The BSE Inquiry / Statement No 23

Scheduled to give evidence on 02/04/98

 

 

THE BSE INQUIRY

Statement of Mark Purdey (23 March 1998)

1. The purpose of my statement is to describe, from the time when BSE was first identified, my actions and statements about BSE and nv CJD and the reasons for my actions and statements. In doing so, I give some background to explain the reasons for my interest. I have a number of criticisms, which I made at the time, which I describe in my statement. I have other criticisms and views which I have submitted to the Inquiry and which I annex to this statement. I entitled it "Short Written Statement to BSE Enquiry; February 1998". I understand that my criticisms and views will be investigated. In this statement I describe what I said and did as a matter of historical fact.

2. I am a dairy farmer currently farming at High Barn Farm, Elworthy, Taunton, Somerset. I was educated at Forres School, Swanage and then was admitted to the scholarship form at Haileybury College, Hertford. In 1972 I declined a university place to study zoology and psychology, in order to start a pioneering organic farming community in the west of Ireland. I have been farming ever since. I am also an independent scientist involved in the aetiology of TSEs, investigating for environmental factors in isolated clusters of TSE all over the world and have published five articles on the BSE/Organo phosphorus theory in peer-reviewed science journals with one article shortly to be published.

3. The Warble Fly Order 1982

In 1984 I was dairy farming at Dene Farm, Halse near Taunton. I had a herd of 80 pedigree Jerseys. My practice had been to use Derris, which is an organic pesticide, to control warble fly when necessary. The substance was on MAFF’s approved list until 1982. Under the Warble Fly Order 1982, however, the Ministry required farmers to treat warble with organophosphorus ("OP") twice a year. Studies had indicated that there was a chance that OP residues could contaminate cows’ milk after treatment. I was also arguing that these chemicals would cause long-term delayed neuro-toxic damage to susceptible types of cows and humans who were exposed. I feared an epidemic of neuro-degenerative disease would ensue as a legacy of the Warble Fly Order. I had used Derris in the past and it achieved 100 per cent success. Derris is a naturally occurring compound and the warble fly larvae are readily killed by two applications a few days apart. I was aware that if cattle were undergoing simultaneous treatment with fly repellents or worm drenches, as well as the OP warblecide, this could affect the balance in the animal’s chemistry. I was also concerned for the welfare of my wife, Margaret, who was then pregnant as there had been cases where farmers’ wives had miscarried after coming into contact with OPs. The Ministry did not accept my arguments and, as my cattle were not treated as required under the 1982 Order, they imposed restrictions on my livestock. There was also a threat of prosecution. I wrote several letters, to the Prime Minister, the Minister of Agriculture, MPs, MAFF’s Advisory Service ("ADAS"), the District Veterinary Officer at Taunton ("DVO"), the Central Veterinary Laboratory ("CVL") and the Health and Safety Executive. The Ministry however did not change their position in support of OP compounds and against Derris (see Mr Lawrence’s letter of 25 January 1985 and the Chief Veterinary Officer’s letter of 4 February 1985).

4. The Ministry informed me that they intended to treat my cattle with the OP compound and to recover their expenses of doing so from me. I decided to take legal advice and challenge the 1982 Order by way of an application for judicial review. I had the support of Dr Alastair Hay, of the Department of Chemical Pathology, Leeds. My lawyers sought an order quashing the Minister’s Enforcement Notice under which the Ministry would have compulsorily treated my cattle with OPs and an order prohibiting the Minister’s proposed treatment. We argued that the Ministry had been acting unlawfully by enforcing treatment with OPs as they had no powers to make the 1982 Order under the Diseases of Animals Act 1950 which only empowered the Minister to enforce treatment with a vaccine or a serum. On 27 March 1985 Mr Justice Woolf granted me leave to apply for judicial review. On 1 April 1985 at the hearing we reached an agreement with the Ministry. My dairy herd were exempted from treatment and my 26 heifers, which had been grazing in the compulsory warble fly zone, had to be treated with ivermectin, a non OP pesticide which makes cows’ milk unfit for human consumption for 28 days.

5. I continued to campaign about the dangers of OPs. In 1987 I submitted evidence to the House of Commons Agriculture Committee inquiry into the effects of pesticides into human health. I linked OPs with brain disorders such as multiple sclerosis and Alzheimer’s disease. I also authored and presented my own BBC2 film "Aggrochemicals" which was shown on 3 June 1988. In 1988 I was appointed an environmental/rural adviser to the BBC Community Programme unit and was responsible for helping in the selection of their films for three years.

6. My reaction to the Wells et al article on BSE in cattle

The article by Dr Wells and others appeared in the "Veterinary Record" in October 1987. I wrote to "Farmers Weekly" in December 1987 querying why the journal had dubbed my postulated link-up between OP exposure and BSE as "ill-informed rumour mongering". I said that –

"My own independent survey on some of the farms inflicted with this crippling neurotoxicity have revealed that warble fly liquids containing "phosmet" and a brand of feeding stuff (compounded from intesticide-treated raw materials) are the common denominators upon these farms. Either, or both, of these inputs could serve as the delayed neurotoxic culprits to those genetically susceptible Holstein cattle bewitched by BSE."

I also pointed out in my letter that Drs Cavanagh and Bouldin had observed "intraneuronal ballooning vacuoles" and "neurofibrillary proteinaceous conglomerations" in the grey matter of the brain stem in degenerating nerve tissue of animals poisoned by OPs. These features resemble major aspects of BSE pathology.

At the time it was believed that Holstein cattle were more prone to BSE. We now know that BSE is a cross-breed problem.

7. The Tyrell Committee report, published 12 July 1990

I wrote a letter to the Farmers Weekly about the report which was published on 3 August 1990. I commented that it seemed "rather foolish that none of the investigative organisations concerned were channelling much energy into solving the missing links surrounding the pathology and prerequisites underlying this "slow viral condition"". I commented further that "I find it interesting that the 250 or so cattle that have grown up through my dairy unit were consistently fed the brands of cake alleged to contain the BSE agent, yet not one of them has developed BSE symptoms. Perhaps the unique feature of my herd is that I have consistently refused and avoided the use of anti- cholinesterase-based insecticides and wormers in my management."

8. "Churnside Birthday" (BSE (No2) Order 1988 : RBSE reference 91/13933)

On 14 July 1991 I wrote to the Chief Veterinary Officer at MAFF as well as the DVO at Taunton about my pedigree jersey cow, "Churnside Birthday", that I had bought into my farm from a chemically run farm and which had developed a "staggers" disorder. After observation, my vets considered that the cow was afflicted with BSE. I raised with the Chief Veterinary Officer the conception that exposure to synthetic or naturally occurring neurotoxicants such as anti-cholinesterases or aluminium containing pollutants were upsetting the cow’s neuro-psychiatric equilibrium. I also pointed out a publication where OPs had been shown to induce spongiform encephalopathy in three victims. I asked for a guarantee that before I handed over the afflicted cow, I should be granted independent access for examination of CNS tissue. Mr Meldrum, the Chief Veterinary Officer, however replied on 25 July 1991 that the Department could not grant me independent access for examination of central nervous system tissues. On 13 November the DVO at Taunton wrote to me to inform me that the laboratory examination identified lesions consistent with BSE and that disease was confirmed in the animal.

9. In early 1992 the Ecologist magazine published my first peer reviewed article on my theory drawing links between BSE and organo-phosphate usage. One of my peer reviewers was Professor Lacey. In my article I said that there was a growing body of evidence that OP insecticides could play a key role in the development of BSE. I noted that the epidemic was worst in areas designated by MAFF as warble fly eradication zones throughout the 1980s. In those areas all cows had to be treated with OPs. Voluntary treatment of cows was urged by MAFF in areas outside the compulsory zones. There was no record of any cow born and raised on an organic farm dying of BSE. The great majority of organic farms had avoided using the high dose type of OP and it is interesting that many cows on those farms may have been fed the concentrates blamed for the disease. I listed similarities between BSE and chronic low dose OP poisoning and pointed out that the chemical had been shown to trigger cancers. I suggested that it might also "switch on" replication of the abnormal prion protein that was supposed to cause BSE. The Western Gazette of 19 March 1992 reported Professor Lacey as saying that "it looks increasingly likely there may be one or more precipitating agents that trigger off BSE and it is possible that insecticides are involved." The Minister continued however to take the view that it was not possible to draw any conclusions in support of my argument (his letter to Mr King MP of 8 June 1992).

 

10. "Chillaton Damson" (RBSE 92/23076)

 

In the summer of 1992 I refused to hand over "Damson" one of my dairy cows for slaughter although she showed signs of BSE. I wanted to continue to treat "Damson" to test my theory that the OP insecticide used against warble fly could be behind the BSE epidemic. A conventional farmer had treated "Damson" with an OP insecticide before I bought her. I took the view that symptoms of the illness, including aggression and nervousness, were signs that cows were suffering from the delayed effects of low dose OP damage upon selective nerve tracts in the brain. I took legal advice from Pannone Napier, the solicitors, about a possible judicial review of the Ministry’s actions. I also wrote to Mr Meldrum, the Chief Veterinary Officer at MAFF. Mr Meldrum replied on 14 July 1992 that he had no objection to my carrying out tests on "Damson" while she was under restriction but if she had to be slaughtered he would wish to know what investigations I wished to carry out on her carcass. Also on 14 July Pannone Napier wrote to the DVO at Taunton requesting that the Ministry should allow me not less than 2 weeks to treat "Damson" with oxime and atropine or any other preparation recommended on veterinary advice. The solicitors also asked that the Ministry undertake not to serve Notice of Intended Slaughter without 2 clear working days notice. Pannone Napier enclosed a letter from Professor Lacey to me dated 3 July who said that I had "certainly produced strong evidence for a causal effect between exposure to [OP] chemicals and the precipitation of BSE-related symptoms." The DVO at Taunton replied to Pannone Napier in a letter dated July 1992 agreeing to my request that I be allowed to carry out a course of treatment on "Damson". The DVO also said that he had no objection to delaying the service of the Notice of Intended Slaughter to allow treatment to take place, provided that the cow’s welfare was not prejudiced. On 16 July I injected "Damson" with oxime and atropine sulphate, pharmaceuticals carried by troops in the Gulf War as an antidotes to nerve gas. Within 90 minutes the cow appeared to have remitted. On Friday 18 July Mr Budge, my vet and Mr Cohen, the MAFF vet, examined "Damson". Over the following weekend "Damson"’s condition deteriorated. I asked my vet to continue with the injections. On Monday 19 July Mr Cohen visited my farm and told me that "Damson" should be put down. Mr Budge later arrived and said that he had to take further advice before reinjecting "Damson". On 20 July "Damson" was down on the ground. I wanted to go to the High Court to force the Ministry to let me continue the treatment. Mr Cohen then paid me a further visit and I had no choice but to consent to "Damson" being put down on welfare grounds. I was very angry. I thought that someone wanted to avoid the embarrassment of the treatment working. I considered that I was engaging in a scientific experiment. BSE was confirmed on 20 August 1992. I wrote to the Central Veterinary Laboratory ("CVL") on 29 September 1992 about aspects of "Damson"’s case. I wrote that I always assumed that "Damson" had chronic OP induced spongiform encephalopathy. Mr Bradley on behalf of the CVL replied on 5 November that if I was satisfied and agreed the final diagnosis of BSE so be it. If however I was suggesting that the cow had concurrent, chronic OP-induced SE, then CVL wished to see the supporting evidence for my conclusion. I wrote a letter to "Farming News" which was published on 26 March 1993 in which I said that my trials with my own BSE cow Damson were spearheading research into chronic OP pesticide induced BSE. I added that it had been proved that some of the OPs that contaminate the bovine food chain exhibit serotonin agony, cholinestrerase depression and mutagenicity – the dirty three detonators for BSE. (I add that my thinking now is that these facets of OP toxicology are partly irrelevant to the OP induced mechanism). On 21 October 1993 Mr Wilesmith of the CVL wrote to Mr North, a Food Safety Officer, who had written an article entitled "The corruption of science" in UKEPRA News dated 20 August 1993. Mr Wilesmith said that he looked forward to seeing the scientific publication of the effects of oxime which I administered to "Damson". He added that CVL’s understanding of the facts was not as reported in Mr North’s article and that there seemed to be some dispute as to whether the alleged improvement in the condition of the animal was able to be sustained through the administration of the treatment. Mr North sent me a copy of Mr Wilesmith’s letter. My reaction to Mr Wilesmith’s letter was that of course I could not sustain the remission because I had not been permitted to complete the therapeutic course.

 

11. Brainstorm (RBSE 93/14947)

In April 1993 it appeared to me that "Brainstorm", my two and a half year old Jersey cow, had contracted BSE from its mother, "Churnside Birthday" who had suffered from the disease (see paragraph 8 above) and not from feed containing contaminated protein. "Brainstorm" was born after the 1988 ban on using ruminant protein in feed for other ruminants. The animal was fed exclusively on organic feed and yet had all the signs of BSE. Its only link with the disease was that its mother had it. The Government vet visited my farm on three occasions. On the first occasion the vet placed a Form A Order on the cow. The vet and I had observed symptoms of myoclonus and nystagmus, tremors under the skin, hypersensitivity to touch and sound, fear of entering the milking parlour, weight loss, a vacant expression etc. I started treating with magnesium sulphate in the hope of remitting the symptoms. On 10 May the Government vet revisited my farm and in her view "Brainstorm" no longer exhibited the symptoms suggestible of BSE and, in consequence, withdrew the movement restrictions placed on my cow. The veterinary officer said that the cow did not appear to be totally healthy and suggested that my vet should examine it. "Brainstorm" continued to live and milk on the farm until she was slaughtered in the conventional way in the autumn of 1996.

 

12. 1993: correspondence with the Ministry

 

I continued to write letters about my theory. I wrote to Mr King, my member of Parliament, who in turn on 5 April 1993 wrote to Mr Gummer, the Minister. Mr Gummer’s reply on 16 April reiterated the Ministry’s view that "detailed studies of the epidemic of bovine spongiform encephalopathy (BSE) in cattle have not shown any connection between the use of such chemicals, either in a primary or contributory role, and the incidence of this disease. That this disease has been spread by the use of infected feed, the hypothesis on which the disease control policy is based, has been substantiated by analytical epidemiological studies and by the effects now seen on the incidence of disease in the younger age groups of cattle." I did not accept this view and wrote again to Mr King who forwarded my letter and enclosures to Mrs Shepherd, who was now the Minister of Agriculture. On 16 June Mrs Shepherd replied to Mr King saying that she was advised that OP poisoning differs so greatly from BSE that the link was most unlikely. Nevertheless by August 1993 Mrs Shepherd asked for all MAFF studies on OPs, including flea collars used on cats and dogs as well as on cattle and sheep, so that she could make up her own mind on their safety. Mr Wilesmith of the CVL also told me that their extensive investigations had covered my theory but the Ministry admitted that they had not done detailed studies of delayed effects of cumulative low-dose OP toxicity (Western Morning News 20 August 1993).

13. Meeting with the Government’s scientific advisers on 13 January 1994

Following a further letter which I sent to Mr King MP which he forwarded to Mrs Shepherd, she replied on 17 September suggesting that I should meet her scientific advisers. This would enable me to fully explain my views and the advisers in turn could raise any points which they might have for me to consider. I sent Mr King a pre-publication copy of a paper on BSE, which I had prepared for the Journal of Nutritional Medicine. I sent the paper on an "In Confidence" basis. Mr King forwarded my paper to Mrs Shepherd who replied on 14 October that my paper covered a lot of ground and that the Ministry needed to consider it carefully. In the period before the meeting I became extremely concerned that the Ministry had breached the confidentiality of my paper. The Ministry had complained to the Press Complaints Commission about articles by Mr Christopher Booker in the Sunday Telegraph which had supported my theories on BSE and which had criticised MAFF staff. The Ministry included an evaluation of my theories and they included an extract of the paper, which I had sent to the Minister. Mrs Shepherd wrote to Mr King MP about this on 13 December 1993 and in the circumstances said that they did not regard what they had done as a breach of confidence. I did not accept this understanding of the situation.

14. My brother attended the meeting at CVL on 17 January 1994 with me. For the Ministry there were the following representatives – Messrs Bradley, Wilesmith, Livesey, Austin, Jackman (CVL), Dr Woodward (Veterinary Medicines Directorate), Ms Lamb (Pesticides Safety Directorate), Dr Marrs (Dept of Health) and Dr Hope (AFRC Neuropathogenesis Unit, Edinburgh). At the meeting the officials promised a longer look at my theory that OPs had caused BSE, but they ruled out scientists carrying out research into my theory. They seemed interested in my theory as far as it related to pesticide contaminated citrus pulp and cereal by-products but seemed less interested in the links between BSE and OP sheep dips and warble fly. We all agreed however that the disease was slowly dying out. The officials said this was because the scrapie-contaminated food was banned in 1988. I said that in my case this was because particular pesticides were withdrawn or naturally phased out (e.g. virtual eradication of the warble fly) at the end of the 1980s. Mr Eddy of MAFF promised my brother and I a tape of the meeting. He never sent a tape so I was unable to demonstrate MAFF’s failure to address at a later date some of what I had said and requested at the meeting, although at the time I had been encouraged by the seemingly open approach of most of those present at the meeting.

15. I wrote letters on 28 January and 6 February 1994 to Mr Eddy at MAFF following up the meeting on 17 January. He replied on 2 June. He said that the idea, which I mentioned in my letters of in vitro experiments, was interesting but there was no obvious model system to do such experiments. He also said that I did not have any unique or particular chemical from the OP family, which could be used at the present time to do those experiments. In respect of citrus pulp, Mr Eddy said that if the OP content of citrus pulp was responsible for the initiation of BSE it is very unlikely that BSE would have occurred only in the UK. This was because citrus pulp was an imported feeding stuff, which would be used in other countries as well. I found such statements as "there is no evidence that well preserved, uncontaminated pulp is toxic to ruminants" as a seemingly deliberate misrepresentation of my concern over OP contaminated pulp. Being disappointed by this response, I wrote to Mr Waldegrave, who was by then the Minister of Agriculture on 8 July. I said that "if we were going to get to the root cause of the BSE epidemic, thus preventing further all round catastrophe to our livestock industry and possible threat to public health, then it is utterly essential that truly "independent" scientists are consulted immediately and the entrenched "mindset" of MAFF’s political officials questioned". I said (page 2 of my letter) that there were three or four likely candidate chemicals which could be introduced "in vitro" to the prion protein at a range of low dose rates. As for citrus pulp, I said that I thought that I had made it clear that it was the OP contamination element of citrus pulp that was the mainstay of my reasoning. The whole point was that pulp samples had repeatedly revealed significant residues of both pesticide and carvone contamination together and in real life UK dairy herds had been consuming ever increasing quantities of pulp since the early 1980s (page 4 of my letter). On 28 September 1994 Mr Dixon replied on behalf of the Minister. He said that the epidemiological evidence of the BSE epidemic still supported the feed borne hypothesis for the origin and recycling of the infection. He also said that in respect of the use of citrus pulp, there was no evidence of a link between the incidence of BSE and the use of this feed. I wrote further letters on 15 and 27 October. In his reply dated 10 November 1994, Mr Dixon argued that I was not fair to suggest that the Ministry had not considered my theory in a scientifically objective light, but from a politically orientated mind set standpoint. He denied that the Ministry had a completely closed mind on my theory. I wrote a further letter to Mr Dixon on 15 November. Mrs Gurnhill replied on behalf of the Ministry on 1 December and said that there was nothing to be gained by repeating statements of fact, which I disputed. My reaction was to question MAFF’s insistence that everything that they said was fact. I had evidence to show that some of what they were saying was inaccurate.

 

16. 1994 –other events

 

My peer-reviewed articles were published in the Journal of Nutritional Medicine in March 1994, J Nutr Med; 4: 43-82. On 16 June I delivered a paper to the British College of Allergy and Environmental Medicine at a symposium at the Royal College of Physicians in London. I questioned whether contaminated feed was responsible for the BSE epidemic. I said that some 15,000 cattle which never received contaminated feed because they were born after the ban on feed made from animal components had been diagnosed with BSE. In addition some 9,500 of almost 10,000 BSE cases born after the feed ban ("BABS") were from dams who never showed symptoms of the disease. This ruled out the possibility that most BABS cases were due to maternal transmission. I went on to argue that exposure to OP chemicals was responsible for triggering BSE in the UK. The pesticides could disrupt normal protein production, leading to the formation of mutant protein, which causes BSE. I wrote to Mr Wilesmith on 1 December 1994. I referred to a letter from Professor Satoshi Ishikawa, the Dean of the Medical School of Kitasato University, Japan, dated 22 December 1992 who had said that he felt that my "description of mad cows and warble fly to organophosphates compounds is exactly true". Mr Wilesmith replied on 19 December 1994. Mr Wilesmith argued that I was being misled on the pathology. He suggested that it was strange that there had not been a plethora of papers describing the histopathological changes associated with the TSEs as similar to OP poisoning, chronic or otherwise. I thought that it was interesting that MAFF had now admitted the existence of chronic OP poisoning, a phenomenon that they had already dismissed as illusory beforehand. I was not surprised that they were trying to break down the pathological correlation that Professor Ishikawa had raised in his letter. Professor Ishikawa cites that specific neurons are vacuolated in OP chronic poisoning. These were the same neurons, which Wells et al also cited as vacuolated in their first paper on BSE pathology.

17. On 10 December 1994, the Daily Telegraph published an article by Peter Bunyan, the chief scientific adviser to MAFF. He based his arguments on many inaccurate accusations levied at my theory, namely that no OPs were used on Guernsey and that organic farms did not record the history of chemical usage and nutrition. When criticising the positive effects of my drug therapy on BSE suffering cows, he omitted to say that MAFF had already placed a Form A notice on a cow before its recovery. I complained to the Press Complaints Commission about the article but never received a satisfactory response from MAFF.

 

18. 1995

 

Medical Hypotheses accepted for publication two articles, which I wrote on the BSE epidemic. On 4 April 1995 I submitted a memorandum to the House of Commons Agriculture Committee hearings on the efficiency and effectiveness of pesticide licensing in the UK. In my memorandum I argued that the links postulated between chronic low-level chemical toxicity and various neuro/psychodegenerative syndromes, which included BSE, had to be attended to forthwith. Mr Waldegrave, the Minister, wrote to Mr King on 5 June about my theories and made erroneous statements such as "OPs are not used in Guernsey".

 

19. Research by the MRC

 

Lauderdale Productions, an independent television company, was contracted by Channel 4 to make a documentary about the OP perspective related to BSE. They contacted Dr David Ray, of the Medical Research Council at Leicester, who had just professed an interest in my theory and had invited me to lecture to his Department at the University of Leicester. The Television Company commissioned Dr Ray to test my theory experimentally. David Ray was aware that my theory homed in on the particular OP, Phosmet. Nevertheless the Television Company and the MRC agreed to conduct tests with a chemical that was conveniently available called DFP. DFP is a markedly different type of OP to Phosmet, which is not used on farms. Reluctantly I agreed to this compromise test but on the basis that the oxone metabolite of DFP, the metabolite common also to Phosmet, was used. As the process of the tests was kept secret from me so that the film would contain a surprise element, I was surprised to learn that the oxone metabolite had never in fact been used in the trial. I was aware from the start that recombinant prion protein without a glycolipid anchor was employed. This however weakened the relevance of this trial to duplication of the effects of this chemical in the real world, because I considered that the glycolipid anchor could play a major role in any interaction between OPs and prion protein and their putative role in triggering BSE. When the MRC received the results, they discarded a minute amount of dose proportional binding of DFP to the prion protein, as mere contamination of the protein with an impurity. I was surprised that despite this no tests had been carried out to ascertain any possible protease resistance of the prion protein, even though this was an agreed criterion of the original proposal. When Channel 4 came to pay for this work, I understand that the MRC replied that the work had already been paid for. They did not state who had paid but they did say, "MAFF owned the work".

20. Mrs Browning, the junior Minister at MAFF, wrote a letter to the Daily Mail in November 1995 in which she claimed that my theory on OP initiation of the BSE epidemic had been researched and could not be substantiated. She also gave a written answer to a Parliamentary Question on 19 December 1995 in which she said that government scientists had concluded that my ideas were unsubstantiated as they failed to explain a number of key facts about the disease. She said that the MRC test had found no evidence that OPs bind to the BSE prion protein. She also said that SEAC had not found any evidence in support of my theory.

21. I wrote to Mrs Browning in November 1995 protesting about her letter to the Daily Mail. I wrote to the Minister again on 3 January 1996 informing her that to date I was not aware of any actual government research that has challenged my hypothesis, except for their "hi-jacking" of the research that was originally initiated by Channel 4 TV and the MRC Toxicology Unit. I received a reply from Mrs Browning’s Private Secretary dated 1 February 1996 in which she said that my scientific theory was not tenable. My reaction was predictable. Mr Hogg, who was by then the Minister of Agriculture, wrote a letter to Mr King on 9 January 1996, commenting on Mr King’s letter of 4 December 1995 which enclosed a letter from me. Mr Hogg said that in the light of the MRC research it would not be appropriate or justifiable to use public funds to carry out further research to test my ideas.

 

 

22. My activities since March 1996

I have continued to press the case for my theory since March 1996 in lectures, the media, in correspondence and meetings. Further inaccuracies still emanated from the Ministry. One example was a letter in August or September 1996 from Mr Hogg to Mr King (quoted in Mr King’s letter to me of 24 September 1996) where the Minister stated that MAFF had evidence from the authorities in Switzerland that Phosmet was not used in that country. Switzerland had witnessed 250 odd cases of endemic BSE in its cattle herd.

23. My meeting with SEAC

Prior to February 1997, Lord Lucas, the MAFF spokesman in the House of Lords, gave a written answer to a question from Lord Lester in which he said that the Government had asked SEAC to re-examine my theory. He also indicated that the Government was aware of new research from the Institute of Psychiatry into the effects of Phosmet on prion protein cell cultures. The research in question consisted of experiments commissioned by myself and funded by well-wishers. I was angry that Lord Lucas had erroneously stated that the basis of the OP hypothesis had not been published in peer-reviewed journals, despite the fact that Mrs Gurnhill of MAFF in a letter dated 7 February 1995 acknowledged that one of my articles was peer-reviewed.

24. I was invited to attend the 41st meeting of SEAC, which was held on 15 April 1997 at MAFF, Tolworth. Also present were Sir Colin Berry, Professor Ian Shaw, Professor Tony Dayan, Professor Ian Aitken, Professor Quentin McKellar, Dr Chris Powell from the Veterinary Products Committee, Mr Horton of the Veterinary Medicines Directorate and Dr Tim Marrs of the Department of Health. After the discussion SEAC asked Sir Colin Berry and Professor Shaw to assess my theory on paper. On the basis of their findings, SEAC would decide whether to advise the Government to fund research into my theory. I was concerned that Sir Colin Berry and Professor Shaw were members of the Government’s Advisory Committee on Pesticides. Would they be able to act impartially? I felt that their response (SEAC 44/1) was toxicologically na´ve and full of inaccuracies and misrepresentations of what I had actually said. For instance, they used data solely from the manufacturers of Phosmet. On the basis of this data, they argued that Phosmet would only contaminate the fat of treated animals and would not get into the liver, kidney and muscles. On the basis of this, they argued that Phosmet would not get inside cells. They said that Phosmet would not make contact with prion protein and therefore interact with it. Thus they argued that Phosmet would be unlikely to play a role in the causation of BSE. However, in counter evidence I presented data from peer-reviewed published articles by several teams who had carried out experiments with Phosmet. The articles demonstrated that Phosmet does penetrate liver, kidney and muscles, at twice the intensity that it penetrates the fat. Yet the SEAC conclusions took Sir Colin’s and Professor Shaw’s evidence from the manufacturers as gospel and completely ignored my evidence.

25. Along with other grievances that I had about SEAC’s conclusions on the meeting, I was amazed that they never even considered the findings of the Institute of Psychiatry, which was the prime motivating factor for the SEAC hearing in Lord Lucas’s statement. I was also aggrieved that SEAC said that there was no evidence that OPs were involved in causation of nv CJD, when I pointed out that no studies by the CJD Surveillance Unit had ever been carried out to investigate this possibility.

 

 

 

 

 

 

 

 

Issued on behalf of the witness by:

The BSE Inquiry

Press Office

6th Floor Hercules House

Hercules Road

London SE1 7DU

Tel: 0171 261 8383 / 8385 / 8377

Fax: 0171 803 0893

Website: http://www.bse.org.uk

email: press.office@bse.org.uk