was the first . This was followed by Coumaphos, Triclorfon and last but not least, Phosmet.

Researching any subject is difficult and costs time and money but when the subject is a closed book it becomes nigh on impossible. The obstacles become even worse when the people who should be helping are becoming more and more obstructive. I cite The Veterinary Medicines Directorate, The Health and Safety Executive, Local Environmental Health Offices, The Department of Health, and of course the mouthpiece for the chemical companies, The National Office of Animal Health.

The shepherds got together and pooled information and what a wonderful group of people they have turned out to be. Black’s Veterinary Dictionary 1973, 10th edition became the focus of much attention.
There we discovered the symptoms of Crufomate poisoning if the cattle were overdosed. At the same time we were looking at the Government document APS/1 which stated that if one OP made one ill, then one should never ever use another OP. Pity the cattle couldn’t talk at the time. Over a period of time, some cattle must have been subjected to treatment with four different organophosphates. Finding scientific data on all of the compounds used turned out to be a test of patience and frustration for me. Coumaphos and Triclorfon presented no problem. Crufomate was something else again.

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The people I tried to get information from turned out to be either unwilling or unable to help. I suspect the former. After seven years of searching we eventually ran around the house shouting "Eureka". The Health Authority New Jersey, U.S.A. placed it on their web site. For the benefit of all I will repeat it here.

SUMMARY
Crufomate can affect you when breathed in and by passing through your skin. Crufomate can damage the testes. Breathing Crufomate can cause rapid fatal organophosphate poisoning with headache, sweating, nausea and vomiting, diarrhoea, loss of coordination and death. Repeated exposure may cause personality changes. High or repeated exposure may damage the nerves.

IS THERE ANYONE OUT THERE WHO IS STILL IN ANY DOUBT ABOUT WHERE BSE ORIGINATED FROM?
The BSE inquiry was a complete waste of tax-payers' money. The manufacturers of Crufomate were Dow Agrosciences Ltd. Their submission to the enquiry stated that they had withdrawn from the animal health business about 1980 and had no records of that part of their business prior to their withdrawal. Was this because they saw everything going pear shaped I ask. They now have a copy of the hazard fact sheet, I sent them a copy, and they should waste no time in putting it in the public domain. There are a number of interesting factors about organophosphates which are not widely known. They were originally designed as nerve gases and then supposedly modified to be used as insecticide. They are extremely efficient at destroying certain enzymes in the blood of all warm blooded creatures, man being no exception. The first enzyme we investigated was cholinesterase.This facilitates messages getting to and from the brain. The expected norm in man varies between 40 and 80 units per 100 mls of blood. When I was blood tested I had 8.25. The cholinesterase enzyme will try to put itself right over a period of time but never reaches its starting point. It is essential that blood tests and done within 24 hours of exposure. Discovering that the enzyme Paraoxinase is important to the functioning of the heart muscles was interesting to say the least. The destruction of this enzyme leads to Cardiac Arrest which is usually fatal. The most amazing factor of all the scraps of information is that there are any cattle, sheep, or farmers, left alive in the UK after so many years of enforced abuse.We need to look carefully at all the Government bodies and agencies which have been involved in his gigantic cover-up.

1. Local Environmental Health Offices supervised the sheep dipping at all farms. Their officers were no better equipped the most farmers. When we collapsed in 1992, there was a blank refusal to help. We needed to remove spent dip from our yard and were told to do it ourselves. When our local councillor called a meeting of local farmers to discover if there were any other victims in the locality, the authority refused to send a representative.

They stated; IF THESE PEOPLE WERE MADE ILL, IT IS THEIR OWN FAULT, THEY WERE GIVEN GUIDELINES.

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2. The Health and Safety Executive. They have a great deal to answer for. The Medical Services Document MS 17 is their responsibility. When they came to rewrite this paper the draft paper actually mentions the Suicide Impulse of many victims. The fact that hundreds of shepherds have committed suicide after using OP sheep dips hasn't yet occurred to them. The MS 17 never reached the farmers and the rewrite was completed without the suicide clause. They later went on to threaten campaigners with libel action and at the same time closed down a wool grading factory at Carnforth because they couldn't guarantee the safety of the workers from organophosphatespoisoning. In 1991 they will in the process of finalising their own research into the health of farmers to the use of organophosphates. The research was devastating. They were aware then that organophosphates degrade through heat and age to become tetraethyl pyrophosphate. They should have been aware that it took only 45 minutes to destroy 20 head of cattle in Texas. Their reaction to this set of devastating research defies belief. They called a meeting. The HSE the VMD and the National Office of Animal Health all attended on 25.2.1991 and now would you believe THEY HAVE ALL LOST THE MINUTES OF THAT MEETING. IT HASN'T PASSED MY NOTICE THAT IF THEY HAD TOLD THE TRUTH AT THAT TIME MY FAMILY WOULD HAVE BEEN SAVED A GREAT DEAL OF TRAUMA AND MANY HUNDREDS OF FARMERS WOULD STILL BE ALIVE. 3.The Veterinary Medicines Directorate is the agency which is supposed to investigate all adverse reactions to veterinary products. They have yet to find a confirmed case of organophosphate poisoning among the farmers who have managed to find their way through the maze of forms. Every report which have looked at very blandly states that there is insufficient evidence to support the diagnosis. They even managed to ignore the reports from HSE doctors which support or confirm the diagnosis. Papers appear to be lost or destroyed as do medical records.
Marks out of ten for the VMD = Zero.
Whilst the minutes of the 1991 meeting may have been destroyed, the people who were in attendance are still around. They should be called before the select committee on health at the House of Commons and asked for explanation of the research and their own involvement in suppressing this information.

The Veterinary Products Committee are responsible for the licensing of all these products. They certainly have a laid-back attitude to the user's welfare. There is no communication between themselves and the victims. Letters to any of these quangos are part of a game called Pass the Parcel. The letter Is passed to another Ivory Tower for reply and when you finally get an answer you will have forgotten what the question was in the first place.

The HSE will never implement the 1968 Medicines Act against the chemical companies on the shepherds' behalf. Section 6 relating to substances at work is quite explicit. The shepherds are entitled to a Police Investigation - always supposing that Murder by Remote-control is still not legal in Britain today.

Brenda Sutcliffe.

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The BSE Inquiry / Statement No 271
Mr David Farrant
(not scheduled to give oral evidence)

Dow AgroSciences
Statement of David Farrant to the BSE Inquiry
[This witness has not been asked to give oral evidence in Phase 1 of the Inquiry]
Dow Agriculture had an Animal Health division between approximately 1960 and 1981 when the group was disbanded. In that period the division did sell a product for warble fly based on the active ingredient crufomate with a registered name of Ruelene. However we have no records available from the period and our statement in answer to your questions has been drawn up based on one or two people’'D5s memory of the period. We cannot therefore guarantee the accuracy of the statement.

Agricultural Chemicals
1. Dow AgroSciences has a range of insecticides, fungicides and herbicides approved by the Pesticides Safety Directorate for use in crop protection on farms.
2. The products are approved for use on various agricultural crops. We have no products used on livestock.
3. Full approved product labels, technical training for distribution and Safety Data Sheets are supplied.
4. The organochlorine molecules have been replaced in many crop situations by organophosphate products because of the environmental persistence of organochlorine molecules. The change has been driven by environmental and regulatory authorities worldwide.

Warble Fly Treatment
5. Dow Agriculture, as the company was at the time, did have an animal health division and sold a treatment for warble fly. This was approximately 1960 to 1981 when the animal health group was disbanded.
6. The active ingredient was crufomate.
7. The brand name for the product was Ruelene.
8. Ruelene 25E –'D0 the rate used was a 1:3 dilution with water to give a 6% pour on using 1 fluid oz/cwt bodyweight up to a maximum of 8 fl.oz. Later (late 1970’'D5s) Ruelene 7R was produced which was a ready to use pour on formulation used at the same rate as the 25E.
9. The dosage in the UK was the same as in other countries.
10. A regulatory package that met the requirements of all countries at the time of sale was produced.
11. As far as we are aware no specific studies were undertaken on the effects of combination treatments.

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Contact with Government Departments
12. At the time Ruelene was sold the then Animal Health Group in Dow were in discussions with the government on an eradication programme but we understand Ruelene came off the market before the programme came into force in the UK.

David Farrant
Registration Specialist
UK and Eire

Issued on behalf of the witness by:
Website: http://www.bse.org.uk
email: inquiry@bse.org.uk

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1.The term organophosphate (OP) is generally understood to mean an organic derivative of phosphoric or similar acids. There are many different OPs and they differ to some extent in their properties. Many OPs inhibit an enzyme known as acetylcholinesterase (the effect of which is described in paragraph 2). This is a class effect of OPs, but not all OPs (e.g. glyphosate) demonstrate this effect. Some OPs react with other proteins such as neuropathy target esterase, and this reaction is associated with the effects detailed in paragraph 5.

2.Inhibitors of acetylcholinesterase affect certain nerve junctions in animals, as well as parasympathetic effector sites (the heart, lungs, stomach, intestines, urinary bladder, prostate, eyes and salivary glands). The transmission of impulses across nerve junctions involves the release of a transmitter chemical, which, in the case of many nerves, is acetylcholine. To stop the nerve continuing to transmit the message, the transmitter, acetylcholine, must be broken down immediately after it has had its effect. This breakdown is brought about by an enzyme, acetylcholinesterase. By inhibiting the enzyme acetylcholinesterase, OPs prevent the nerve junction from functioning properly. In the case of most OPs and all medicinal and pesticidal anticholinesterase OP products this effect is either reversible, the rate of re-activation of the enzyme being dependent on the chemical structure of the OP, or recoverable by synthesis of new enzyme.

3.OPs can be carefully selected, on the basis of their chemical structure, so that they are very effective agents against their target pest or insect and the risk to humans can be controlled by following the recommended precautions. The efficacy of OP products as pesticides and as human and veterinary medicines relates to the inhibition of acetylcholinesterase in the target pest species.

4.In humans, anticholinesterase OPs have broadly similar actions to those seen in other species. Acetylcholinesterase inhibition causes acute effects in humans and other mammals. The symptoms in humans, which generally occur when acetylcholinesterase activity has been reduced by about 50%, may include: headache, exhaustion and mental confusion together with blurred vision, sweating, salivation, chest tightness, muscle twitching and abdominal cramps. The severity of the effects depends on the degree of acetylcholinesterase inhibition. The more severe effects can include muscle paralysis leading to severe difficulty in breathing, so requiring respiratory support. Convulsions and unconsciousness can occur. Recovery depends on elimination of the OP product from the body and return of acetylcholinesterase activity. However, as noted in paragraph 1, not all OPs are anticholinesterases, and compounds such as glyphosate exhibit quite different toxic effects. Furthermore some non-OPs are anticholinesterases and these compounds have similar toxicity to anticholinesterase OPs, an example of this being the carbamate insecticides.

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5.Some OPs may also work by another mechanism, that is, causing an OP-induced delayed effect on the peripheral nerves. This is known as OP induced delayed polyneuropathy (OPIDP). OPIDP is a delayed effect caused by die-back in the long nerves, thus affecting the limb extremities. OPIDP is associated with, but not necessarily caused by, inhibition of another enzyme known as neuropathy target esterase (NTE). The capacity of OPs to inhibit NTE and cause OPIDP does not correlate with their capacity to inhibit acetylcholinesterase. Any OP product which is shown by laboratory tests to be likely to produce OPIDP in humans, will not be authorised in the UK. A number of studies of OP products currently or previously used in UK sheep dip, have shown them to have no potential to produce delayed polyneuropathy in animal tests.

6.Another known toxicological effect of OPs in humans has been termed the intermediate syndrome. This can follow severe acute poisoning, sometimes as a result of a suicide attempt, and causes temporary paralysis of the proximal muscles (muscles nearest to the central line of the body e.g. respiratory, neck and upper part of limb muscles; the distal muscles of the limb are not affected so grip strength may be preserved). Since this includes the respiratory muscles, respiratory support is necessary to keep the patient alive. The precise reasons for the development of intermediate syndrome are not clear but explanations which have been advanced include myopathy (muscular damage), depolarisation blockade (blocking impulses at the neuromuscular junction and paralysing the muscles) and Guillain-Barre syndrome-like effects (muscle weakness, numbness and pins and needles in limbs).

7.There are postulated long-term effects of OPs following long-term low-level exposure. Some studies on low-level exposure have shown subtle effects (e.g. slower reaction times) in specialised tests for neurological function, whereas others have shown no change in different neuropsychological and neurophysiological tests. The alleged theories and mechanisms are sometimes not related to acetylcholinesterase activity.

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When using organic compounds of phosphorus, such as these insecticides are, one has to bear in mind two potential dangers - that from residues in the carcase - to people eating the meat; and the danger of the cattle being rendered ill by the dose. However, these compounds have been the subject of extensive trials both in Britain and overseas.

Crufomate poisoning as a result of over-dosage results in distressed breathing and a staggering gait; also a tendency to rermain lying down. Atropine is an antidote. (see also Trichlorphon.)

In 1965 the British Veterinary Association supported the use or organophorus systemic dressings, recomending application between October and November 15 or between mid-March and the end of the warble season. (but not between mid-November and mid-March because of the location of the parasite in the host).

In 1968 a warbles eradication scheme covering a central zone of 50 square miles, surrounded by a 5-mile outer zone, was reported. Between 85-90 per cent of the cattle - over 17,000 in all - were sprayed annually with coumaphos and crufomate. The average number of warbles per animal reduced from 13.7 to nil in two years. After five years the average incidence was 0.8 warble per head. Poisoning was not observed with either drug.

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TRICHLORFON (THE LANCET 27.2.1993)

Cluster-type Outcome

Of 15 infants born in 1989 and 1990 in a small Hungarian village (Rinyaszentkirály), 4 had Down's syndrome. Thus, the recorded rate (266.67/1,000) exceeded the expected rate (1.17/1,000) 228 times. Other unusual findings were noted: 7 other babies had congenital abnormalities, and of 15 live births, 6 (40%) were twins (although the expected rate was 2%). All four cases with Down's syndrome had trisomy 21, but their parents were healthy; however, the origin of an extra chromosome 21 was maternal meiosis II. This is in contrast to the typical nondisjunction that occurs in maternal meiosis I. Two complementary studies were therefore organized to investigate the phenomenon.

The clinical examination of all 61 children born in the village between 1980 and 1988 did not detect any occurrence of Down's syndrome. As a further check, we looked at the records for children born in the neighboring seven settlements less than 20 km from Rinyaszentkirály. Only one case of Down's syndrome was found, and the observed rate corresponded well with the expected baseline rate. Thus, we concluded that the spatial clustering of Down's syndrome was restricted to Rinyaszentkirály and to just the 2 years, 1989 and 1990.

Subsequently, we organized a case-control study. The involvement of classical hazardous environmental factors such as alcohol consumption, radiation, drug ingestion, microbial infections, maternal disorders, etc., were not found. The confounders, e.g., demographic factors such as maternal age, birth order, and previous fetal loss, also did not show any significant differences among groups studied. However, all mothers of Down's syndrome cases reported frequent fish consumption.

Follow-up investigations showed that the territory of Rinyaszentkirály includes several fish ponds, and a new director of fish farms introduced chemical fast bathing of fish in 1988. These fish were taken out of the ponds and treated with 500 mg/l Flibol (40% trichlorfon) for 5 to 10 min to eradicate parasites and then were returned to the pond. Trichlorfon is an organophosphorus insecticide, which is also known as chlorofos, metrifonate, and trichlorphane; brand names include Dipterex and Flibol. After the treatment, fish seemed to be lifeless on the surface of the water for hours. Dead fish were noted both by inhabitants and those supervising the cleaning operation. The inhabitants of Rinyaszentkirály were not told about the new technology, but fishing was prohibited during these periods (March and May in 1988 and 1989); however, people often took out the comatose fish by hand for consumption in this impoverished village. The estimated initial trichlorfon content of the fish was about 100 mg/kg (acceptable daily intake is 0.01 mg/kg). All mothers of Down's syndrome babies consumed poisoned fish during the critical period, i.e., on the day of conception. This chemical treatment of farmed fish was banned in 1990. All 30 children born after the ban between, 1991 and 1994, are healthy, thus the cluster ceased. In addition, Doherty et al. (8) confirmed the aneugenic effect of trichlorfon in experimental studies.

Thus, the possibility that high-dose trichlorfon is a germinal mutagenic agent deserves further attention.

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THE GREAT BSE SCAM

By Kitty Little. M.A. B.Sc. PhD 18-9-98.

On 1st September 1978 a Statutory Instrument that had been issued by the Minister for Agriculture, Fisheries and Food came into operation Warble Fly (England and Wales) Order 1978.-S.I. 1978 No. -1197). For the stated purpose of eliminating Warble Fly, this required all cattle to have their backs and heads treated with a powerful organophosphate nerve poison.

Other countries in Europe used the same organophosphate nerve poison to eliminate the warble fly, but under different conditions. For every poison there is a threshold level below which symptoms do not develop, and with the exception of Switzerland and Britain the doses were kept below the threshold level. Switzerland and Britain used oil to increase absorption of the poison, and in Switzerland a dozen or so animals developed the symptoms of BSE. The oil had raised the absorption dose to just above the threshold. But in Britain a dose four times the recommended dose had been used, with the result that large numbers of cattle developed BSE.

When he read a description of the symptoms of BSE, a military intelligence officer told me that they were identical with the symptoms produced by military nerve gases in animal trials. He assumed - correctly - that I would be interested, since he knew that for the last 40 years, the greater part of my work has been on topics where research results have been falsified.

The main effect of the organophosphate (OP) nerve poisons is to deactivate acetylcholine esterase. The function of this enzyme is to control the levels of acetylcholine in the brain. When it is deactivated, the levels of acetylcholine can rise to several hundred times normal. The changes in the brain giving rise to BSE symptoms do not occur until the acetylcholine levels are well over 100 times normal.
There is a simple blood test for acetylcholine, and if this had been done during active phases of the BSE syndrome it could readily have been shown whether the overdose given during the warblefly treatment had been the cause of the BSE. This should have been the first thing the Ministry of Agriculture considered, but they didn't. It seems that the scaremongers were already in control.

A second effect of these nerve poisons is to modify the structure of certain proteins, known as prion proteins. Mark Purdey gave clear evidence about this to the BSE Inquiry in March. This change happens at much lower doses than those needed to cause BSE symptoms. And so the scaremongers used a confidence trick that anyone who has done O-level Biology should have been able to spot. They pretended that those modified proteins were an infective agent.

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An essential property of any infective agent, whether bacteria, virus or mycoplasma, is that it should be able to reproduce itself. Those prion proteins do not reproduce themselves. They are formed by cells and modified by toxic agents, and that is all. Again, if there is an infection, such as foot-and-mouth disease, it spreads from one animal to another. BSE didn’t. The farmers, the victims of all this, are fully aware of the actions of infectious agents in herds of cattle, and that BSE did not follow that pattern. They are not to give evidence to the BSE Inquiry. Also, if the “new variant CJD” was due to eating beef containing an infective agent, there ought to be many more cases in the United Kingdom than elsewhere. In fact, the incidence is lower in the United Kingdom than in many other countries.

If the pretence that BSE is an infection that could be transmitted to humans was to be kept up, there was a need to provide something that could be interpreted as “transmissible”. A start was made by referring to “TSEs” – “transmissible spongiform encephalopathies” - to get people used to the idea. Again a confidence trick was being employed, that anyone with an elementary knowledge of biology could spot.

It is well known that for blood transfusions or tissue transplants the tissue of donor and recipient have to be compatible, otherwise there is a “foreign body” reaction. In the experiments that have been done to make the idea of TSEs apparently plausible, brain tissue has been transplanted from one animal to another and from one species to another. The expected “foreign body” reactions have been described as transmission of infection. In March, Professors Ebringer and Pirt explained to the BSE Inquiry about immune and autoimmune reactions, but the scaremongers have ignored their evidence.

Professor Southwood’s evidence to the Inquiry was revealing. In 1988 there was no evidence of a BSE-like illness in people, but he had been told “by the Central Veterinary Laboratory” that it was an infection, so just in case it might spread to humans his Committee recommended that over 2 million healthy cattle should be killed and their carcasses destroyed. (The new abattoirs needed for this were already in place). He twice appealed to doctors to try to find some cases among their patients.

As a result of the scaremongers’ disinformation campaign we have had a variety of harmful edicts - banning beef-on-the-bone, doubts about blood for blood transfusions, and dozens of regulations about the surviving cattle, that are harmful and very costly for farmers, and amount to cruelty to the animals. And now there is the suggestion that all the sheep in the country should be killed off. The foundations for this latest confidence trick were also laid in the late 1970s and 1980s.

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Sheep dipping became compulsory: the agents recommended by the Ministry of Agriculture being organophosphate poisons. The “protective clothing” recommended to farmers let the poison straight through.
The Health and Safety Executive had prepared a Guidance Note MS 17, that was revised in February 1986, “Health Surveillance of Workers Exposed to Organo-phosphates and carbamate Pesticides”. Its distribution was blocked. The symptoms described for OP poisoning are the same as those described for some of the “New Variant CJD” victims.

Hundreds of farmers were affected by the OPs in the dip, and more have died of their effects - over 200 so far - than there have been cases of the “New Variant CJD”. Paragraph 32 in the blocked Health and Safety Guidance Note says:

It is only reasonable to expect that many of the sheep that were dipped will have the modified prion protein caused by the OP poisons to which they were exposed, and this would give the scaremongers the excuse for having all our sheep killed, and thus eliminate livestock farming.

We have now arrived at a situation where the BSE “infection” is supposed to have been derived from scrapie in sheep, while the present suggestion is that sheep will get a TSE from the BSE “infection” .

So what about scrapie?

It is a very rare condition. One might expect to find about 2 cases a year in the whole of the North West, or 5 or 6 cases in the South West. In Australia and New Zealand there is no scrapie among the same breeds of sheep. It has been known for centuries not to be infectious. (Even if it were infectious there are far too few cases to have infected hundreds of cattle).

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Since the “scrapie causes BSE” myth was launched there have been strenuous efforts to find some infectious agent for scrapie, with no success. All the evidence points to it being a toxic reaction from some mould or fungus in the ground.
In that connection it is interesting that the vet David Bee gave evidence to the BSE Inquiry in March concerning cattle that, a short time before the BSE outbreak, had developed BSE-like symptoms as a result of eating mouldy feeding stuff.

There remain the “New Variant CJD” cases that have been reported. Experiments reported by Professor John Collinge have shown that it is similar to BSE and different from other types of CJD. This is very strong evidence that these cases are really cases of OP poisoning. Ordinary CJD cases come in a variety of forms and are also non-infectious, which must lead to a suspicion that some of the cases are the result of a reaction to a toxin. The cases that were the subject of a recent High Court action, where the source had been an apparently contaminated growth hormone preparation, are examples of an autoimmune reaction.

The scaremongers are providing more and more lurid headlines:- “Mass testing for BSE -breakthrough will show if millions have killer disease”, “The making of a modern plague”, and so on. But what are the facts? Since Professor Southwood made his plea to the medical profession 27 alleged cases have been reported in 11 years. They are meant to have “caught the disease” by eating beef, but at least one, and probably three or more of the victims have been vegetarians. A cluster of the cases occurred near an OP factory in Kent, when an accident resulted in some of the products being dispersed into its surroundings One alleged case was a man who had never shown any CJD symptoms, and had died of something completely irrelevant. It had been “diagnosed” at post mortem.

Most people are now exposed to OPs. They are in insect sprays, pesticides, on wheat (and therefore in bread), on cereals, fruit and vegetables that have been sprayed with pesticides, and so on. They are not in beef or mutton (lamb), so that those are the safest foods to eat if one is afraid of getting the “new variant CJD”.

As well as high doses of OPs that are above the threshold level for the toxic reaction leading to BSE and the debilitating symptoms in farmers, Gulf War veterans who were sprayed with the OP nerve gas, and the “new variant CJD” cases, there is a considerably lower threshold for the production of modified prion proteins. The confidence tricksters are hoping that the change due to all the other causes of exposure to OPs will have occurred in a sufficient number of people for them to be able to suggest that since a large number of people have caught the “infection” in due course all of them and probably many more will develop “New Variant CJD”.

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If a sufficient number of people fall for that scam, the way will be wide open for the scaremongers to arrange for the total destruction of our livestock industry. That appears to have been the object of the exercise. Fish, eggs and milk have also been under attack, so that we would be deprived of our indigenously produced proteins - and our merchant navy is now virtually non-existent.

There remains the question: what should be done about it? We have had over 2 million healthy cattle killed, unnecessarily. There is a threat that large numbers of healthy sheep might be killed, also unnecessarily. Having got away with so much, the scaremongers in what might be called the “BSE Industry” are coming out with more and more outrageous suggestions, while the Ministry of Agriculture is forking out millions of pounds to feed that hungry “cuckoo in the nest”.

The BSE Inquiry will not be over till next June, and even then its report will be about who has done what, and not the consequences of their actions. There is every reason to think that at least some of the actions of the scaremongers and “BSE industry” are criminal, but a criminal investigation also takes time, and by then these people could have done totally irreparable damage to the country. The sequence of events very strongly suggests that that has been their intention.

I would suggest that the Government should take immediate action to:

1. Withdraw all funds going to the scaremongers and the “BSE Industry”.

2. Cease to spend anything implementing niggling and petty laws that harm people. (We have been a Christian nation for almost two millennia, and Christ’s teaching on such laws was unambiguous. They should be ignored).

3. Use the money released from those sources to properly compensate farmers, so that they can build up our livestock industry again.

4. Immediately repeal all Orders etc, from and including that of 14 June 1988 onwards, that seem to have been designed for the purpose of harassing farmers, animals, butchers and others. Reimburse people who have been fined or had their businesses harmed by those unjustifiable Orders, etc.

5. Have the Health and Safety Guidance Note MS17 circulated to all farmers, and to all people handling organophosphate preparations. (Including Prince Philip, who got a brush-off from the Ministry of Agriculture over the deaths of birds and animals as a result of crop-spraying on the Sandringham estate, the Ministry being at fault).

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   Dated 2/3/2007.

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