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La strana storia di Mark Purdey e la mucca pazza

Sin dal 1988, Mark Purdey, un allevatore del Somerset, ha sostenuto l'ipotesi che gli scienziati non abbiano studiato a fondo le cause della BSE. Autodidatta e senza finanziatori ha indagato sui complessi meccanismi biochimici del cervello, arrivando a pubblicare un rivoluzionario e documentato studio su un'autorevole rivista medica, ottenendone però soltanto attacchi, verbali e fisici. Lo studio di Purdey inizia con l'esame delle funzioni dei prioni, le proteine cerebrali la cui alterazione sembra essere responsabile della BSE. I prioni hanno il compito di proteggere il cervello dalle proprietà ossidanti di alcune sostanze chimiche attivate da agenti esterni come i raggi ultravioletti. La sua ipotesi è che quando i prioni sono esposti a una carenza di rame e un eccesso di manganese, il manganese prende il posto del rame cui normalmente il prione si lega. In tal modo, la proteina perde la propria funzione. La prima insorgenza della BSE in Gran Bretagna, ricorda Purdey, si ebbe negli anni '80, quando il Ministero dell'Agricoltura impose a tutti gli allevatori il trattamento degli animali con un pesticida a base di organofosfati chiamato Phosmet, impiegato a dosi molto più alte che nel resto del mondo. Il pesticida veniva versato lungo la colonna vertebrale degli animali. La ricerca di Purdey mostra che il Phosmet cattura il rame. In quegli stessi anni il mangime degli animali veniva arricchito con sterco di polli proveniente da allevamenti dove gli animali erano nutriti con manganese per aumentare la quantità di uova prodotte. I prioni contenuti nel cervello dei bovini, in tal modo, venivano contemporaneamente privati di rame e intossicati dal manganese. In Francia, l'impiego del Phosmet divenne obbligatorio inizialmente in Bretagna. 20 dei 28 casi di BSE vennero alla luce proprio in quella regione. Sempre secondo le ricerche di Purdey, la diffusione della malattia coincide con quella del pesticida. Un analogo tipo di avvelenamento potrebbe spiegare la distribuzione della versione umana della malattia. Dei due principali ceppi di vCJD in Gran Bretagna, uno, nel Kent si trova nel pieno di un'area con coltivazioni nelle quali vengono usate ingenti quantità di fungicidi a base di organofosfati e manganese. L'altro ceppo è a Queniborough, nel Leicestershire, dove una fabbrica di vernici (distrutta da un incendio alcuni anni fa, con grave inquinamento chimico sul paese) ha per anni riversato parte degli scarti di lavorazione nel sistema di canalizzazioni usate per irrigare i campi. Nella produzione di vernici viene usato il manganese. Ma Purdey non si è limitato a queste indagini, andando a verificare sul campo la propria teoria sui ceppi di BSE e CJD in Islanda, Colorado, Slovacchia e Sardegna. Ovunque vi siano ceppi di queste malattie, egli ha riscontrato esposizione degli animali e degli esseri umani a carenze di rame e eccessi di manganese. La maggioranza dei ceppi, inoltre, si trovano in aree montane, nelle quali i livelli di luce ultravioletta sono alti. Ma la prova più concreta a sostegno della sua ipotesi viene da uno studio pubblicato da un'équipe di biochimici all'università di Cambridge quest'anno. Essi hanno scoperto che quando il rame viene sostituito dal manganese nei prioni, i prioni adottano precisamente i comportamenti che identificano l'agente infettivo della BSE.

Articoli correlati 

 Siti correlati 

• The French cases of BSE may not have been spread from Britain
  

• On May 5, 1996, I conducted a long distance telephone interview with Mark Purdey of Somerset, England.
  

• Introduction to the Purdey hypothesis on Spongiform Encephalopathy (SE)
  

• The BSE Inquiry . original interview to Mr. Mark Purdey
  

• The "Bse Inquiry" - Supplementary statement by Mark Purdey

• The Organophosphate-BSE Hypothesis
  and CJD
  
• Properties of Organophospates.
  
• Mad cows, Bretons and manganese Guardian - Thursday November 23, 2000
  
• ALTERNATE HYPOTHESES FOR THE ORIGIN OF BSE

THE BSE INQUIRY

DAY 16 - Thursday 2 April 1998 (9.30 am)

Mr. Mark Purdey
Organic farmer.
======================================

MR WALKER: This morning Mr Purdey is here. He has furnished this Inquiry with a statement. I would like to confirm that this is indeed the statement that you supplied?
MR PURDEY: Yes.
MR WALKER: Mr Purdey would like to begin this morning by speaking a bit about his theories. He thinks that might take a maximum of 20 minutes. I have said to him that would be absolutely fine by me, and I am sure it would be by the Committee. If he looks like going beyond 20 minutes, I might interject and ask him if he could draw it to a close because I will then want to start on the chronological account that he gives in his statement, so that we can get through today. Would that be acceptable, Mr Purdey?
MR PURDEY: Yes.
SIR NICHOLAS PHILLIPS: That is fine with us. Because you have a 20-minute time limit, do not talk twice as fast as you normally would in order to get it in, because these ladies are making a transcript as you go along.

MR PURDEY: Yes, organophosphates were basically the in vogue pesticide of the 1970s and 1980s. They are derived from very insidious roots in the natural world, where they were first identified as a natural ingredient in the Calabar bean, which was a bean used in West Africa in witchcraft trials for killing people in convulsive paralytic agony. It basically attacked the nerves. It is also found as an ingredient in snake and spider venom. It then got taken up synthetically for use initially as the military nerve gases, and then slightly less toxic versions of the chemical were used in agriculture, horticulture, the domestic environment, et cetera. There are many different times of OPs. Broadly, they are the systemic types. Those are ones that are fat-soluble in fat, and they pass through the skin and into the living organism, whether it is a plant or an animal. Then there are the non-systemic types that just remain on the surface of the treated crop or animal. All types of organophosphates have very, sort of, idiosyncratic properties. This is very important to sort of gauge, particularly in its possible relationship to BSE.
There are chronic effects which have different symptoms and markedly different pathology to the acute effects. They cause their toxic effect by actually deforming the conformational shape of certain brain proteins, notably acetyl cholinesterase. Once they are released in the environment, there are many environmental variables that dictate the way that they break down and how toxic they are in the environment. As a result, rarely, epidemics of neurodegenerative disease has surfaced as a result of organophosphate usage.
Mammals, such as humans, exhibit a varied individual susceptibility to the toxic effects of these chemicals. This is mainly based in the liver where each individual expresses different activities of enzymes that are capable of detoxifying these chemicals as they come into our bodies. Also, if somebody is undergoing current therapy with other chemicals, such as anti-depressants or the contraceptive pill, this makes you much more susceptible to low doses of organophosphates that you are exposed to.
Some OPs and other neurotoxic chemicals are well recognised to produce a delayed type of neurotoxic syndrome. This is largely based on the conformational change to another protein called neurotoxic esterase. I think these neurodegenerative syndromes, the cause of them exhibits a sort of multi-factorial aetiology. There is a template there where you can find the presence of a chemical trigger factor, a genetical susceptibility factor, perhaps a factor of stress, and maybe in time, some infectious agent. Looking at BSE, when it first came on the scene I was very sceptical of the official theory. Firstly, in the USA and Scandinavia, they rendered their meat and bonemeal in exactly the same way as was incriminated in Great Britain, yet they have not had a single case of BSE, despite scrapie going into the meat and bonemeal. 
British UK meat and bonemeal was sold all over the world, particularly to the Middle East, which received thousands of tons for its cattle population. Yet, according to vets I know who operate in the Middle East, in the large dairy herds there, they have not had a single case of BSE. There have been also 30,000 plus born-after-the-ban cases of BSE in cattle in this country. There have been also 300 cases of born-after-the-ban in Switzerland. This has been blamed conveniently on leakage of minute amounts of meat and bonemeal that have slipped over from pig and poultry rations where meat and bonemeal was still permitted.
But if it is leakage of small amounts, how come large amounts being exported to countries like the Middle East caused no cases in those countries? Various trials in the US have also injected different strains of scrapie agent into cattle, and it has failed to produce the disease. It has produced a neurodegenerative disease, but more akin to amyotrophic lateral sclerosis, which is a motor neurone disease.
There are also cases where some animals and entire farms were struck with BSE, yet had never been exposed to the feed. This suggests at the very least that meat and bonemeal cannot serve a single role as a cause of the disease. There must be some other phenomenon. It perhaps could indicate that meat and bonemeal is not involved at all.
I started looking at chemicals as a possible cause, and I suppose I had a hunch about it. So I had to look at what was unique to Great Britain, because in Great Britain we had had an epidemic of BSE. What was the unique factor? And I went to the cumulating medical indices, and I found a column entitled "Chemical-induced" under "spongiform encephalopathy". I became aware that various chemicals such as cuprizone, disulfuran, dithiocarbamates and some anti-depressant drugs after prolonged therapy had produced spongiform-encephalopathy-like diseases. Indeed, some cases in the literature of organophosphate poisoning have performed spongiform-encephalopathy-type disorders.
So I am proposing that chronic OP poisoning, as opposed to acute, underlies the cause of BSE, perhaps involving exposure to OPs at the vulnerable foetal stage, in the in-utero stage. That is an aspect that has not been officially looked at.
Looking at the biochemistry, either organophosphates have had some direct co-valant interaction with the prion protein -- I no longer think this is a possible cause -- or they have had an indirect OP interaction with the prion protein via some other disturbance to a protein which is sort of metabolically linked to the prion protein in the cell, or the organophosphate has increased susceptibility of the cell to attack from some external disease agent, perhaps an agent that is found in meat and bonemeal.
The mechanism, I think, is organophosphates are well recognised -- when they penetrate inside the central nerves -- they are well recognised to generate a free radical chain reaction. Free radicals are unpowered electrons that are highly reactive and can link on to certain sites on proteins and cause a whole myriad of effects such as aggregation of proteins, a phenomena that is found in prion disease.
But what organophosphate or groups of organophosphate were unique to the UK? This is what I had to get to the basis of. It seemed that in the warble fly eradication of the late 1970s, early 1980s, and up to the end of the 1980s, there was a type of organophosphate used called Phosmet that I homed into as a possible candidate for the cause of this disease.
It was started in 1975 in a small way. In the 1980s, it really increased in use, particularly in 1982 when the Warble Fly Order changed, and it became compulsory to treat twice a year instead of once a year. Then in 1985, the other type of low dose organophosphate called Fenthion was actually removed, or virtually, in effect, removed off the list of approved chemicals, and farmers had no choice but to use this phosmet variety.
Phosmet is particularly unique in that it is an organophosphate that contains a phthalimide moiety. That is a fraction of a chemical that hinges within the phthalimide group, that has quite different effects to organophosphates, although their effects are neurological.
What I identified with Great Britain, what was unique, was that we were using particularly high doses of phosmet, 20 milligrammes per kilogramme of body weight under the Warble Fly Order, with a repeat 14-day treatment twice a year, compulsory treatment, using a systemic formulation, that means a formulation that is designed to go through the skin and kill the warble fly inside the cow, instead of on the outside surface of the skin. I feel that exposure in early life, or perhaps in-utero of the cow, was perhaps an important facet.
And exposure has to be to a susceptible cow as well. That is one that is perhaps lacking a low level of the detoxification enzymes, the enzymes that are involved in degrading and detoxifying the chemical.
But I have to look at other countries, obviously, to try and stand this theory up. It turned out that very few countries licensed phosmet in its systemic formulation. The other countries that did were Southern Ireland, France and Switzerland and the Channel Islands, but they licensed it at a much lower dose and in a systemic formulation still. In France and Switzerland, the use was voluntary. In Southern Ireland, it was only compulsory for a very short period of time, from 1978 onwards, but as a once-a-year treatment, and there were two other types of lower dose organophosphates used at the same time. But phosmet was licensed in its systemic formulation also in Australia and New Zealand, which are BSE-free countries, supposedly. Obviously, I had to address this because this was a challenge to my theory.
When I started looking at the situation a bit further, I realised that because the chemical was systemic and therefore had to be fat-soluble to work -- that meant that when an animal was treated, the chemical combined into the fat of the cow -- so when you killed that cow after treatment, and then fed it back through meat and bonemeal, you would start to get a sort of bio-accumulating effect of the chemical.
It was a bit like revisiting the DDT disaster of the 1950s and 1960s, where DDT built up in the food chain as each animal ate back the remains of another animal which had been treated with a chemical.
Eventually, when you exceed a threshold level, a certain level of toxicity, then that would switch on, say, theoretically, BSE.
But in New Zealand and Australia, the chemical was only used at the lice dose rate, which is 10 milligrammes per kilogramme of body weight, and there was no repeat treatment. And also in Australia and New Zealand, farming is very extensive, and there was very little actual use of this chemical, plus the fact that they did not feedback meat and bonemeal. Even though meat and bonemeal was produced in these countries, it was largely exported to other continents for feeding.
So I think if one did an overall analysis of the total amount of use, then it would seem that New Zealand and Australia were exposed to a much lower dose of the phosmet chemical overall, whether it was via its direct pouron treatment or via the indirect route of contaminated feed, phosmet contaminated feed.
Other countries, like USA, had used phosmet as well, and Hungary, for instance. But they had used it in its non-systemic formulation, as a spray-on and a powder that was applied to the back of the cow to kill off lice and other ecto-parasites. So this chemical would not penetrate through the skin at a sufficient dose to get into the central nervous system, as the systemic version was designed to do. If you look at some of the other animals that have had problems with BSE, such as cats and deer, which have had a more, sort of, naturally occurring type of spongiform encephalopathy, you can also find the presence of use of organophosphate chemicals.
I have been investigating, in Colorado, the deer, where there is a unique cluster of the deer -- "chronic wasting disease" it is called. I have found evidence of phosmet use in alfalfa. This was being fed in the deer reservations where there were chronic wasting disease problems, and was being fed to some of the wild deer that were coming in and being fed and treated as pets by some of the Americans that lived up in the footholes of the Rockies.
Also, the deer were coming into contact with pesticides through -- because they spray along the rivers with types of organophosphates with a similar structure to phosmet for breaking the mosquito life cycle. They spray directly along the rivers from the air, et cetera.
I will just finish briefly by looking at new variant CJD as well. This could either be due to exposure to the same common environmental trigger factor as BSE, or most unlikely in my view, to ingestion of abnormal prion protein like contaminated beef. Although I think we would have to look at the possibility of if some vaccinations, for instance, had become contaminated with bovine material -- perhaps used deliberately -- we should look at that kind of area, where the material could have been injected into the animal.
I cannot understand how the prion, the abnormal protein, which is undegradable to all known enzymes, such as in the digestive tract, can cross the gut wall. Because if proteins are to be taken by the gut wall, they need to be broken down into amino acids to be taken across into the bloodstream. But, of course, one has to weigh up there might be some leakage of this protein, the abnormal protein, through these Peyer's patches, or if someone has a worm infection, or had gastro-surgery, perhaps ulcers, Crohn's disease, these may increase susceptibility to intake of the abnormal prion through the gut wall. But there is a unique pathology of new variant CJD and BSE that is characterised by a specific prion protein glycoform pattern which could merely reflect the way that glycoproteins, such as prion protein, are recognised to glycosylate more intensively in younger people and younger mammals. So when someone is young, the prion protein glycosylates in a very intensive manner, but when you get older -- so it does not glycosylate so intensively.
So what we might be seeing here is some incidental factor with this unique pathology, which is merely a reflection of immature mammalian development, which you would expect in people whether they have the disease or not. So it may be irrelevant to the disease process, et cetera.
Perhaps this explains also why new variant CJD has not, as far as I know, occurred in the elderly. But OPs should be explored in the role of new variant CJD because it seems to be that the people who work with pets or with farm animals are the people who are going own with the disease.
SEAC have regularly cited that it is people in these occupational groups, who work with pets or farm animals, that are most susceptible to CJD. It is they who would be occupationally exposed to systemic organophosphates which are used on cats, dogs and on farm animals. Aspects such as head lice shampoos that contain -- some of them contain organophosphates; aspects such as hallucinogenic drugs should be looked at, that mimic and duplicate some of the bio-chemical effects of organophosphates; anti-depressants -- prolonged therapy on anti-depressants has produced CJD-like-disease syndromes, and this should be looked at; the intensive amount of organophosphates in vegetables.
There have also been clusters occurring of CJD at Tucson in Arizona, where there were five cases in a missile-producing factory. Interestingly, in missiles, they use cuprizone, which is a missile propellant that fuels the rockets. It was this chemical that was used in the Compton Laboratories deliberately to switch on scrapie disease in mice.
There have also been five cases of the new variant occurring in a select area of Kent, although it seems that the CJD Surveillance Unit would not agree on this. And there is also one of the other CJD new variant cases who used to visit the area regularly. Kent is an area that is virtually unique in growing hops and top fruit. On hops and top fruit, according to the Ministry of Agriculture statistics, there are a hundred times more systemic organophosphates sprayed on these crops than there are on cereal and grassland that is grown generally over all the other areas of the UK.
So people that are living in the hamlets and villages where it seems this new variant CJD occurs, they are going to be exposed to the spray drift of these repeated applications of systemic organophosphates. So when spraying goes on in the valleys, it kind of basins -- the contaminated air basins out in the valleys. Also there was a big leak from an organophosphate factory at Yealding on 17th April --

SIR NICHOLAS PHILLIPS: Could I interrupt you for two reasons, 
(a) because you have overshot your time, and
(b) because I think you are now repeating a matter which you have already given to us in your latest --

MR PURDEY: Yes, I was finishing really. Basically, I think the slaughter policy was a mistake because they failed to eradicate other forms of this disease, scrapie, off Iceland, where they slaughtered all the sheep and chronic wasting disease in deer, where they slaughtered whole deer reservations and the disease still came back. This suggests, all of this, the presence of an environmental factor in the cause of this disease.

MR WALKER: Thank you very much. I am going to take my jacket off. I hope you will feel free to do the same. What I would like to do at the start of my questions is something which I do with all our witnesses, to explain the distinction between Phase 1 and Phase 2 of the Inquiry. I think you have been sent some material about this. I want to recap it because it is very important that people understand it. 
Phase 1 of the Inquiry involves establishing and reviewing the facts. That is the phase that we are in at the moment. It will take us some time to review the facts with a number of witnesses during the course of this year. At the beginning of next year, we plan to reach Phase 2. 
The Committee have called Phase 2 "Clarification, conflict of evidence and potential criticisms". So it is very important that all witnesses understand that Phase 1 is not about any criticisms of the witnesses. If there are any potential criticisms for witnesses to deal with, then there will be a letter sent out towards the end of this year and people will be asked for their response. But that is a long way down the line.
Today I am just going to be asking you questions about what you did at the time, what you said at the time, and your reasons. I might also ask you whether you think something could have been approached differently, and if it had, what the effect of approaching it differently would have been. But neither I nor the Committee today will be making any criticisms of you at all, either explicit or implicit, in our questions. That is not what we are seeking to do. If I ask a question, or a member of the Committee asks a question, and you think that involves some suggestion of criticism of you, whether explicit or implicit, any question that you should have done something differently rather than could have done something differently, I want you to tell us, then we can stop and make sure we are sticking to the purpose of today, which is simply to establish and review the facts. Is that acceptable to you?
MR PURDEY: That is fine, yes.
MR WALKER: One other general thing. In my questions today, I am going be asking you to try to put yourself back in the position you were at the time in question.
MR PURDEY: Yes.
MR WALKER: That means not using hindsight. It is very difficult to do it, but I want you to try as much as you can to tell the Committee what was in your mind at the time. Just occasionally, I might ask you to look back with hindsight. If I want you to do that, I will say so. Unless I say so, please tell the Committee how you saw thing as at the time in question.
MR PURDEY: All right.
MR WALKER: Thank you. You have very kindly taken a lot of trouble to work through the history of events in a chronological order, which is the order that is most helpful to us. That is the order that I am going to follow in my questions to you. The first thing that you have done in your statement, after some introductory material, is to tell the Committee something about the Warble Fly Order, in particular the Warble Fly Order of 1982. And you had some concern about a suggestion that you should be obliged to use particular pesticides in accordance with what the Ministry said were the requirements of the Order.
You have referred, in paragraph 3 of your statement, to some correspondence. You wrote several letters, among others to the Prime Minister and the Minister of Agriculture. I do not believe that we have been able to find the actual letters that you wrote to the Prime Minister or to the Minister of Agriculture.
We have found a reply, and I would like to take you to that.

=====start original file=====
1 If we could have the year book for 1985,
2 YB 85/1.25/1.1. I think it is the fourth page after
3 divider 1. This is a letter dated 25th January 1988
4 from Mr A J Lawrence, who is in the Ministry of
5 Agriculture at their Tolworth Office, writing to you.
6 Do you remember receiving this letter?
7 MR PURDEY: Oh yes, yes.
8 MR WALKER: He refers to the letters that you had written.
9 In the second paragraph, he says that he thought it
10 would help if he explained briefly about the measures
11 taken to try to eradicate warble fly.
12 MR PURDEY: Yes.
13 MR WALKER: In the third paragraph, he told us that the
14 campaign began in the autumn of 1978, relying initially
15 on compulsory treatment of affected animals in the
16 spring, with voluntary treatment of all susceptible
17 cattle in the autumn.
18 MR PURDEY: Yes.
19 MR WALKER: Then things moved on in 1981. Compulsory
20 treatment on all cattle where infestation was known to
21 occur was introduced. Then, in March 1982, measures
22 were introduced under which warble fly was made a
23 notifiable disease, and compulsory spring treatment of
24 the whole herd on the infected premise was applied and
25 followed by the compulsory treatment of the whole herd
Day 16
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1 again in the autumn. I think this is the twice-yearly
2 compulsory treatment you described just now.
3 MR PURDEY: Yes.
4 MR WALKER: Then he goes on about the effectiveness of the
5 campaign, and proposed a yet further development. He
6 says:
7 "Further measures were introduced last year [1984]
8 which provided for infected areas to be imposed [I think
9 he means 'designated'] when disease problems arise in
10 specific areas of England and Wales."
11 He goes on to say once there had been such a
12 designation, stringent rules were applied within them,
13 including the compulsory treatment of cattle. A number
14 of such areas have recently been designated in the Wales
15 and the south-west, he says.
16 As I understand it, it went beyond a particular
17 farm. If you were in a particular area, there was an
18 obligation, according to the Ministry, to apply these
19 pesticides?
20 MR PURDEY: Yes, originally it was often whole counties in
21 the early stages of the disease, then it was narrowed
22 down to 3-kilometre zones around each farm towards the
23 end of the 1980s.
24 MR WALKER: Then he goes on to explain about the sort of
25 treatments that are involved. He says:
Day 16
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1 "Cattle are treated systemically for warble fly
2 using approved liquid 'pouron' dressings, in the main
3 prepared from organophosphorous compounds, although
4 there is an injectable solution with the trade name
5 'Ivomec', which is prepared from a naturally occurring
6 organism. These preparations kill larvae at any stage
7 of their migration through the host animal. Derris, on
8 the other hand, is a contact insecticide and is only
9 effective when applied directly into the hole which the
10 warble larvae makes through the skin ..."
11 Derris, am I right in thinking this was the
12 non-organophosphate treatment you had been using on your
13 cattle?
14 MR PURDEY: Yes, it is a powder that you just apply to
15 cattle that are infected with the disease only. As the
16 warble bursts out from under the skin, in the spring you
17 have to rub the paste -- you mix up a paste and you rub
18 it into the warble fly larva. If you do it diligently
19 it kills it, it is effective. This was approved by the
20 Ministry, I believe, up until 1982.
21 MR WALKER: Certainly what Mr Lawrence is quite clearly
22 saying in this letter is that Derris was unacceptable to
23 the Ministry by January 1985?
24 MR PURDEY: Hmm, hmm.
25 PROFESSOR FERGUSON-SMITH: Can I interject and ask about
Day 16
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1 ivermectin, did you use that as well or --
2 MR PURDEY: Well ivermectin was not permitted in dairy
3 cows. Well, it was permitted in dairy cows, but you --
4 PROFESSOR FERGUSON-SMITH: But you could not use the milk
5 for quite some time?
6 MR PURDEY: 28 days. So effectively that gave the general
7 rule that beef cattle could get ivermectin, whereas
8 dairy cows had to be treated with organophosphates to
9 avoid throwing milk away.
10 PROFESSOR FERGUSON-SMITH: So you did not use that. It is
11 widely used for all sorts of parasites?
12 MR PURDEY: Yes, lice and ...
13 MR WALKER: Could you tell me a little bit more about the
14 ivermectin? In this letter, what Mr Lawrence is saying,
15 as I understand it, is that it is not obligatory to use
16 an organophosphate compound in the sense that it is
17 possible to use Ivomec, an injectable solution prepared
18 from a naturally occurring organism. I would like to
19 clarify the answers you were giving Professor
20 Ferguson-Smith. Had you used Ivomec in the past?
21 MR PURDEY: No I had never used it, no -- I had always used
22 Derris. I had no warble problem in the year that I was
23 forced to treat -- it was a sort of prophylactic
24 measure, that formal basis of some of my ...
25 MR WALKER: Tell me if you are not able to say this, but at
Day 16
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1 this time, in the mid 1980s, did you have any idea of
2 how many other farmers were using Ivomec?
3 MR PURDEY: Basically, it was only the beef suckler farmers
4 with beef herds that were not selling milk that were
5 using it, because it was convenient. It did not have
6 the taboo attached to organophosphates that had
7 circulated in the farming community, because we knew
8 that sometimes cows would die after treatment with
9 organophosphate compound. So it was a dirty word,
10 really, in the farming industry at that time.
11 MR WALKER: Now, the remainder of this letter goes on to
12 talk about different aspects of Derris, and then to
13 refer to the licensing requirements of the Medicines
14 Act, and the question of the sale of milk following
15 application of systemic dressing. The conclusion is:
16 "Whilst it is true that organophosphorous
17 compounds are used widely, there is no evidence that
18 repeated exposure is rendering the human and animal
19 population more subject to cholinesterase depression on
20 this account. Neither is there any indication that the
21 organophosphates at present in use, having been
22 previously tested for this facility, are responsible for
23 chronic, psychiatric or neurological disturbances."
24 Then he closed the letter.
25 Is there anything more you would like to say about
Day 16
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1 that particular letter?
2 MR PURDEY: I suppose that last statement was in answer to
3 me, my fears that I expressed to him that it could cause
4 neurodegenerative disease both in the cattle that were
5 being treated and perhaps in the human operator, because
6 I was aware of a few cases where farmers had
7 accidentally splashed themselves, where they had
8 developed neurological systems as a result, though there
9 were not many at that time. You know, I suppose it was
10 the early days of the widespread organophosphate use on
11 farms.
12 MR WALKER: There was another letter sent to you from the
13 Ministry of Agriculture.
14 SIR NICHOLAS PHILLIPS: Just before we go to that, could
15 you in a few words educate us about the warble fly, how
16 its cycle goes, where the larvae migrate, and what
17 happens to cattle if you do not treat it?
18 MR PURDEY: Yes. The warble fly has an annual life cycle
19 where it spends about 11 months inside the cow. The
20 life cycle starts where the fly bursts out the back of
21 the cow -- it is a rather grotesque-looking organism,
22 you know, creepy, and it bursts out through the hole on
23 the hide, on the back of a cow, and then goes on the
24 wing and will fly after the cattle herds. There used to
25 be -- when warble flies were around, cattle used to go
Day 16
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1 into a frenzy. They would hear this buzzing noise -- it
2 had a very characteristic sound -- and they would charge
3 across the field with their tails up in the air. It was
4 always the weakly cow that would be struck by the warble
5 fly, because it would manage to catch up with it. It
6 would settle just above the hoof, on the leg, and inject
7 eggs under the skin. Those eggs would then hatch and
8 they would migrate up through the cow.
9 I mean, it was a pretty nasty parasite and I was
10 behind an eradication campaign, but using Derris of
11 course. I suppose the motives for the campaign were
12 because it was damaging the leather by bursting up
13 through the skin on the back. The leather did not have
14 any value after that. That was the motive behind the
15 campaign, plus a welfare issue to cows.
16 MR WALKER: I was going to take you on, unless there was
17 anything more on this letter from Mr Lawrence, to the
18 letter you received from Mr Rees, the Chief Veterinary
19 Officer. We have it just a few pages on at YB
20 85/2.04/2.1. After the divider 2, I think it is the
21 second page. Is that it there?
22 MR PURDEY: Yes.
23 MR WALKER: This is a letter dated 4th February 1985 from
24 Mr Rees, who was then the Chief Veterinary Officer,
25 again at Tolworth. Do you remember receiving this
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1 letter?
2 MR PURDEY: Yes, I do.
3 MR WALKER: And he writes to you:
4 "I am writing in reply to your letter of
5 28th December to the Director General of ADAS, Professor
6 Bell ..."
7 ADAS, of course is the Ministry of Agriculture's
8 Agricultural Development and Advisory Service.
9 "... and to your various letters to Mr Scudamore,
10 at Taunton, and Mr Stephens, director of the Central
11 Veterinary Laboratory at Weybridge."
12 He adds:
13 You will no doubt have heard from Mr Edward Du
14 Cann replying to the points you raised with him, which
15 to a considerable extent cover the same ground."
16 One thing I notice that Mr Rees seems to have left
17 out is Mr Lawrence's letter of 25th January. I suppose
18 with all that correspondence going around, he could be
19 forgiven for not picking up on that one.
20 Then he goes on to talk about treatments for
21 warble, and he refers to various reasons, why he says
22 that Derris would not be a viable alternative. The
23 letter then turns to the question of licensing,
24 referring to the independent technical experts on the
25 Veterinary Products Committee. Then, after that, it
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1 turns to the biochemistry of organophosphorous
2 compounds. He concludes by saying:
3 "The use of systemic pesticides is essential if
4 they are going to eradicate warble fly, and that is
5 reflected in the current legislation."
6 I do not think he refers to Ivomec. Am I right in
7 thinking that Ivomec is a systemic warblecide even
8 though it is not an organophosphorous compound?
9 MR PURDEY: Yes, it is. It is injectable -- well it was
10 injectable in those days. You injected it into the cow,
11 and then it circulated the blood and it worked just like
12 an organophosphate, but it had a different toxicological
13 mechanism of killing the warble bug. It worked on a
14 different area of the nerves.
15 MR WALKER: He concludes by says:
16 "I must urge you to reconsider your decision and
17 cooperate with MAFF in our agreed intent to eradicate
18 the parasite."
19 Did you reconsider your position?
20 MR PURDEY: Yes, I was not prepared to -- I mean, my wife
21 was in the early stages of pregnancy at that time. I
22 was aware of miscarriages being caused by people who had
23 been handling, and my wife was milking the cows. We had
24 to handle the cows on their backs which -- we had this
25 oil that you poured along which would stick on the back
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1 of the cow for often up to several days, before it
2 rained and washed it off. We had to handle the cows by
3 sort of banging them on the back to get them into the
4 cow shed -- a rather primitive system. So yes, I was
5 not really convinced that I should use this.
6 MR WALKER: Now, in paragraph 4 of your statement, you
7 describe how you came to seek leave to apply for
8 judicial review. Indeed, you were granted leave to
9 apply, as I understand it, before the matter came to be
10 argued in court, or perhaps on the day, I am not sure
11 which. You reached agreement with the Ministry?
12 MR PURDEY: There was a hearing, yes, and there was a sort
13 of compromise deal struck after the court hearing.
14 MR WALKER: Yes. As I understand it, the court hearing was
15 one where the court considers whether you have an
16 arguable case and the court held that you did have an
17 arguable case. As sometimes happens once the court has
18 said you have an arguable case, the Government then
19 decides perhaps they had better not take it all the way.
20 The agreement that you reached is described at the
21 end of paragraph 4. There seem to be two aspects to
22 it. One is that the dairy herd were exempted from
23 treatment, is that right?
24 MR PURDEY: Yes, the main dairy herd, yes, did not have to
25 be treated or anything.
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1 MR WALKER: You did not have to apply any insecticide to
2 them?
3 MR PURDEY: Yes.
4 MR WALKER: Then the 26 heifers, which you say had been
5 grazing in a compulsory warble fly zone, they had to be
6 treated with ivermectin?
7 MR PURDEY: Yes, that is right.
8 MR WALKER: This is the product we have just been
9 discussing?
10 MR PURDEY: Yes.
11 MR WALKER: And you agreed to that. Did you have concerns
12 that ivermectin might produce the same results as
13 organophosphate, in the sense of undesirable effects?
14 MR PURDEY: I was a bit concerned, but I did study the
15 literature on ivermectin and the area of the nerves that
16 it exerted its toxic effect. I was not so concerned
17 because I was aware that cholinesterase, which is one of
18 the targets with organophosphorous compounds has a very
19 crucial balancing effect on the nervous equilibrium, and
20 this got me very concerned because cholinesterase is
21 involved in all areas of the body, whether it is control
22 of the muscles, the glands, the psychiatric centres, et
23 cetera. It was a risk I just was not prepared to take.
24 MR WALKER: I would like to take you on now to the period
25 immediately following the article by Dr Wells and others
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1 in the Veterinary Record in October 1987, unless there
2 is anything else you would like to say about the period
3 up until then. Is that okay?
4 MR PURDEY: Yes.
5 MR WALKER: We can put away year book 1985. We need to take
6 out the year book for 1988. Right at the front of that
7 year book, just behind divider 1, I think we have a
8 photocopy of a letter that you wrote to the Farmers
9 Weekly.
10 MR PURDEY: Yes.
11 MR WALKER: Our reference is YB 88/1.08/1.1. In the
12 right-hand column there, is that a letter you sent to
13 the Farmers Weekly?
14 MR PURDEY: Yes, that is right, yes.
15 MR WALKER: At this time. It was published on 8th January.
16 You begin by referring to some criticisms, substantially
17 a letter from KJ Ellis about Farmers Weekly's own item
18 on BSE. We have not got the earlier articles, but I am
19 inferring from this that once the Veterinary Record had
20 been published, talking about bovine spongiform
21 encephalopathy, that generated some material in the
22 farming press?
23 MR PURDEY: Yes.
24 MR WALKER: You, in your letter, queried why Farmers Weekly
25 had dubbed a postulated link-up between
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1 organophosphorous exposure and this neurological
2 degenerative condition as "ill-informed
3 rumour-mongering". Who had postulated the link between
4 organophosphorous exposure and BSE?
5 MR PURDEY: Well, there was one journalist who had been in
6 contact with me during my warble fly high court battle,
7 and he phoned me up, and I told him about: this is what
8 I was expecting, an epidemic of neurological disease.
9 Then he writes part of a column on the front page -- one
10 of the front pages of the editorial column. He was just
11 putting an input in. He postulated this, as you know,
12 sort of scare-mongering. I naturally rose to that and
13 thought I would get the issue into the platform and get
14 it under debate by, you know, bringing it out in this
15 letter.
16 MR WALKER: It was actually you that postulated it?
17 MR PURDEY: Yes, it was me who postulated it.
18 MR WALKER: Then, in the article, you made some observations
19 about Farmers Weekly, and then went on to say that
20 plenty of research had been done into the known delayed
21 neurotoxic reaction inflicted upon genetically
22 susceptible organisms exposed to lower dosages of
23 certain organophosphates, and described some
24 similarities between those and the symptoms seen in BSE
25 cattle. In particular, you drew attention to the work
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1 of Cavanagh and Bouldin, who had observed vacuoles,
2 which they had described as unique to
3 organophospherous-induced neuropathy.
4 MR PURDEY: Yes.
5 MR WALKER: Then you went on:
6 "My own independent survey on some of the farms
7 inflicted with this crippling neurotoxicity have
8 revealed that warble fly liquids containing phosmet and
9 a band of feeding stuff compounded from
10 insecticide-treated raw materials are the common
11 denominators upon these farms."
12 Could you tell the Committee a little bit about
13 your own independent survey?
14 MR PURDEY: Yes, there were, in the early stages of BSE,
15 quite a lot of cases emerging in Devon where I was
16 farming at the time. Through my vets, I managed to
17 trace some of the farms where the first cases had arisen
18 in Devon. Obviously, I had to sort of tread carefully
19 because there was quite a lot of taboo already attached
20 to BSE. But I telephoned up just five of the farmers
21 who had had cases in the Devon area that I managed to
22 find out, and just questioned them about their
23 feedingstuff policies, and their usage of warble fly
24 within the lifetime of the cow. By "lifetime", I mean
25 that I looked at when they were in the womb as well, so
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1 it was like nine months before their date of birth
2 I went back.
3 What struck me -- I know this was a very limited
4 survey, very anecdotal in a sense -- but every case that
5 had been treated with the phosmet brand of warble fly
6 liquid -- so that is how it came about. I mean, it was
7 not a very professional survey, but nonetheless I asked
8 straight questions, and that was a common denominator in
9 every case that I looked at.
10 MR WALKER: Your letter concluded in a paragraph which
11 straddles the two pages:
12 "Is Farmers Weekly for free thought and
13 development of the farmer or for shielding the
14 embarrassing hiccups boomeranging directly from the
15 compulsory clinical regimes resurrected from the
16 multi-national ministerial alliance."
17 What was the multi-national ministerial alliance?
18 MR PURDEY: You are embarrassing me.
19 MR WALKER: I am sorry, I do not want to embarrass you at
20 all. I wanted to know more about it.
21 MR PURDEY: Yes. Well, I suppose I was -- even then had a
22 rather cynical view over this. It is the way that
23 I perceived those ministerial bodies. I felt --
24 I suppose I had a bit of a chip on my shoulder, but
25 I think there was some sense to what I was saying that
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1 there did seem to be this cohesion between the interests
2 of the multi-nationals selling chemicals and the
3 Ministry of Agriculture, particularly at that time. A
4 lot of the research that the Ministry was doing was
5 always tailored on the side of looking at effects of
6 agrochemicals, rather than looking at the alternative
7 biological means of control. Being an organic farmer,
8 this was obviously causing me a sort of problem.
9 MR WALKER: Now the Farmers Weekly editor has put a little
10 comment at the end of your letter:
11 "The Ministry's Central Veterinary Laboratory says
12 it is satisfied that the organophosphorous compounds do
13 not cause BSE. 'This link has been researched and
14 rejected' said a spokesman ..."
15 And that is the end of my quote.
16 Did you know anything about research at that time
17 by the Central Veterinary Laboratory into a possible
18 link with organophosphorous compounds?
19 MR PURDEY: No, but I did later. I learnt about it later.
20 MR WALKER: Later in the year, I think, towards the end of
21 the year, an article by Mr Wilesmith and others was
22 published in the Veterinary Record. Do you recall what
23 they said in that article about organophosphorous
24 compounds?
25 MR PURDEY: Yes, I do.
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1 MR WALKER: What did they say?
2 MR PURDEY: They were looking at whether BSE was a result
3 of the immediate effects of some novel chemical
4 substance that had been introduced into agriculture, et
5 cetera. And they concluded that there was no such
6 association.
7 MR WALKER: Do you recall what the basis was for that
8 conclusion?
9 MR PURDEY: Presumably because they could not find any
10 correlation in time of year or state of pregnancy with
11 exposure to organophosphates. I later found out that
12 apparently only 80 per cent of the cases of BSE that
13 they had examined had exposure to organophosphate
14 chemicals. But I disagree with that, the way they did
15 their survey.
16 MR WALKER: Yes. One aspect I was going to ask you about
17 was that they observed that there had been cases of BSE
18 in herds which had not been exposed to organophosphate.
19 Would that, to your mind, mean that organophosphates
20 necessarily did not play a part in BSE?
21 MR PURDEY: No, not at all.
22 MR WALKER: Why not?
23 MR PURDEY: Well, firstly the survey failed to look at the
24 in-utero period. They looked just at in the lifetime of
25 the cow. They did not look at exposure of animals in
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1 the womb. I also felt that they should look at the
2 chemical history of the parents, if there was any
3 unforeseen genetical damage that chemicals such as
4 organophosphates were having. Also, perhaps look at the
5 treatment to the bull that had sired this particular
6 animal. I think it should have gone much further back.
7 I know that is very easy to say and that would have
8 involved an awful lot of work, but I think to do a
9 thorough job of looking at -- because it is known in
10 toxicology that you have these long-term delayed
11 effects, in-utero effects, as subtle teratogenic
12 disturbances, for instance.
13 Also, it is known that subtle mutations in both
14 the male and the female parents could have knock-on
15 effects on the next generation. Also, I think the
16 organophosphate was in the food chain because it was fat
17 soluble. It was coming in the feed itself. And I think
18 this was an acceptable avenue that should have been
19 looked at.
20 PROFESSOR FERGUSON-SMITH: Had anybody looked at levels of
21 organophosphates in meat and bonemeal at that time, do
22 you know?
23 MR PURDEY: Not that I know of. I cannot find any
24 published studies of -- having said that, the
25 manufacturers did a study -- this is recent -- the SEAC
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1 Committee had presented to me the results of the
2 manufacturers' study that showed a level of phosmet
3 combining into fat, which seemed to plateau off, which
4 is quite interesting. I had forgotten the level it was
5 in-fat at. Instead of going away, it did plateau off,
6 I think, six days after the experimental treatment,
7 which was quite interesting.
8 MR WALKER: Thank you. Unless there is anything more you
9 would like to say about what you thought of the work by
10 Mr Wilesmith as published in 1988, I was going to move
11 on a little?
12 MR PURDEY: Yes, I just thought it was inadequate in
13 relation to what was known in toxicology at the time.
14 MR WALKER: In February 1989, the Southwood Working Party
15 reported. One of their recommendations was there should
16 be another group of experts set up to look at programmes
17 for research. That group of experts reported towards
18 the end of 1989, and their report was published in July
19 1990. I expect you remember that report?
20 MR PURDEY: Yes. Yes, I do.
21 MR WALKER: And you wrote a letter to Farmers Weekly about
22 it, I think on 3rd August 1990. I would like to take
23 you to that. That means we can now put away our bundle
24 for 1988 and take out the year book for 1990. Our
25 reference is YB 90/8.03/1.1. I think this is a
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1 letter -- am I right -- that you wrote to Farmers
2 Weekly, and they published on 3rd August under the
3 heading "Look for the missing BSE link". This is the
4 letter you wrote, is it not?
5 MR PURDEY: Yes.
6 MR WALKER: And if I can just quote the first paragraph:
7 "Reading your various reports of the BSE
8 committee's findings, et cetera, it seems rather foolish
9 that none of the investigative organisations involved
10 are actually challenging much energy into solving the
11 missing links in the pathology and prerequisites
12 underlying this slow viral condition. If such research
13 were conducted with positive results, then that would
14 place any practical remedial directions into a more
15 worthwhile context."
16 I stop quoting the first paragraph there. Then
17 you describe some of the things you have mentioned to
18 the Committee already, in particular about the more
19 weakly individual cattle being susceptible. You also
20 refer to a new breed of sheep being scrapie-resistant.
21 Then you go on to describe your own experience and the
22 fact that none of the cattle in your herd were as yet
23 showing symptoms. You described then the litigation and
24 the compromise agreement that you reached with MAFF.
25 You then went on to say:
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1 "I have also discovered that all of the registered
2 organic herds which do not use these substances [that is
3 the organophosphorous substances] yet may have fed the
4 brands of cake containing the infective BSE agent have
5 also had no cases in their home-reared cattle. In fact,
6 the only two cases found in these herds were in two
7 cattle that had been purchased in from chemically
8 managed farms."
9 Could you explain a little about the work you had
10 done for this purpose?
11 MR PURDEY: Yes. There has been a survey done which looked
12 at all organic herds in great detail. We have a copy of
13 it here. This survey showed precisely that there had
14 been no cases of BSE in fully converted organic farms
15 and in home-reared cattle that had been home reared on
16 those fully converted organic farms. Conversion to an
17 organic farm is a three-year process, so it is quite
18 feasible that on a fully converted organic farm, you
19 could just get a case of BSE from something that had
20 happened to the cow, like when it was bought in from a
21 chemically run farm, et cetera, because of the
22 incubation period that has been postulated for this
23 disease. But I think it seems very cut and dried that
24 there had been no recorded cases.
25 I think there was one case that was a bit suspect
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1 where they had a case on a fully converted organic farm,
2 but it was one that was only just converted so that
3 there was a link back to possible exposure to
4 organophosphate. But, I mean, we do not live in a
5 cocooned world. Organophosphate will penetrate even
6 organic farms, but obviously at very low doses because
7 they are not being intentionally used.
8 SIR NICHOLAS PHILLIPS: Were organic farmers at this time
9 happy in general to use compound feedstuffs?
10 MR PURDEY: No, they were not. But you could be a
11 registered organic farm, livestock farm, and you were
12 allowed to use -- 20 per cent of your concentrated feeds
13 could come from conventional feedingstuffs. As far as
14 all the cake merchants I have talked to, they assured me
15 that every brand of concentrates in those days had meat
16 and bonemeal in it as a protein supplement.
17 SIR NICHOLAS PHILLIPS: So this would not be explained by
18 the possible theory that they simply were not feeding
19 MBM. Most organic farms you would have expected to be
20 feeding some of this?
21 MR PURDEY: I was not an organically registered herd
22 through the 1980s. I unwittingly fed an awful amount of
23 concentrates that came from conventional sources because
24 I was farming my land organically, but buying in feed
25 that was inorganic.
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1 SIR NICHOLAS PHILLIPS: But in general the amounts would be
2 less than in an organic farm?
3 MR PURDEY: Yes, they would, quite considerably less. But
4 it was banned -- the Soil Association, who are the
5 governing body, did ban it I think a year before, 1987,
6 I believe. So you could not use brands with it in
7 then.
8 MR WALKER: Just returning to your letter published on 3rd
9 August, you then went on to note that these chemicals
10 had been used at London Zoo, and I think that by that
11 time it was known that there had been some animals at
12 London Zoo who had come down with a disease like BSE.
13 Then you referred to the world of pet cats. I think by
14 the time you wrote this letter, it was known that there
15 had been at least one cat that had come down with
16 spongiform encephalopathy. Then you go on to --
17 MR PURDEY: Yes.
18 MR WALKER: Then you go on to describe what is known as the
19 "neurotoxicological level". You concluded by drawing
20 attention to the fact that some schools had banned beef,
21 while nevertheless the Government was promoting the use
22 of anticholinesterase headlice shampoos, which as
23 I understand it contained these organophosphorous
24 compounds?
25 MR PURDEY: Some of the brands, not all, but similar acting
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1 chemicals.
2 MR WALKER: Again, your letter has led to a comment from the
3 editor. I will just quote it:
4 "It seems that diseases like BSE are far from
5 simple cause and effect affairs, which is why their
6 epidemiology is so difficult and why it is the farmer
7 who must ultimately make his own choice of system for
8 dealing with BSE on the basis of the best risk
9 assessments he can make."
10 What did you think of that comment from the
11 editor?
12 MR PURDEY: Well, I suppose the farmer was in direct
13 contact, having direct observations with what was going
14 on, but in a sense it was a very mysterious disease.
15 You know, any intuitive feeling you have was obviously a
16 theory. So I think it is very hard for farmers to be
17 able to gauge exactly what was going on, particularly
18 when all we were reading in the press was that this was
19 caused by meat and bonemeal, et cetera. We were so
20 bombarded in the press with the sort of mind-set causal
21 hypothesis that it was meat and bonemeal that caused
22 this, and scrapie had jumped from sheep into cows, et
23 cetera. I think it was the more thinking farmer and the
24 more intuitive farmer who was challenging conventional
25 wisdom, you know down at the pub, et cetera.
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1 I think thinking farmers were very wary, you know,
2 of accepting the Government's hypothesis as gospel, just
3 on the basis of their observations, because stories go
4 round the farming grapevine, farms that milled up their
5 own feed, for instance, I had heard of one or two cases
6 where they had had BSEs. Even on one of the Ministry's
7 own experimental farms, where it was an all-grass silage
8 farm, where they did not feed cereals, that was the
9 experiment, to rear beef cows on a cheap low-cost
10 system, feeding grass and silage. This was on Exmoor at
11 this farm. The manager of that farming unit told me
12 that he had four cases of BSE in these animals on this
13 experimental unit. I found that very interesting.
14 MR WALKER: Yes. When was that? Was that at this time or,
15 can you recall?
16 MR PURDEY: 1990 I heard about that, yes. Then that was
17 confirmed by one of the Ministry officers in Taunton.
18 MR WALKER: That was a bit later on the confirmation, was
19 it? Could it be useful just to hear a little bit more
20 about this now? If it was confirmed to you, was there
21 any explanation offered for it?
22 MR PURDEY: Yes, there was an explanation that the calves
23 were brought in at sort of four or five days old, but it
24 was rather vague. I was told that, you know, some of
25 the calves were brought in and some were reared on the
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1 unit. So I suppose that seems a fair point, that if
2 there is maternal transmission, say, of meat and
3 bonemeal, and infectious agent in meat and bonemeal by
4 maternal transmission, then those calves could have
5 brought in -- even with the chemical fear -- they could
6 have been incubating the disease, could have been
7 switched on in the womb. But apparently two or three --
8 the farm manager told me that two or three of the cases
9 were not brought in, but I am not 100 per cent certain
10 of that. That was sort of hearsay, I would suppose.
11 PROFESSOR FERGUSON-SMITH: On that particular farm, were
12 they using OPs?
13 MR PURDEY: Yes, they were using the warble fly liquids,
14 yes, yes.
15 MR WALKER: I wanted to ask you a bit about what was
16 happening in the Ministry of Agriculture at this time.
17 For that purpose, I would like to distribute a document
18 that the Ministry produced, their departmental report.
19 I do not know whether you have seen this before?
20 MR PURDEY: No.
21 MR WALKER: This is a departmental report. It deals with
22 the Government's expenditure plans for 1991/92 to
23 1993/94. It is quite an interesting document, this, for
24 a number of reasons. One reason is until that time,
25 there used to be quite a big publication, the Public
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1 Expenditure White Paper, which dealt with all aspects of
2 Government. But at about this time, the Government
3 decided to introduce individual reports from
4 departments. So this is the very first time, as
5 I understand it, that the Ministry had produced their
6 own departmental report setting out their expenditure
7 plans.
8 MR PURDEY: Yes.
9 MR WALKER: They talk a bit about the activities of the
10 Department. So far as we have been able to ascertain,
11 it is the first time in a report of this kind that they
12 deal in a little bit of detail with pesticides. One of
13 the things that I wanted to show you was paragraph 90,
14 which is towards the back of this document. They are
15 talking here about food safety, which is the heading on
16 the previous page, prior to paragraph 284. They talk a
17 bit about the food safety directorate, and then they go
18 on to talk about the report of the independent committee
19 on the microbiological safety of food. That is
20 paragraph 88.
21 In paragraph 89, they deal with
22 nutrition-labelling and date-marking and things like
23 that. Finally, for my purposes, in paragraph 90, they
24 mention some other aspects. It is the second sentence
25 that I wanted to draw attention to:
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1 "A full review was carried out during the year of
2 the Government's strategy for the control of
3 pesticides. As a result, the number of scientific staff
4 engaged on registration work is being increased
5 substantially in order to speed up the processing of new
6 pesticides and review of older ones, for both of which
7 planning targets have now been set. The rolling
8 programme of surveillance monitoring for pesticide
9 residues in food is to be enhanced by the inclusion of
10 results obtained by food manufacturers and retailers. A
11 bio-technology unit was established at the beginning of
12 1990 to coordinate the Ministry's wide range of
13 interests in the increasingly important science of
14 genetic modification."
15 Then they give a table, Table 20, called
16 "Pesticide Assessment: Staff Numbers and Outputs".
17 There we have some data indicating what has been
18 happening in past years up to 1990/1991, and then some
19 estimated figures for subsequent years. We see a
20 dramatic increase that they are planning, which has
21 started, and they are planning should continue in the
22 number of scientific staff at the Data Evaluation Unit.
23 Were you aware, at this time, that the Ministry was
24 embarking on a sort of major growth in its number of
25 staff looking at pesticides?
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1 MR PURDEY: Yes, I think we were sent out -- there was
2 quite a lot of articles about it in the farming press
3 certainly, and the environmental press, which said that
4 this was going on, you know.
5 MR WALKER: And I should also mention that, at paragraph 70,
6 reference is made to pesticides as being a particular
7 area of high priority. This is page 27 of the report.
8 MR PURDEY: Yes.
9 MR WALKER: The last sentence of paragraph 70. If you have
10 the last sentence of paragraph 70 there, I think we see
11 that the only thing that is mentioned ahead of
12 pesticides as being a particular area of high priority
13 is research into BSE itself.
14 MR PURDEY: Yes.
15 MR WALKER: Now, there are also some other references in
16 this document to a consumer panel and to a new entry on
17 publicity and information. I wanted to ask you whether
18 at this time you were detecting any change in the way in
19 which MAFF approached its tasks?
20 MR PURDEY: No, not really, no.
21 MR WALKER: Now --
22 MR PURDEY: Not with me personally. Yes, I did not feel
23 any let-up at all from the previous stance, should
24 I say?
25 MR WALKER: Thank you. Now, we can put that document away,
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1 I think. What I would like to turn to now is a little
2 bit about the course of events in your own herd.
3 I found this most conveniently set out in the article
4 that you wrote for the Journal of Nutritional Medicine
5 which we have some copies here. So if we can pass that
6 up -- sorry, I have found it. I will ask you later on
7 about the events which led you to write this article,
8 but at the moment, it is just the description that you
9 give of what happened at your farm that I wanted to
10 refer to. I think I find the relevant passage at page
11 68. This is a section of your article which has a
12 subheading "The Magnesium-induced Prolonged Remission".
13 What you say about your herd is this, and I quote:
14 "Some 400 head of Jersey cattle have been
15 home-reared through the author's own organically managed
16 farm since the beginning of the 1980s. They were all
17 exposed to the animal protein feed prior to the ban in
18 1988, yet none of these cattle have ever contracted BSE.
19 In line with our organic standards, special brands of
20 concentrated cake have been fed since 1988 which have
21 been selected to contain minimal pesticide and solvent
22 residues. No OP products are ever used.
23 "In January 1990, eight four-year-old cows were
24 purchased for this farm for pedigree breeding purposes.
25 They came from an intensive factory-style dairy farm in
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1 West Wales. OPs and other insecticides had been used
2 routinely on this farm. In April 1990, one of these
3 cows, called Mustard, started to develop the classic
4 early symptoms of BSE, anxiety evoked by handling,
5 aggressive outbursts of kicking, eye-flicking, tremor,
6 loss of milk yield and appetite, hyperaesthesia,
7 hyperacusis, reluctance to enter doorways, et cetera.
8 Curiously, Mustard spent a substantial part of her time
9 at the free access mineral trough, licking at the
10 magnesium and selenium-enriched powder, instead of
11 eating forage silage with the rest of the herd. It was
12 initially assumed that her mineral fetish indicated that
13 her symptoms were chronic hypomagnesia-related.
14 Consequently, two 400 ml bottles of magnesium sulphate
15 were subcutaneously injected into her on alternate days
16 in early June. Within 48 hours, Mustard's neurological
17 symptoms remitted, leaving her in seemingly good health
18 once again."
19 Just at that stage, after the treatment in June,
20 what did you conclude about Mustard?
21 MR PURDEY: Because I had not seen BSE before, I thought
22 this was a rather severe case of chronic hypomagnesia,
23 which is a magnesium deficiency syndrome, because these
24 were all symptoms of magnesium deficiency in the nervous
25 system.
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1 MR WALKER: And the treatment for magnesium deficiency
2 seemed to have worked?
3 MR PURDEY: Well, yes, that is going into the future.
4 MR WALKER: I think it is useful to carry on with what
5 happened after that:
6 "By November 1990, both Mustard and another cow
7 called Birthday ..."
8 I interpose, I think that is Churnside Birthday
9 that you have told us about in your statement.
10 MR PURDEY: Yes.
11 MR WALKER: "... who had also originated from the same
12 chemically managed herd delivered calves. But
13 immediately after calving, both of these cows contracted
14 an unusually lengthy bout of milk fever syndrome
15 (parturient paresis) which necessitated the subcutaneous
16 infusion of four 400 ml bottles of calcium borogluconate
17 and magnesium each over a week's duration in order to
18 stabilise and remit the syndrome. None of the remaining
19 58 cows in the herd suffered from any degree of milk
20 fever that year.
21 By April 1991, Birthday started to develop the
22 classic symptoms of BSE, but not quite so dramatically
23 as Mustard had the previous year, although ataxic and
24 paranoid schizophrenic symptoms were more prominent. As
25 experienced during classic syndromes of magnesium

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1 deficiency, contact with both potash-rich fields and wet
2 weather exacerbated Birthday's symptoms. Total
3 remission of her symptoms was induced 36 hours after
4 subcutaneous injection of the first bottle of magnesium
5 sulphate. Symptoms returned moderately by early June
6 and MAFF vets who were called in diagnosed early stage
7 symptoms of BSE, issuing a Form A BSE Suspect Notice on
8 the cow. Further treatment with two bottles of
9 magnesium sulphate induced total remission once again,
10 and at the beginning of September, MAFF vets withdrew
11 the BSE notice altogether."
12 I close the quote there. What I would like to do
13 is to just take you to some of the correspondence that
14 had occurred at this time. Before I do, can I confirm
15 by this time you had moved to High Barn Farm?
16 MR PURDEY: Yes, this was all on High Barn Farm, all this.
17 MR WALKER: The first letter I want to take you to is in
18 July 1991. We have it in the year books for 1991. The
19 year book for 1990 can go away. Hold on to the article,
20 because we will come back to that.
21 In YB 91, if you go into tab 7. There is rather a
22 lot in our 1991 year book. We are going to have to
23 divide it into two, I think, quite soon. I think the
24 first document after tab 7 is a letter dated 14th July
25 1991. It is sent from you to the Chief Veterinary
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1 Officer at MAFF. Is that right? Is this a copy of a
2 letter that you sent?
3 MR PURDEY: Yes, that is right.
4 MR WALKER: In paragraph 1, you describe what had happened
5 to Churnside Birthday:
6 "Over the last two or three months, this cow
7 started to develop what appeared to be a chronic
8 staggers type of disorder, which was partially rectified
9 after administering magnesium sulphate into the cow.
10 However, after blood tests were taken for magnesium, et
11 cetera, no mineral deficiency could be identified within
12 the cow, and my vets are now considering that this cow
13 is afflicted with BSE, and will be contacting
14 yourselves."
15 Then you go on to describe your keen interest in
16 environmental toxins. You say a bit about the
17 conception that exposure to neurotoxicants upsets the
18 cow's immunological equilibrium. In the third paragraph
19 you say:
20 "If your vets endorse my vet's verdict of BSE,
21 I would like to attain some form of guarantee from
22 yourselves before I hand over the afflicted cow that
23 I may be granted independent access for examination of
24 CNS tissue."
25 On the last paragraph of this page, you go on to
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1 outline various correlations which suggest why BSE could
2 be a sequel to an acute or chronic neurotoxicant
3 disorder some years earlier to the surfacing of the
4 outward symptoms.
5 What I would like you to do is to take you to some
6 of the things you have said about those correlations, if
7 I may? Is that all right?
8 MR PURDEY: Yes.
9 MR WALKER: Just over the page you refer to some cattle
10 herds within the UK, as well as all herds within some
11 other countries, having consumed the alleged prion
12 contaminated feeds, yet remaining completely devoid of
13 BSE outbreak to date.
14 MR PURDEY: Yes.
15 MR WALKER: Then the following paragraph, you refer to the
16 fact that in your own farm you had not used the systemic
17 pourons.
18 After that you go on to refer to the fact that
19 registered organic herds may well have fed the cake in
20 the 20 per cent that was bought in the cake allowance
21 previously permitted by the Soil Association standards.
22 Then you refer to the point about use at London
23 Zoo, and pet cats which, we had seen earlier. Then you
24 turn to journals which showed that certain environmental
25 toxins, such as aluminium and anti-thiamine agents, and
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1 some others, had increased permeability of the
2 blood-brain barrier, and had disrupted the -- is that
3 pinocytotic?
4 MR PURDEY: Yes, pinocytotic vesicles.
5 MR WALKER: -- pinocytotic vesicles in the vessel walls. I
6 was interested there that some of the things that you
7 referred to, they included not only anti-thiamine
8 agents, radiation, anaesthesia, but also cycad nuts.
9 MR PURDEY: Yes.
10 MR WALKER: I think this was a study on Guam?
11 MR PURDEY: Yes, Guam, yes, that is right. A very
12 interesting study.
13 MR WALKER: You referred to various general articles. I
14 think what happened on Guam had been the subject of a
15 book by Oliver Sachs, had it not, called "Island of the
16 Colour Blind"?
17 MR PURDEY: This was the first milestone in accepting the
18 role of chemicals, albeit it naturally-occurring, in the
19 triggering off of well-known neurological diseases like
20 Alzheimer's, which is very similar to TSE, and
21 Parkinson's and motor-neurone disease. So to me this
22 was very interesting research that I homed into right
23 away.
24 MR WALKER: I think the disease on Guam was called lytigo
25 bodig?
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1 MR PURDEY: It was called something like that, yes.
2 MR WALKER: It was studied by Professor Gajdusek whom we
3 know did some studies into kuru and other aspects of
4 spongiform encephalopathy?
5 MR PURDEY: Yes, and Peter Spencer as well, who did a lot
6 of work.
7 MR WALKER: Having referred to that, you went on to a
8 demonstration that anti-cholinesterase chemicals had
9 overdriven the regions of the digestive tract that were
10 intensively supplied with cholinergic receptors. Then
11 you went on to refer to research teams investigating the
12 delayed neurotoxicity of certain anti-cholinesterases
13 and reported spongiosis.
14 Over the page, you refer to the work by Bouldin
15 and Cavanagh that we mentioned earlier on this morning.
16 Then about halfway down that page in a paragraph --
17 perhaps I should read the whole paragraph:
18 "Other dairy farmer colleagues of mine also report
19 that their diagnosed cases of BSE temporarily responded
20 dramatically to magnesium and calcium treatment.
21 Interestingly, these same mineral deficiencies were
22 considered along with chemical neurotoxins to be the
23 essential prerequisites for triggering the Guam
24 syndromes. The very fact that some of the BSE symptoms
25 are reversible suggests that not all symptoms can be
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1 accountable to the direct physical damage created by the
2 infective prion agent. Perhaps hyperparathyroid
3 activity is involved here as a sequel to exposure to
4 chemical neurotoxins well known for overdriving the
5 neuroendocrine system."
6 Then you went on to say that in research trials on
7 the Guam degenerative disorders and the Birmingham
8 research into anti-cholinergic effects, it showed that
9 it was apparent that there were similar pathological
10 duplications involved in the BSE syndrome, and finally
11 suggested that whether it was a question of identifying
12 the neurotoxic trigger or eliminating one, doing the
13 necessary research would be an advance into
14 comprehension of slow viral encephalopathies with
15 knock-on benefits for public health at large?
16 MR PURDEY: Yes.
17 MR WALKER: There are a number of references in this
18 letter. How long did it take you to prepare this
19 letter?
20 MR PURDEY: I do not think this is very long, not compared
21 to this article, burning the midnight oil for many
22 nights, many nights.
23 MR WALKER: Thank you. You tell us in paragraph 8 that
24 Mr Meldrum replied to you on 25th July 1991 saying that
25 the Department could not grant you independent access
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1 for examination of central nervous tissue.
2 Unfortunately, we have not been able to locate a copy of
3 that letter at the moment. Can you recollect whether he
4 dealt with the points that you were making about the
5 correlations between BSE and these other diseases?
6 MR PURDEY: No, no. No.
7 MR WALKER: You cannot recollect that?
8 MR PURDEY: No, he did not. He just answered the fact that
9 I could not have central nervous system tissue.
10 SIR NICHOLAS PHILLIPS: Did he explain why?
11 MR PURDEY: He just said that it was against -- you know,
12 the law was that it could only be analysed in Government
13 laboratories. It was MAFF property. Once the cow was
14 taken under a BSE order, it became MAFF's property,
15 and ...
16 SIR NICHOLAS PHILLIPS: That would not explain why MAFF
17 could not release a bit of the cow back to you if it
18 wanted to.
19 MR PURDEY: Well, exactly.
20 SIR NICHOLAS PHILLIPS: But no explanation was given other
21 than it was their policy not to do so?
22 MR PURDEY: Yes, that is right.
23 SIR NICHOLAS PHILLIPS: I see.
24 MR WALKER: I would like to finish off this bit of the
25 story before we break for coffee. If we go on to tab 11
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1 in our bundle, the second document behind tab 11, our
2 reference is YB 91/11.13/1.1. Do you see there a letter
3 dated 13th November 1991 from the Taunton office of the
4 Ministry of Agriculture, Fisheries and Food. The
5 veterinary officer is writing to you and your wife at
6 High Barn Farm. Is that a letter you received?
7 MR PURDEY: Yes.
8 MR WALKER: This letter says:
9 "As you are aware, the brain of your bovine
10 animal ...", the cow, "... identification number
11 JB122-178 ...", which I think is Churnside Birthday,
12 "... was collected for examination following slaughter
13 on 29th September 1991. The examination was intended
14 solely to confirm whether or not the animal was
15 suffering from bovine spongiform encephalopathy and no
16 attempt could be made at providing a differential
17 diagnosis."
18 Can you tell the Committee what that means, that
19 no attempt had been made to provide a differential
20 diagnosis, or what did you understand it to mean?
21 MR PURDEY: I suppose that meant that they had not looked
22 at any other possibility; that all they were looking for
23 was whether it was BSE positive or not. There was this
24 phenomena of BSE negative, where some cows were coming
25 back that had been taken under the BSE order, exhibiting
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1 the symptoms of BSE, and were coming back BSE negative.
2 There were one or two publications in the Veterinary
3 Record, for instance, about BSE negative.
4 MR WALKER: By that, you mean the number of cattle that had
5 been assessed by a vet as likely to be suffering from
6 BSE?
7 MR PURDEY: Yes.
8 MR WALKER: And that had led to them being slaughtered under
9 the slaughter policy?
10 MR PURDEY: Yes.
11 MR WALKER: Then, when examination of the head took place,
12 the information led to the conclusion that this cow,
13 while it had shown the symptoms of BSE, did not in fact
14 suffer from that disease?
15 MR PURDEY: Yes, that is right. I think it did not show
16 the ballooning vacuoles, the swelling of the brain. But
17 it could have just been at an earlier stage of the
18 disease and had not yet demonstrated that kind of
19 pathology.
20 MR WALKER: The interesting question is exactly what the
21 animal was suffering from if it had not shown the
22 lesions characteristic of BSE.
23 MR PURDEY: Yes.
24 MR WALKER: What you were then told, in the second
25 paragraph, was that they had received the result of the
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1 laboratory examination, and that lesions consistent with
2 BSE were in fact identified with the result that the
3 disease is therefore confirmed in that animal.
4 I would just like to take you back to the --
5 PROFESSOR FERGUSON-SMITH: Can I interject and ask: I just
6 wonder if that letter says, "We were not excluding any
7 other form of spongiform degeneration which could have
8 had a toxic effect"?
9 MR PURDEY: Yes.
10 PROFESSOR FERGUSON-SMITH: He was covering, is that right?
11 MR PURDEY: I did not think that, but now, yes, that is a
12 possibility. Yes.
13 MRS BRIDGEMAN: If I may make a comment? This strikes me
14 as a standard letter into which they have inserted your
15 address and your bovine animal number, so it can apply
16 universally; but that is perhaps something that we can
17 explore.
18 MR WALKER: I wanted to take you back, to finish off the
19 story, by looking at your article again which you have
20 loose, I think, just there.
21 MR PURDEY: Yes.
22 MR WALKER: On page 69, if you look at the course of events
23 there, we have reached the third to last paragraph on
24 page 69 of the Nutritional Medicine article. There you
25 say:
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1 "Despite the fact that the pyschoneurological
2 symptoms of the early stages of BSE never recurred,
3 Birthday started to lose weight, her muscles atrophied,
4 she developed a dejected appearance, and on
5 September 29th when an extreme bout of wet weather set
6 in, she collapsed in a muddy gateway and was unable to
7 rise. MAFF vets were called in, who instantly reimposed
8 the BSE notice and slaughtered her. Her post-mortem
9 revealed BSE positive lesions."?
10 MR PURDEY: Yes.
11 MR WALKER: Just to conclude, the story is of a cow that
12 exhibits some symptoms which might be attributed to BSE,
13 but then recovers from those after dosing with
14 magnesium, only later on to display the symptoms again
15 and eventually to need to be slaughtered?
16 MR PURDEY: Yes.
17 MR WALKER: Well, I am going to come on, after the coffee
18 break, to the article you then wrote in The Ecologist
19 describing what happened. Perhaps if we might break for
20 coffee now. Would that be convenient?
21 MR PURDEY: Yes.
22 MR WALKER: We will resume in about 20 minutes.
23 (11.05 am)
24 (Short break)
25 (11.30 am)
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1 MR WALKER: I think I said after coffee I would take you to
2 the article in The Ecologist. Perhaps we could
3 distribute that? We have an article entitled "Mad Cows
4 and Warble Flies: A Link Between BSE and
5 Organophosphates?" I think this is published in volume
6 22 of The Ecologist, in their issue for March and April
7 1992; is that right?
8 MR PURDEY: Yes.
9 MR WALKER: In this article, I think you begin by describing
10 the suffering of Churnside Birthday.
11 MR PURDEY: Yes.
12 MR WALKER: After having described the way in which she was
13 put down, at the end of the third paragraph you say:
14 "All the pleas made to MAFF for various
15 post-mortem neuropathological explorations were rejected
16 outright."
17 A. Yes.
18 MR WALKER: Then you say a little bit about the prion theory
19 and BSE negative cows that we discussed earlier.
20 MR PURDEY: Yes.
21 MR WALKER: Then, under the heading "Genetic and
22 Environmental Factors", you say:
23 "Much of the scientific establishment seems to be
24 ignoring the importance of the genetic and environmental
25 factors which influence slow virus diseases."
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1 MR PURDEY: Yes.
2 MR WALKER: Then you refer to some things which you say
3 need investigating, in the final paragraph on that page.
4 You refer to large differences in the incidence of BSE
5 between different herds and the geographic differences
6 in the spread of the disease.
7 MR PURDEY: Yes.
8 MR WALKER: Then we have a section which is entitled "The
9 Organophosphate Link". You begin by saying:
10 "A striking feature of BSE epidemiology in Britain
11 is that the epidemic is at its most intensive in the
12 areas which were designated by MAFF as 'warble fly
13 eradication zones' approximately three years
14 previously."
15 I think that we will come on to the more detailed
16 explanation that you give of that in the article in
17 1996.
18 MR PURDEY: Yes.
19 MR WALKER: Just while we are dealing with it here in The
20 Ecologist, in the next sentence you said:
21 "All farmers were legally obliged to treat their
22 cattle with one of three pouron quasi-systemic
23 'phenylphosphorothioate' types of organophosphorous
24 insecticide known as phosmet, famphur and Fenthion."
25 At this stage, was it still possible to use
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1 Ivomec?
2 MR PURDEY: Oh yes, yes.
3 MR WALKER: There was the possibility then of using
4 something other than an organophosphorous?
5 MR PURDEY: Well, really only on beef cows, unless you
6 wanted to bankrupt your business by throwing milk away
7 for 28 days.
8 MR WALKER: I think that most of the points that you
9 describe in this section are points that we have covered
10 already, references to the zoo and cats and so on.
11 I was going to take you on to the next section
12 headed "Neurological Effects of OPs". This is the
13 middle column on page 53. You say there that:
14 "Acute poisoning by organophosphates causes the
15 nerves to go into 'overdrive' due to the excessive
16 release of acetylcholine at the synapses (nerve
17 junctions)."
18 You talk about the neurotoxic effect. At the
19 bottom of that column, you say:
20 "The pattern through which the nerves degenerate
21 in these victims of OP precisely duplicates several
22 types of motor neurone diseases such as Friedrich's
23 Ataxia and amyotrophic lateral sclerosis."
24 You draw attention to some work that has been done
25 in that regard.
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1 Then, having done that, at the foot of the
2 right-hand column on page 53, you say:
3 "An important link between the slow viral
4 encephalopathies (such as scrapie and BSE in animals,
5 and kuru and CJD in humans), and the human 'non-viral'
6 degenerative diseases (such as Parkinson's, motor
7 neurone and Alzheimer's disease) is suggested by the
8 similar way in which all these diseases develop."
9 Then you go on to describe the ways in which they
10 show the clinical symptoms over time. Then the next
11 section of the article is headed "A Reduced Capacity for
12 Detoxification".
13 You say in the left-hand column on page 55 that:
14 "There is evidence that there may be a reduced
15 capacity for detoxification in the BSE cow due to a
16 deficiency of calcium and magnesium."
17 I wonder if you could describe that evidence a
18 little to the Committee?
19 MR PURDEY: That would be some of the detoxification
20 enzymes that are involved in breaking down chemical
21 pathways, when they are detoxifying are actually
22 activated. There are cofactors in enzymes that are
23 often minerals or vitamins, for instance, and magnesium
24 certainly plays a role in the degradation in activating
25 enzymes involved in these detoxification pathways. But
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1 I think it goes a lot further than that, my current
2 thinking, you know, there are many more things.
3 SIR NICHOLAS PHILLIPS: That sounds more like that there is
4 a theory rather than there is evidence?
5 MR PURDEY: There is evidence, yes. Magnesium is involved
6 in activating certain enzymes in the detoxification
7 pathways from ...
8 MR WALKER: I think the evidence that you refer to here are
9 some of the things that you have seen in your own herd,
10 the symptoms appearing and then the effect of treatment
11 with magnesium?
12 MR PURDEY: It would be referring to both observations in
13 my own herd and then relating that to the published
14 scientific literature, various articles that cited the
15 role of magnesium, for example.
16 MR WALKER: I was interested by the right-hand column on
17 page 55, where you say:
18 "In response to a letter of mine pointing out this
19 magnesium connection, the head of MAFF's BSE
20 Epidemiology Unit, John Wilesmith, stated that in MAFF
21 trials, therapy with magnesium had also resulted in a
22 temporary remission of the clinical signs of BSE."
23 MR PURDEY: Yes.
24 MR WALKER: I have that letter at the moment.
25 MR PURDEY: Yes, it is the first page of one letter that
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1 I faxed to Brian McHenry just a couple of nights ago,
2 where he says that magnesium can either cause an
3 ephemeral remission of symptoms or an acute worsening of
4 symptoms in cows that are suffering from the early
5 stages of BSE. Those are the exact words from memory.
6 MR WALKER: Did he have any explanation for that?
7 MR PURDEY: No, he did not elaborate at all. I was
8 obviously interested that this was squaring up with some
9 of my observations and my colleague farmers.
10 MR WALKER: Thank you. I was going to go on in the article
11 to the following page, page 56. After a section
12 entitled "Enabling Toxins to Bio-accumulate", you then
13 turn on to the question of BSE negative cows. You say
14 that you had read reports of cases where cattle were
15 being slaughtered with BSE symptoms, but proving BSE
16 negative on post-mortem.
17 Then you say that when you read those reports you
18 contacted one of the farmers concerned, who informed you
19 that all three of his herds had been regularly treated
20 with OPs, but it was the two herds farmed on the clay
21 soils that were producing the BSE cases. What was the
22 significance of that, to your mind?
23 MR PURDEY: At that time -- I would disagree with it
24 today -- I thought, because chalk soils are
25 notoriously -- they contain a lot of calcium and
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1 magnesium; and my natural assumption was that the cows
2 grazing over the chalk, being farmed over chalk, would
3 have a much higher status of calcium and magnesium, a
4 correct status. The homeostasis of calcium is
5 controlled by the parathyroid gland, so you can never
6 exactly have too much unless there is a disorder in the
7 parathyroid gland.
8 But whereas I postulated that perhaps this farmer
9 was having problems on the clay farm with magnesium.
10 Indeed, he did confirm that he had to treat, with
11 magnesium, on the clay farm, whereas on the chalk farm
12 he did not get a problem. But you would probably expect
13 that anyway. But it is not quite as simple as that.
14 There are a lot of other sorts of complications with
15 levels of potash and so on which can set magnesium and
16 calcium out of balance, for instance.
17 MR WALKER: Then I was going to go to the last paragraph,
18 but one which begins at the foot of page 56, where you
19 say that:
20 "Standard MAFF questionnaires to farmers with BSE
21 cows only included questions on chemical exposure in the
22 early stages of investigation into the disease.
23 Moreover, MAFF were only concerned with a link between
24 BSE and 'acute' chemical exposure, rather than with the
25 well-known 'delayed' toxic effects of organophosphate
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1 poisoning. Yet John Wilesmith, MAFF's chief
2 epidemiologist, claimed in a letter to me that my
3 concerns and hypotheses have been covered by the
4 Ministry's extensive detailed research into BSE."
5 The reference that you give for saying that MAFF
6 were concerned with a link only concerned with a link
7 between BSE and acute chemical exposure, I am not quite
8 sure what it is.
9 MR PURDEY: It was the article to which you referred to
10 earlier, one of the original epidemiological trials
11 where it talked about establishing any such association
12 between the immediate effect of a novel chemical used on
13 farms at the time when -- I think they looked at 83 or
14 168 herds from memory.
15 MR WALKER: You are referring to the article in the
16 Veterinary Record in 1988?
17 MR PURDEY: That is right, yes.
18 MR WALKER: Finally you concluded the article by commenting
19 that:
20 "... a link between BSE and organophosphate
21 treatments is more than plausible, yet MAFF refused to
22 carry out the necessary research to prove or disprove
23 the OP theory."
24 MR PURDEY: Yes, publicly, yes.
25 MR WALKER: Thank you. Now I think that I have covered with
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1 you most of the points that you dealt with in paragraph
2 9 of your statement, which is where you deal with this
3 Ecologist article. I was going to take you to the
4 Western Gazette report, unless there is anything else
5 you want to say about the article itself, no?
6 Then the Western Gazette report is in our year
7 book 1992, if that could be provided please. You will
8 need some help with that other bundle to put it away.
9 I hope that you will find it behind tab 3. Our
10 reference is YB 92/3.19/1.1. I think, in fact, it is
11 halfway between divider 3 and divider 4. Have you found
12 it there? This is a report in the Western Gazette, 19th
13 March 1992. There is reference made to your theory and
14 to the Ecologist article. In the fourth column, we have
15 a comment from Professor Lacey. I quote:
16 "Leeds University professor of Microbiology,
17 Richard Lacey said 'it looks increasingly likely there
18 may be one or more precipitating agents that trigger off
19 BSE and it is possible that insecticides are involved.
20 More study is urgently needed. There is something
21 desperately amiss with the Ministry's approach to the
22 problem."
23 That is the close of the quote there from
24 Professor Lacey. There is then a description in this
25 article of the cases of BSE deaths following the ban,
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1 and the discrepancy between the predictions of the
2 Southwood Report on the number of cases of BSE and the
3 latest figures from the National Farmers' Union. There
4 then follows a further quote from Professor Lacey:
5 "The number of young animals dying should have
6 begun to fall not rise. This strongly suggests the
7 offal ban has not stopped the spread of the disease."
8 At this stage, at any rate, you seemed to have
9 had Professor Lacey on your side?
10 MR PURDEY: Yes. I mean, he was quite an ardent supporter
11 in the early days; and he refereed two of my articles
12 which both recommended publication. In fact, his was
13 the most positive peer review of all the peer reviewees.
14 MR WALKER: Are you referring to The Ecologist article?
15 MR PURDEY: The Ecologist and the Journal of Nutritional
16 Medicine, yes.
17 MR WALKER: We will come on to the Journal of Nutritional
18 Medicine in a moment. If we can just note what
19 Professor Lacey had to say then, I think we move on in
20 this bundle to the letter from the Minister to Mr King.
21 We find that at YB 92/6.8/2.1. This is a letter of 6th
22 June to Mr King. It is about halfway through before you
23 reach divider 7. I think you need to go on a bit.
24 6.8/2.1. That looks like it. Now, this is a letter
25 sent to the Rt. Hon. Tom King, who I think was your MP?
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1 MR PURDEY: Yes.
2 MR WALKER: And had passed on some of your concerns to the
3 Ministry?
4 MR PURDEY: Yes.
5 MR WALKER: And there is some discussion about
6 organophosphates and motor neurones. They are
7 considering the contents of your article, they say.
8 They then turn to genetic susceptibility but say they
9 cannot draw any conclusions on the information currently
10 available.
11 So that the stance that is taken by the Ministry
12 at this stage is simply one of "we cannot say very
13 much". Would that be roughly right?
14 MR PURDEY: Yes. I mean, at this stage I did experience,
15 perhaps, a slight loosening of the reins. I did feel a
16 slight gap in the clouds appearing, a bit of light
17 appearing, when Gillian Shephard was Minister of
18 Agriculture.
19 MR WALKER: This was actually written by John Gummer,
20 I think, this letter.
21 MR PURDEY: Well, yes, this would just be prior to that.
22 Sorry, I have got the wrong -- yes, that is okay. That
23 would be just prior to the loosening-up period.
24 MR WALKER: Now, also just a period on the chronology here.
25 We are in early to mid 1992. I think we might mention
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1 Mustard again. If I take you back to your article in
2 the Journal of Nutritional Medicine at page 69, you say
3 that:
4 "In January 1992, due to a shortage of milk quota,
5 the whole dairy herd was moved on to another farm
6 (chemically managed) which had spare quota available to
7 accommodate them. When the herd returned to the organic
8 farm in mid-March 1992, two cows, Mustard and another
9 cow called Damson (who also originated from the same
10 chemically run farm)," this was the same farm that
11 Churnside Birthday had come from too, "were both
12 manifesting the early stage symptoms of BSE.
13 "One 400 ml bottle of magnesium was subcutaneously
14 injected into each cow at the beginning of April. Both
15 cows remitted within 48 hours of treatment."
16 MR PURDEY: Yes.
17 MR WALKER: So they both got better?
18 MR PURDEY: Yes. Normally, with magnesium sulphate, if it
19 was an acute magnesium problem, the cow would invariably
20 remit in one hour to two hours. What was odd about cows
21 -- in fact I would now guess that BSE was the problem
22 if a cow took 48 hours to respond to the magnesium
23 treatment. I know a lot of other farmers who found this
24 48-hour response -- when initially they would think the
25 disease was a magnesium disease, he would inject and
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1 have to wait for 48 hours for recovery. Whereas, if it
2 was a pure magnesium disorder, you would get recovery
3 within an hour ordinarily. This was interesting.
4 MR WALKER: Then in the article, you say:
5 "Damson started to relapse, albeit only
6 moderately, within 1 month of that treatment."
7 MR PURDEY: Yes.
8 MR WALKER: That brings you on to paragraph 10 of your
9 statement, where you deal with Chillaton Damson. You
10 tell us that you refused to hand her over even though
11 she showed signs of BSE, because you wanted to continue
12 to treat her to test your theory about the OP
13 insecticide.
14 MR PURDEY: Yes.
15 MR WALKER: And you wrote to Mr Meldrum, and he replied on
16 14th July 1992. In our 1992 year book, which you have
17 open in front of you, if you could turn on up to tab 7?
18 I think we will find this at our reference YB
19 92/7.14/2.1. This is a letter you received from
20 Mr Meldrum.
21 MR PURDEY: Yes.
22 MR WALKER: The Chief Veterinary Officer. In paragraph 1,
23 he points out that:
24 "Notification is in our own interest as, if the
25 suspect cattle were to die before there had been
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1 inspection, you might lose out on your compensation."
2 Then he goes on to say that he appreciated that
3 your prime concern is to have the opportunity to carry
4 out further investigations. He says:
5 "I have no hesitation in agreeing to your carrying
6 out further tests on your animal while it is under
7 restriction, with the proviso that it is subject to
8 regular clinical inspection by a veterinary officer.
9 The overriding concern is for the welfare of the animal,
10 and if at any time it is deemed to be suffering
11 unnecessarily, it will be slaughtered."
12 Then he went in the next paragraph to the question
13 of examinations on CNS tissue. He said that with regard
14 to carrying out such examinations after slaughter, he
15 must ask for further information before agreeing to vary
16 their procedures. He made reference to their concerns
17 about the way in which it was investigated. So he asked
18 you for some information.
19 Now, the letter ended by saying that he could
20 assure you that the Ministry had not closed their eyes
21 to the needs of individual farmers, or to the fact that
22 symptoms characteristic of BSE may be caused by other
23 syndromes. He went on to say that treatment with
24 magnesium sulphate had been known to produce complete
25 recovery of some suspects which were clearly affected by
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1 hypomagnasemia, not BSE. He concluded by saying:
2 "None of their investigations linked either
3 clinical signs or development of lesions of BSE with
4 prior treatment with organophosphorous drugs."
5 Then I think that you then deal with subsequent
6 events in the part of paragraph 10 that carries over the
7 page.
8 SIR NICHOLAS PHILLIPS: Just before we go on, can you help
9 me with this? You are here talking about concluding
10 that the symptoms of this illness was attributable to
11 delayed effects of low dose OP damage.
12 MR PURDEY: (Nods)
13 SIR NICHOLAS PHILLIPS: That again was something that you
14 had referred to in paragraph 9.
15 MR PURDEY: Yes.
16 SIR NICHOLAS PHILLIPS: But when you were looking at making
17 the point that no cow born and raised on an organic farm
18 had died of BSE, you then commented:
19 "The great majority of organic farms had avoided
20 using the high dose type OP."
21 MR PURDEY: Yes.
22 SIR NICHOLAS PHILLIPS: I infer from that that some of them
23 would have been using the low dose type of OP. That
24 raises the question why were they not getting these
25 symptoms if you think it was a low dose effect?
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1 MR PURDEY: Basically, it was well known within farming
2 circles that you could actually sign the form that you
3 treated your cows and never actually carry out the
4 treatment, and an awful lot of farmers have phoned me
5 who did this, who have said that, you know, they are the
6 only farmer in their road who has not had problems with
7 BSE, even though they all fed the same brand of
8 feedstuff. There were actually very few cases where
9 organic farms fell within the compulsory zone. I was
10 one of them, and there was somebody else in Wales who
11 also fell, and they managed to wriggle out of having
12 their cows treated without going to court. I went to
13 court and quashed the order at that time. But I did
14 know one organic farmer who used the Fenthion brand,
15 that is the active ingredient Fenthion, which was used
16 at the 5 milligrammes per kilogramme body weight, as
17 opposed to the 20 milligrammes per kilogramme body
18 weight phosmet chemical.
19 SIR NICHOLAS PHILLIPS: Thank you.
20 MR WALKER: I think you said just now you went to court and
21 quashed the order. In fact, from what you have told us
22 earlier, it was not quashed. What happened was that an
23 agreement was reached between you and the Ministry which
24 meant that you did not have to do what they had said
25 previously you would have to do?
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1 MR PURDEY: Yes, but in the High Court case, I demonstrated
2 that the Ministry were acting illegally by enforcing
3 treatment with a chemical dressing. We argued that
4 under the Animal Diseases Act the Ministry were only
5 empowered to treat with a vaccine or serum. And we
6 argued that an organophosphorus compound was neither a
7 vaccine or a serum. Therefore, the Ministry order was
8 nullified.
9 MR WALKER: That was your argument, and the Ministry took it
10 sufficiently seriously at least to reach an agreement
11 with you, but the court did not actually pronounce a
12 judgment quashing the order?
13 MR PURDEY: Well, subsequent to 1985, the Act was amended
14 very rapidly to add "chemical dressing" after "vaccine
15 or serum".
16 MR WALKER: The point was dealt with by legislation, but so
17 far as the legal record is concerned, the order had not
18 in fact been set aside by a court?
19 MR PURDEY: No, I suppose I was the only farmer that had
20 recognised this problem, yes, in the wording.
21 MR WALKER: Thank you. Now, we then have the description of
22 what happened in relation to Damson. I was not going to
23 go into the detail of that. We have all had a chance to
24 read the story of what happened to Damson, but I was
25 going to take you to Mr Bradley's letter of 5th
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1 November, which I think comes towards the end of that
2 story. We have that in the same bundle just after tab
3 11, if you could turn on to it. Our reference is YB
4 92/11.05/1.1. This refers to a letter of 29th September
5 1992, which I do not think that we have found. What
6 Mr Bradley goes on to say about that is that:
7 "We [I think that means the Central Veterinary
8 Laboratory] wish to follow up and clarify some of your
9 statements."
10 Then, in the next paragraph, Mr Bradley goes on to
11 say:
12 "That Damson had BSE confirmed is beyond
13 dispute... If you are satisfied and agree the final
14 diagnosis of BSE, so be it. However, if you are
15 suggesting that the cow had concurrent chronic
16 OP-induced spongiform encephalopathy, we would like to
17 see the supporting evidence for this conclusion with the
18 agreement of your veterinary surgeon. This would
19 include a clear description of the clinical signs with
20 dates of examination, the nature, result, and
21 interpretation of the blood tests, and when the blood
22 samples were collected in relation to the clinical signs
23 and treatments. We would also like to have the detail
24 of the frequency and method of administration and dose
25 of the drugs used. Although I may be able to obtain
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1 some data from colleagues in the Veterinary Field
2 Service, it would be convenient if you could also
3 indicate the origin and date of acquisition of Damson,
4 and the treatments with dates, doses, drugs and routes
5 of administration with particular reference to OP
6 compounds."
7 Was this something you went on to take up and give
8 all these details?
9 MR PURDEY: Yes, I think I sent the majority of the details
10 to Ray Bradley after that, yes.
11 MR WALKER: And then there are some other aspects of your
12 letter that he raises, asking for documents in relation
13 to the references that you have given. Then, in the
14 paragraph which straddles the page, he says that you had
15 suggested that MAFF should initiate some research.
16 At present, he said, you had presented no new
17 information which suggests this is necessary. But
18 should you be able to present convincing evidence that
19 there is a deficit, your suggestion could be
20 reconsidered.
21 "However, it would be helpful to us in considering
22 any proposals for further research to have a clear
23 statement of the objective or the hypothesis to test."
24 What was your reaction to this response to your
25 letter?
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1 MR PURDEY: Well, I felt sort of that it was putting the
2 onus on me to do the research, which -- obviously I am a
3 very small farmer and I have not got much money, so to
4 do the sort of extent of tests that would be necessary
5 to provide some sound scientific evidence that would in
6 my mind spearhead MAFF to take it up was obviously out
7 of my pocket. All I was able to do was to do what I had
8 been trying to do, to test BSE cows on my farm in
9 relation to the healthy cows on my farm. I felt I was
10 in a no-win situation. I was limited in what I could
11 actually do to achieve that requirement that Ray Bradley
12 was putting on me.
13 MR WALKER: Now, before we leave the 1992 bundle, I just
14 wanted to take you to the letter that we have behind tab
15 12. This is a letter of 22nd December 1992, sent to you
16 by Satoshi Ishikawa, who is the Professor and Chairman
17 of the Department of Ophthalmology at the School of
18 Medicine, Kitasato University in Japan.
19 Did you remember this letter?
20 MR PURDEY: Yes, very much so.
21 MR WALKER: In this letter Professor Satoshi Ishikawa says
22 that:
23 "Your description of mad cows and warble fly to
24 organophosphates compounds is exactly true."
25 That must have been encouraging.
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1 MR PURDEY: Yes, it was. It was a good New Year's present
2 actually. It arrived on January 1st, from memory.
3 MR WALKER: Do you know how Professor Ishikawa had become to
4 be interested by all that?
5 MR PURDEY: Professor Ishikawa is a sort of long-standing
6 global author on low dose chronic organophosphate
7 poisoning. He was involved in identifying this whole
8 region in Japan, the Seikou(?) district, where he
9 identified a sort of chronic neurotoxic syndrome,
10 particularly amongst children in that area. He had been
11 using the treatments that I was trying to use on my cows
12 on humans with great success, where he was actually
13 curing people with a range of neurodegenerative diseases
14 after a six-month course of treatment. In a sense, he
15 was one of my gurus at this particular stage of my
16 research.
17 MR WALKER: Is there anything more you would like to say
18 about that letter before we leave 1992?
19 MR PURDEY: I think what was interesting is he was citing
20 vacuolation in the particular neuronal tracts and the
21 nuclei, like the red nucleus, the vestibula, the
22 reticular formation, which correlate precisely with the
23 regions that Wells et al identified as the regions that
24 were vacuolated in their first Veterinary Record paper
25 back when BSE first arose. So Ishikawa seemed to have
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1 raised this correlation in a pathological sense, but as
2 far as the exact detail of the pathology, I am obviously
3 not certain, because it is, you know, couched rather
4 sort of vaguely. I wanted to investigate this a lot
5 further.
6 MR WALKER: Thank you. That brings me on to 1993. So we
7 can put away this 1992 year book, and you can take out
8 1993. I would like to begin with your letter to Farming
9 News. YB 93/3.26/1.1. It is first document after
10 divider 3. Here we have a letter published in Farming
11 News on 26th March 1993, headed "False Link Made in BSE
12 Case". Is this a letter you sent?
13 MR PURDEY: Yes.
14 MR WALKER: You begin by saying you were enraged to read in
15 many national newspapers last week that links were being
16 suggested between the farmer who contracted CJD disease
17 and his consumption of milk from his BSE-suffering cow.
18 MR PURDEY: Yes.
19 MR WALKER: Then you go on to refer to chemically induced
20 CJD. What was it that enraged you about reading this in
21 the national newspapers?
22 MR PURDEY: Well, I knew that there were no prion protein
23 cell lines expressed in the memory system. Therefore,
24 if prion protein is indeed the infectious commodity, in
25 whatever form, then I could not see, unless of course
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1 the udder was damaged by some mechanical damage and
2 caused an inflammation -- and it is known that prion
3 protein is involved in the lymphatic system, and
4 therefore any inflammation might have prion proteins
5 present; but if a cow has got mastitis, then its milk is
6 not sold. I could not really see the scientific logic
7 in what they were saying.
8 In particular, I was aware that kuru mothers who
9 had breast-fed their children, there was no association
10 between kuru developing in the children of kuru mothers
11 who breast-fed their children, who had themselves
12 developed kuru at a later stage. Kuru is another prion
13 disease, similar to new variant CJD, BSE.
14 MR WALKER: Then, later on in this letter, you said that
15 your trials with your own BSE cow, Damson:
16 "Were spearheading research into chronic OP
17 pesticide induced BSE. It has been proved that some of
18 the OPs that effect the bovine food chain also exhibit
19 serotonin agony, cholinesterase depression and
20 mutagenicity", what you described as, "the dirty three
21 detonators for BSE".
22 Is there anything more that you would like to say
23 about this letter?
24 MR PURDEY: Yes, I mean I still hold to some of that.
25 I remember when I met the Ministry in 1994, James Hope
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1 pointed out to me that they had found no mutagenic
2 association in any cell line with BSE. That is not to
3 say that there is not one, but you know, I hold quite
4 high regard for James Hope, and in a sense I thought
5 that maybe it was not a mutagenic mechanism that was
6 involved, it was something post-translational, that is
7 after the protein has been synthesised in the genetic
8 material, that it was some covalent modification,
9 perhaps after the protein had been synthesised that
10 changed the shape of the protein.
11 SIR NICHOLAS PHILLIPS: Mr Purdey, I noticed in some of
12 your earlier letters or articles that you had yourself
13 been referring to BSE as a "slow viral infection". It
14 sounds as though by this time you had been converted to
15 the prion theory?
16 MR PURDEY: Yes, the further I went on, and I started
17 reading Stanley Prusiner's work. And I think, even
18 though I do not hold to some of the aspects of Stanley
19 Prusiner's and his associates' work, I think that it
20 seems that the prion protein must have some pathogenic
21 ability that is unusual in relation to other proteins
22 that are known to be deformed in the disease.
23 MR WALKER: The next stage in the chronology, I think, is
24 Brainstorm, who was a cow whose mother Churnside
25 Birthday we have been talking a bit about, because in
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1 paragraph 11 of your statement, you tell us that in
2 April 1993 it seemed that Brainstorm was exhibiting
3 symptoms of BSE?
4 MR PURDEY: Yes.
5 MR WALKER: You started treating with magnesium sulphate in
6 the hope of remitting the symptoms?
7 MR PURDEY: Yes.
8 MR WALKER: And on 10th May, the Government vet revisited
9 the farm and took the view that Brainstorm no longer
10 exhibited symptoms of BSE, and withdrew movement
11 restrictions that had been placed on the cow?
12 MR PURDEY: Yes.
13 MR WALKER: Just for the record, I think we have the letter
14 from the Ministry confirming that just behind divider 5
15 in this bundle. If you turn on to that? It is the
16 second document after divider 5. We see here a letter
17 of 11th May, YB 93/5.11/1.1. Is this a letter that you
18 received?
19 MR PURDEY: Yes.
20 MR WALKER: After the first paragraph which describes what I
21 have just recounted, the second paragraph says that:
22 "Mrs Crea reported that although exhibiting no BSE
23 symptoms, the cow did not appear to be totally healthy."
24 There was then a suggestion that you should have
25 her examined by your own vet. Is there any significance
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1 to that?
2 MR PURDEY: I think the first two visits, they obviously
3 thought there was a possibility of BSE because of the
4 symptoms that we observed. It was on the third visit
5 that the symptoms that were suggested of BSE had
6 remitted. And this is why they are saying that -- yes,
7 I mean I would agree with her prognosis at that time,
8 that, you know, it did not look as though the cow had
9 BSE, although I was still aware of -- I was unhappy
10 about the cow. I still thought, you know, that I could
11 still see signs of it. But they were very subtle. She
12 also inspected the cow in the field. When you get them
13 in the building and they have got BSE, the symptoms are
14 exacerbated and the stress of being in the building
15 brings out the symptoms, but on the third visit we
16 examined the cow in the field, and I think, you know,
17 those signs just were not present.
18 MR WALKER: Now, at about this time too, there was further
19 correspondence between you and the Minister or rather
20 your MP and the Minister. If we could look at that? We
21 need to go back to April, so back in the bundle to
22 divider 4. The first document after divider 4 is YB
23 93/4.16/1.1. This is a letter from Mr Gummer to your
24 MP, Tom King.
25 Mr Gummer begins in his letter, which is dated
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1 16th April 1993, by thanking Mr King for a letter of 5th
2 April, which had enclosed letters from you and from
3 Professor Ishikawa. Is that the letter we had seen of
4 December of the previous year?
5 MR PURDEY: Yes, it was.
6 MR WALKER: Then he goes on to say that the hypothesis of
7 spread of disease by infective feed had been
8 substantiated by epidemiological studies. In the next
9 paragraph, he says:
10 "Although there are superficial similarities in
11 histopathology, there are important differences as
12 between BSE and organophosphate toxicity ...", which he
13 says have been agreed and extensively studied and
14 documented by neuropathologists.
15 He then turns to a point about CJD, and says that
16 the Department of Health would be interested to see case
17 reports and medical literature on that.
18 Finally, he concludes by saying:
19 I would add that much research is underway to
20 investigate the many aspects of this group of diseases,
21 including studies on the mechanisms which lead to the
22 development of disease. I enclose a copy of the interim
23 report on research of the Spongiform Encephalopathy
24 Advisory Committee which describes this, and which
25 Mr Purdey may be interested to see."
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1 Can I ask you what your reaction was when you
2 learnt of this letter?
3 MR PURDEY: Well, when I read the list of research that was
4 being carried out, I could not see anything at all that
5 was relevant to my hypothesis, nothing at all. It
6 seemed to be all tailored to investigate the official
7 scrapie leap theory as the cause, and some work on the
8 prion protein, but that obviously involved -- you know,
9 they were saying that the abnormal prion from sheep had
10 jumped into cows and mutated, or whatever it was.
11 MR WALKER: Now, I think you have mentioned in your
12 statement that you wrote again to Mr King and that
13 letter was forwarded on to the new Minister of
14 Agriculture, Mrs Shephard. We see her reply just after
15 divider 6. Our reference is YB 93/6.16/1.1. This is a
16 letter dated 16th June 1993, from Gillian Shephard to
17 Tom King, referring to a letter that Mr King had sent
18 Mr Gummer on 17th May. In the second paragraph,
19 Mrs Shephard said this:
20 "Although OPs can react with a variety of
21 biological substances, I am advised that OP poisoning
22 differs so greatly from BSE that the link is most
23 unlikely. Clinically, OP poisoning is so dissimilar to
24 BSE that the two are unlikely to be confused, and there
25 is no evidence to link any immunotoxic or mutagenic
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1 effects of OPs with BSE. The papers provided by
2 Mr Purdey have no bearing hypothesis. Two of them are
3 concerned with conditions in man which have some
4 features clinically similar to CJD, but not
5 pathologically. I would add that research on BSE is the
6 responsibility of our Central Veterinary Laboratory,
7 where there is also considerable expertise in OP
8 toxicity in farm livestock."
9 That is the end of the quote. Again, what was
10 your reaction to receiving a copy of that letter?
11 MR PURDEY: Well, firstly I do not agree that -- she had
12 not differentiated between acute OP poisoning and
13 chronic OP poisoning, which show markedly different
14 symptoms and pathology. It was a mainstay of my theory
15 that this was a chronic problem, if you like, a high
16 dose chronic problem. And this had been sort of
17 ignored. This vague generalisation was in a sense a
18 misrepresentation of what I was actually saying.
19 Also, I can never recall having linked the
20 immunotoxic effects of acute high doses of
21 organophosphates to BSEs because work has shown that in
22 mice the immune system is actually required for the
23 disease process to ensue, because when they have
24 engineered mice with an immune knock-out, they cannot
25 develop the disease.
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1 So, I think what is relevant is the fact that
2 organophosphates will actually accelerate some aspects
3 of the immune and cytokine system, which could have
4 great relevance to the BSE disease process, I believe.
5 This was really a misrepresentation of what I was going
6 trying to say. But I agree I had linked the mutagenic
7 effects of OPs to the disorder; but my work has evolved,
8 and I no longer really feel that mutagenicity has a role
9 in the disease.
10 PROFESSOR FERGUSON-SMITH: Still, at that time you still
11 felt that the disease was caused by a combination of an
12 environmental factor and the prion, is that not right?
13 MR PURDEY: Yes.
14 PROFESSOR FERGUSON-SMITH: It seems that this particular
15 letter does not recognise that.
16 MR PURDEY: Yes, that is right.
17 MR WALKER: There seems to have been some movement in
18 Government thinking about what they should do about
19 organophosphates shortly after this, because we have in
20 our Purdey references bundle -- if I could ask you to
21 keep hold of the bundle you have at the moment, but also
22 to be given the Purdey references bundle, and turn to
23 tab 10 -- we have, at tab 10, an article from the Sunday
24 Telegraph dated 22nd August 1993. It is by Greg Neale,
25 the Environment Correspondent for the Sunday Telegraph.
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1 If you can be shown the document? You see it begins:
2 "The Government is reviewing the safety of
3 chemical veterinary products, including some used in the
4 home, amid fears that they could be linked to illness in
5 farmers using sheep dip, or even bovine spongiform
6 encephalopathy - BSE or 'mad cow' disease.
7 "Gillian Shephard, the Agriculture Minister, has
8 ordered the review of all veterinary products containing
9 chemical organophosphates, including flea collars used
10 on cats and dogs as well as on cattle and sheep ...
11 "An Agriculture Ministry spokesman said yesterday
12 that the review did not mean there were grounds for
13 linking 'mad cow' disease with OPs as has been suggested
14 by some researchers."
15 Then, later in the article, reference is made to
16 what is said by a spokesman at the Animal Health
17 Division, which is consistent with what I have just
18 quoted. Then Ian Gardiner, the head of the NFU, on farm
19 policy, is quoted as saying:
20 "So far, nothing has happened that increases the
21 probability that the Ministry's hypothesis of what
22 caused BSE is wrong. Government advisers have advised
23 the minister and the NFU has no basis on which to differ
24 from that advice."
25 Then the article goes on. Sir Richard Body, the
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1 MP for Holland with Boston and former chairman of the
2 Select Committee on Agriculture Pesticides, said:
3 "We have not got on top of BSE, and there is a
4 grave suspicion that there are other reasons for it. The
5 Ministry made up its mind too quickly."
6 What did you know about the proposed review at the
7 time?
8 MR PURDEY: Well, I did not know anything about it at all.
9 Certainly in relation to BSE, I was not aware that there
10 was any proposed review into looking at the chemicals as
11 a possible link to BSE or CJD.
12 MR WALKER: I would like to take you, I think, to the piece
13 that appeared in the Western Morning News at about that
14 time, unless there is anything more about what you would
15 like to say about what we see from the Sunday Telegraph
16 here?
17 MR PURDEY: No.
18 MR WALKER: That means, I think, that we can put away this
19 bundle. We come back to the bundle that you have open.
20 If you turn to tab 8, our reference is YB 93/8.20/1.1.
21 This is an article in the Western Morning News which is
22 headed "Pesticide May Lead to Mad Cow Disease". I think
23 here that you say that -- or rather are quoted as saying
24 that -- you believe evidence was growing that the OP
25 chemicals could be linked to the disease, and that
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1 Government scientists believe mad cow disease was
2 triggered by contaminated cattle feed, but critics claim
3 that OP chemicals may have been to blame.
4 There is then a quote from the MAFF spokesman
5 saying that it is quite clear that feed is the main
6 source of the infection, although mother to calf
7 transmission could not be ruled out. Then reference is
8 made to the review that is proposed by Gillian Shephard,
9 and a quote from you, if I can take the second
10 paragraph:
11 "The Ministry's epidemiologist, John Wilesmith,
12 tells me that their extensive investigations have
13 covered my theory, but they admit not having done
14 detailed studies of delayed effects of cumulative low
15 dose OP toxicity."
16 MR PURDEY: Yes.
17 MR WALKER: When had Mr Wilesmith told you that?
18 MR PURDEY: I was referring to -- when I said "they", I was
19 referring to the Ministry in general. I had heard a
20 taped interview with a member of, I think, the
21 Veterinary Products Committee or the Veterinary
22 Medicines Directorate, who stated that when he was asked
23 whether he had looked at the chronic low dose effects,
24 he said "No, they had not".
25 MR WALKER: Unless there is anything more that you want to
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1 say about that article, I would like to move on to --
2 MRS BRIDGEMAN: Could I just ask one question? It so
3 happens later in this article that somebody suggests
4 that the Department of Health ought to be involved.
5 I wonder whether throughout this story, up to this
6 stage, you had had any direct dealings with the
7 Department of Health rather than the Ministry of
8 Agriculture?
9 MR PURDEY: No, I had not, no.
10 MRS BRIDGEMAN: Was this because it did not occur to you,
11 or for some other reason?
12 MR PURDEY: I suppose because I was a farmer, I was
13 immediately involved with the agriculture. I think BSE
14 was always considered a farming issue, an agricultural
15 issue. But they did come in at a much later date.
16 SIR NICHOLAS PHILLIPS: Could I just ask about this
17 article? It reports MAFF making the point that there
18 was clear evidence linking BSE to feed. At this stage,
19 was that something that you would have regarded as
20 simply incompatible with the theories that you were
21 putting forward, or something that could accommodate
22 these theories?
23 MR PURDEY: Well, there were a few slight, sort of, weak
24 points of my theory which I was trying to grapple with
25 at the time, which, you know, the Ministry have pointed
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1 out. One was the Channel Islands, which was never a
2 compulsory warble fly eradication zone. Having said
3 that, exactly the same systemic types of phosmet were
4 used on the island for control of lice. Because it is a
5 very warm winter climate on the islands, that is
6 conducive for lice to breed.
7 I still did not feel particularly happy with that
8 line of attack on my theory. I did not feel that
9 I addressed it. I thought maybe, you know, that
10 feedingstuffs had a role in taking in the
11 organophosphates that are bioconcentrated -- such as the
12 systemic phosmet -- that are bioconcentrated in the fat
13 of the meat and bonemeal, and fat was a large account of
14 the cattle feed rations on the Channel Islands because
15 they were producing Channel Island milk, which was very
16 high fat milk.
17 I am a Channel Island cattle breeder myself, and
18 it is common policy to use even protected fat, and
19 rations up to 20 per cent of animal fat in the
20 concentrate feed. I think perhaps this could explain
21 why you have this particularly high incidence of BSE,
22 particularly on Guernsey Island. I was also stressing
23 that maybe the genetics of the Guernsey cow, what would
24 have been close inbreeding of the Guernsey cow on the
25 Channel Islands, and of the Jersey on Jersey Island, and
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1 this may have lead to low levels of detoxification
2 enzymes in the livers of Guernsey Cows. Perhaps -- and
3 this is total hypothesis, but I was requesting at the
4 time that that should be looked at at the meeting I had
5 with the Ministry in due course.
6 SIR NICHOLAS PHILLIPS: Thank you.
7 MR WALKER: Could I just ask you a bit about the Department
8 of Health? We saw in that letter of 16th April 1993
9 from Mr Gummer that he said that the Department of
10 Health would be interested to see your references.
11 I noticed that when Gillian Shephard wrote, she said
12 that the references that you had provided were concerned
13 with conditions in man which have some features
14 clinically similar to CJD, but not pathologically?
15 MR PURDEY: Yes, I think maybe they had overlooked the
16 spongiform. But I suppose they could have been arguing
17 that this particular type of pathology in BSE, which is,
18 as I was describing earlier, this intensive
19 glycosylation was not similar to the type of spongiform
20 encephalopathy in the couple of articles that I produced
21 as references. It could have been a very fine point,
22 but I do not know.
23 MR WALKER: All I was seeking to draw from this was that at
24 least in April of 1993, MAFF were saying to you that the
25 Department of Health would be interested in some
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1 references. It seems from the letter of June 1993 that
2 you indeed sent the references on to MAFF?
3 MR PURDEY: Yes, I did, yes.
4 MR WALKER: So they could no doubt pass them on to the
5 Department of Health. But that the only comment that
6 you were getting back about the references that you had
7 sent in was that they had no bearing on your hypothesis,
8 as far as I can see from this correspondence?
9 MR PURDEY: Well, I sent in a considerable number of
10 references. I can remember, I think, about 40 published
11 peer-reviewed articles that dealt with -- because no one
12 had put this together, I was just substantiating facets
13 of the whole BSE disease issue with this particular
14 specific article from the published peer-reviewed
15 literature by way of assimilating my case. That was,
16 after all, the only means of my disposal, because I did
17 not have a laboratory and I had to rely on other
18 published peer-review evidence from experimental work,
19 et cetera.
20 MR WALKER: Thank you. Now, the next thing I would like to
21 take you to is an article by Dr Richard North, which is
22 the next page in that bundle. Our reference is YB
23 93/8.20/2.1.
24 This is an article headed "The corruption of
25 Science", which appeared in something called UKEPRA News
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1 on 20th August 1993. Do you know what UKEPRA stands
2 for?
3 MR PURDEY: I think it is better to ask Richard North.
4 Maybe someone present understands.
5 MR WALKER: In this article, Richard North describes some of
6 the work you had been doing, and he also described,
7 I think, what had happened in relation to Damson, is
8 that right?
9 MR PURDEY: Yes, I think so, yes. I was not actually aware
10 of this exact article. I was aware of an article that
11 Richard North had written in The Times. I think that
12 this was virtually the same article by the looks of it.
13 MR WALKER: I have taken you to it because it is referred to
14 in a letter that you have told us about in paragraph 10
15 of your statement, the letter of 21st October. If you
16 turn on to tab 10, it is just before the end of tab 10,
17 just ahead of tab 11. Our reference is YB
18 93/10.21/1.1. This is a letter that Mr Wilesmith of CVL
19 sent to Mr North, who begins by saying:
20 "Dear Mr North, I have been asked to write to you
21 about your article 'The Corruption of Science' in UKEPRA
22 News of 20th August, to draw attention to a number of
23 facts that seem germane to the issues you have raised."
24 In this third paragraph, he refers to the causes
25 that were tested against the then known facts. In the
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1 second to last sentence, he says:
2 "At those meetings a number of experiments were
3 reported which clearly show that material from brains of
4 animals showing clinical signs of BSE can pass on an
5 infectious neurodegenerative disease to some other
6 species of animals. It is difficult to see how evidence
7 of this kind could support a theory that BSE is simply
8 due to chronic OP poisoning."
9 Was your theory that it was simply due to chronic
10 OP poisoning?
11 MR PURDEY: Yes, I mean it could have been as a result of
12 some knock-on effect of organophosphate. For instance,
13 in my Journal of Nutrition and Medicine article,
14 I hypothesise that the organophosphate somehow, by
15 malforming the prion protein, would then evoke an
16 autoimmune attack on the extra large sort of molecular
17 conglomeration of the prion fibril at the end of the
18 disease process. This could set off a type of
19 autoimmune attack that did not display the normal
20 inflammation that one would expect in the pathology of
21 an autoimmune disease, merely because prion protein
22 seems to have a role in activating lymphocytes, et
23 cetera.
24 So when the prion protein is damaged, you would
25 not have the normal inflammatory attack. So by

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1 injecting in material with perhaps a mutant prion, if
2 you like, brain protein would then invoke the same
3 response to that protein as was invoked in the original
4 cow which -- so the pathology would mirror exactly what
5 had happened in the first generation BSE case.
6 I had also suspected that as organophosphates are
7 known to generate free radicals and kick off chain
8 reactions of free radicals, that this too, when you take
9 out brain material and subject it to homogenisation,
10 which is what you do in a laboratory in a transmission
11 trial, you actually draw out the ion, which is a free
12 radical itself, and that kicks off and continues this
13 chain reaction free radical attack. When that is
14 injected into a host animal, in a sense that free
15 radical disease is passed on into the next generation.
16 So I did not necessary agree, now, that you needed
17 a sort of virus agent to produce transmission. I think
18 it was totally compatible with my theory that this
19 disease could be transmitted.
20 MR WALKER: Yes. Then later in this letter we turn to the
21 next page, in the third paragraph, on that page, what
22 Mr Wilesmith says is that he looks forward to seeing the
23 scientific publication of the effects of toxin
24 administered to the suspect case in your herd. He adds
25 some comments to that:
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1 "I have received personal correspondence from Mr
2 Purdey and would point out that he has not met a wall of
3 official or scientific indifference, but we have tried
4 to point out to him the strengths and weaknesses of his
5 theories just as others do in the scientific world. We
6 have in fact recently offered to meet Mr Purdey."
7 We will see in a moment the letter of the
8 preceding month which contains that offer.
9 MR PURDEY: I cannot recall them ever having pointed out
10 the strength of my theory at all.
11 MR WALKER: I think that does bring me to the letter
12 suggesting a meeting, which is the preceding month, just
13 before tab 10. Our reference is YB 93/9.17/1.1. This
14 is a letter sent from Gillian Shephard to your MP, Tom
15 King. In the second paragraph, Mrs Shephard says:
16 "In view of the highly technical nature of the
17 issues involved, I suggest that Mr Purdey should meet my
18 scientific advisers so that he can fully explain his
19 views and they, in turn, can raise any points which they
20 may have for Mr Purdey to consider. Before this can be
21 arranged, however, it is important that Mr Purdey
22 supplies the detailed references mentioned. I also
23 suggest that the objectives of the meeting are clearly
24 set out and agreed. This would prepare the way for any
25 discussion to be as beneficial as possible. If Mr
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1 Purdey was also able to supply a pre-publication copy of
2 his paper for distribution to the appropriate experts on
3 a strictly 'in confidence' basis (as is usual with such
4 papers), then this would also facilitate the
5 understanding of his hypothesis."
6 I think you tell us that in fact you did forward a
7 pre-publication copy of your paper, and arrangements for
8 such a meeting were indeed made?
9 MR PURDEY: Yes, yes.
10 MR WALKER: Yes find an acknowledgment of your pre
11 publication paper arriving in October. And if you would
12 turn on to our reference YB 93/10.14/1.1, it is just
13 before the letter we were looking at a moment ago. This
14 is a letter dated 14th October 1993 from Gillian
15 Shephard to Tom King again. The Minister writes:
16 "Thank you for your letter of 1 October enclosing
17 a pre-publication copy of Mr Purdey's paper on BSE. I
18 can confirm that a copy of the paper has been sent to
19 the Veterinary Medicines Directorate and that his points
20 will be noted and borne in mind during the consideration
21 of the OP sheep dip issue by the Veterinary Products
22 Committee.
23 " As you will be aware Mr Purdey's paper covers a
24 lot of ground and we will need to consider it very
25 carefully and my officials will be in touch with him
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1 shortly to arrange a meeting."
2 Now that, I think, has brought us to halfway
3 through your paragraph 13 of your statement, if we could
4 turn to that? Do you have your statement handy?
5 MR PURDEY: Yes.
6 MR WALKER: If you could just turn to paragraph 13. After
7 dealing with this letter of 14th October, you say:
8 "In the period before the meeting, I became
9 extremely concerned that the Ministry had breached the
10 confidentiality of my paper."
11 We saw in that earlier letter, in September, that
12 Mrs Shephard had indicated that the paper could be
13 submitted on strict 'in confidence' terms. You say:
14 "The Ministry had complained to the Press
15 Complaints Commission about articles by Mr Christopher
16 Booker in the Sunday Telegraph which supported my
17 theories on BSE and which had criticised MAFF staff.
18 The Ministry included an evaluation of my theories and
19 they included an extract of the paper ..." that you had
20 sent to the Minister.
21 Mrs Shephard wrote to Mr King about that on 13th
22 December, and in the circumstances said that they did
23 not regard what had been done as a breach of
24 confidence. I would like to look at that with you, if
25 I may? If you turn on in our 93 year book to
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1 divider 12. The second document after divider 12 is a
2 letter dated 13th December from Mrs Shephard to Tom
3 King. Have you found that?
4 MR PURDEY: Yes.
5 MR WALKER: And it refers to a letter from him of 19th
6 November, dealing with your concerns. What the Minister
7 says in the second paragraph is:
8 "Please convey my apologies to Mr Purdey if there
9 has been a misunderstanding. I did indeed promise to
10 treat Mr Purdey's paper on an 'in confidence' basis, but
11 I am sure that nothing we have done runs contrary to the
12 spirit of that undertaking."
13 In the third paragraph:
14 "It is in relation to an article by Mr Booker
15 dated 26th September that my Permanent Secretary wrote
16 to the Press Complaints Commission seeking redress for
17 the way in which the article unfairly criticised MAFF
18 staff. Mr Purdey's theories were an integral part of
19 Mr Booker's argument and were set out in the most public
20 manner conceivable, in the pages of a Sunday newspaper.
21 We did not think it unreasonable, therefore, to include
22 a technical evaluation of the theories, as portrayed by
23 Mr Booker, in our private correspondence with the PCC;
24 the paper forwarded to you by Mr Purdey was an extract
25 from that document. This correspondence was copied only
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1 to the PCC, whose discretion can be relied upon, and to
2 the Editor of the Sunday Telegraph whose columnist was
3 self-evidently already fully acquainted with Mr Purdey's
4 theories.
5 "Under the circumstances, I do not feel this can
6 be construed as a breach of confidence."
7 Did you agree with that?
8 MR PURDEY: Well, I think this was not exactly true, but it
9 did not particularly bore me.
10 MR WALKER: Then the letter went on:
11 "I would, however, like to end this letter on a
12 more positive note. A meeting has been arranged for
13 17th January to enable Mr Purdey to discuss his paper.
14 We have gone to a great deal of trouble to assemble a
15 team of experts in the wide range of fields covered by
16 Mr Purdey's paper, including the flying in of an expert
17 from the Neuropathogenesis Unit in Scotland. I hope
18 that any misunderstanding over the matters raised in
19 this letter does not overshadow what I am sure we all
20 hope will be a useful meeting."
21 Did any misunderstanding about the matters raised
22 in the letter overshadow the meeting which eventually
23 took place?
24 MR PURDEY: No, I do not think so.
25 MR WALKER: Thank you. That then brings us, I think, almost
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1 to the meeting. Just before we do, we need to deal with
2 the written answer of 1st December -- no, sorry. If
3 I could just check a reference? If you would forgive me
4 a moment? Yes, it brings us to the meeting. We can put
5 away the 1993 year book and please take out the 1994
6 one. The reference I was looking for is in fact in our
7 1994 year book, 94/1.12/1.1. This is the very first
8 document in the book. It is dated 12th January 1994 and
9 is a letter to you from Mr Eddy. Do you remember
10 receiving this?
11 MR PURDEY: Yes.
12 MR WALKER: He tells you that in addition to Mr Eddy, and
13 I think others from the CVL, and your brother who was
14 going with you, the meeting was going to be attended by
15 Dr Woodward from the Veterinary Medicines Directorate,
16 Ms Lamb from the Pesticides Safety Directorate, Dr Marrs
17 from the Department of Health, and Dr Hope from the
18 Neuropathogenesis Unit. I assume he was the person
19 being flown down from Edinburgh?
20 MR PURDEY: Yes.
21 MR WALKER: The last point in the letter was they proposed
22 to record this meeting:
23 "That was standard practice at meetings of the
24 advisory panel on badgers and TB and we find that it
25 avoids any later confusion over what was said and what
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1 was not said."
2 The meeting you have described in paragraph 14 of
3 your statement, you said there that the officials
4 promised a longer look at your theory, but ruled out
5 scientists carrying out research into the theory. Who
6 ruled it out?
7 MR PURDEY: Well, it became apparent when I eventually got
8 a letter from Tom Eddy that they had said that because
9 of the considerable number of chemicals and contaminants
10 that I had proposed, which I do not believe was actually
11 the case, it would be far too difficult and expensive to
12 set up the necessary in-vitro trials which I was
13 requesting. I was actually requesting the work that the
14 Institute of Psychiatry had just carried out -- well, 18
15 months ago. That is what I was trying to get tested.
16 MR WALKER: You say in your statement, then, that:
17 "All were agreed the disease was slowly dying
18 out. They said that was because of the food ban, and
19 you replied that you thought it was because particular
20 pesticides were withdrawn or naturally phased out, for
21 example, by virtual eradication of the warble fly at the
22 end of the 1980s."
23 MR PURDEY: Yes.
24 MR WALKER: How was that response received?
25 MR PURDEY: One question that I was asked during the
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1 meeting was by Ray Bradley. I think it was, sort of,
2 quite a good question. He said, "Let us say
3 theoretically that your theory is correct, have we made
4 the right moves to cease the spread of BSE?" And he
5 asked me this question. I sort of went through the
6 possible candidate organophosphates that I thought could
7 be behind the BSE epidemic. I sort of pointed out that
8 warble fly was being eradicated anyway, and therefore
9 the use of organophosphates was considerably reduced,
10 which would obviously have a net effect on the reduction
11 of BSE incidence in years to come, which has borne
12 true.
13 I also pointed out that compulsory sheep-dipping
14 had ceased. Of course, sheep carcasses had been going
15 into meat and bonemeal, which then was banned in 1988,
16 so the residues of organophosphates coming from sheep
17 material resulting from compulsory twice-yearly
18 sheep-dipping, that had been stopped by banning the
19 offal. But I did point out that I was concerned also
20 about the use of an organophosphate called pirimiphos
21 methyl -- it is a organophosphorous powder that is mixed
22 into grain for controlling weebles and mites in the
23 storage silos.
24 What concerned me was that the intervention stores
25 had to apparently be treated at six-monthly intervals;
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1 and the residues of organophosphates were getting so
2 high that to deal with the problem they had to raise the
3 maximum permitted residue level from two parts per
4 million to ten parts per million, which is a five-fold
5 rise in the permitted residue levels in the grain.
6 I understand, though this was hearsay, that a lot of the
7 grain that had been destined for human use went into the
8 animal food chain during the 1980s. I was worried about
9 this particular entry of organophosphates into the
10 bovine food chain around about this time. I did not
11 feel this problem had been addressed. It was in fact
12 addressed later.
13 MR WALKER: Thank you. You then go on to say that although
14 you were promised a tape, you were never sent one. Do
15 you recall whether the meeting was tape-recorded?
16 MR PURDEY: Yes, an official had come from MAFF's Tolworth
17 with Tom Eddy specifically for the purpose of taping the
18 meeting. He had a reel-to-reel tape recorder, and the
19 whole meeting was taped, apart from the interval when we
20 had lunch. At the beginning of the meeting, my brother
21 wanted to tape the meeting. They said "No, there is no
22 need. We will send you a copy of the tape after the
23 hearing". But I never received the tape even though
24 I asked for it.
25 MR WALKER: It has been quite short notice for the Ministry
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1 to try to find a record of the meeting. What they have
2 been able to find we have at YB 94/1.17/2.1, which is a
3 little bit further on. This is a memo from Mr Eddy to
4 Miss Mannix in the Press Office. He said:
5 "We had a very amicable meeting with Mr Purdey and
6 found that we had a surprising amount of common ground.
7 We agreed that neither side would go for knee-jerk
8 reaction, and I do not want to damage what I hope is now
9 a reasonable relationship with Mr Purdey by seeming to
10 go back on this. I would therefore prefer to take the
11 following line ..."
12 Then he sets out a proposed quote, I think, for a
13 press release:
14 "MAFF officials and experts from", and he sets out
15 the various departments, "today met Mr Purdey to discuss
16 the paper he submitted in confidence to the Ministry
17 with his views on the origin of the BSE epidemic. It
18 would not be appropriate for the Department to discuss
19 the details of the meeting as this would breach the
20 confidentiality under which the paper was given to the
21 Department. However it is clear that Mr Purdey agrees
22 with the Department in three important areas namely:
23 that the risk to humans is remote; that the present
24 regulations are adequate to control the disease in
25 cattle and that the number of cases is declining; and on
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1 the importance of recycled animal protein in the spread
2 of the disease."
3 Any comment on that?
4 MR PURDEY: Yes, I mean I think I would agree. I saw this
5 meeting as a light opening up in a stormy sea. Yes,
6 I think we did have quite a lot of agreement,
7 ironically, but maybe the importance of recycled animal
8 protein and the spread of the disease -- yes, I did
9 agree I felt it had a role, but I would not say I felt
10 it was quite as important as the Ministry considered
11 it. I did not think it was totally necessary to cause
12 the disease; that exposure to OP on its own in some
13 cases could trigger off the disease.
14 MR WALKER: I would like to take you on then to March, if
15 I may? If you go on to divider 3? Just after divider
16 3, we find a letter to you from Tom King, your MP. Our
17 reference is YB 94/3.11/1.1. This is a letter dated
18 11th March 1994. He says that he is:
19 "... pleased to hear your comments on the meeting,
20 and I am sure you are right to say that face-to-face
21 discussions of this kind are far the best way to deal
22 with the sort of misconceptions that otherwise arise and
23 also help to remove some of the entrenched positions
24 that get taken. I gather from the 'other side' that the
25 meeting was certainly thought to be helpful and [he
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1 hoped] that it might be followed in other areas where it
2 might also be appropriate."
3 Then he goes on to say:
4 "Your letter raises the further unresolved queries
5 which do exist and I am very interested to see that you
6 have had offers of funds for a Research Project. If
7 those can be confirmed, I think it would certainly be
8 worth raising the idea with MAFF."
9 We have not got your letter to him. Can you tell
10 us a bit about the offers of funds for a research
11 project?
12 MR PURDEY: Well, I cannot exactly work this out, where
13 this came from. I think there was an accurate press
14 report he was referring to, rather than my letter,
15 because I cannot exactly work out where this came from.
16 MR WALKER: At the moment, that is a bit of a mystery.
17 MR PURDEY: I know there was some inaccurate media in the
18 television and newspapers that I had received funding
19 from Europe, a sort a windfall, which I wish I had,
20 but ... Yes, I cannot recall where that comes from,
21 unless it was some very small project that I was
22 spearheading that I have forgotten about. But I have
23 virtually received no funding at all for my research,
24 except for more recently where, you know, various people
25 have put funds into -- well, the Institute of Psychiatry
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1 work, you know, et cetera.
2 MR WALKER: The next document that we have is in June. So
3 we turn on to tab 6 of YB 94/6.02/1.1. It is a letter
4 of 2nd June 1994 from Mr Eddy to you. Do you remember
5 receiving this?
6 MR PURDEY: Yes.
7 MR WALKER: He begins by saying:
8 "I am very sorry not to have replied before now to
9 your letters of 28 January and 6 February."
10 I think you told us before that those were letters
11 you sent following up on the meeting?
12 MR PURDEY: Yes.
13 MR WALKER: In paragraph 15 of your statement, you have
14 drawn attention to some aspects of Mr Eddy's letter, in
15 particular the question of citrus pulp, and his having
16 said that there is no evidence that well-preserved
17 uncontaminated pulp is toxic to ruminants. What Mr Eddy
18 has said about that is that he does recollect that on at
19 least one occasion you and he did discuss the question
20 of citrus pulp. He believes that he did make the point
21 that it seemed to be unlikely to be the cause of a
22 disease largely restricted to this country, because
23 citrus pulp is not something uniquely produced here and
24 is therefore unlikely to be uniquely a component of
25 animal feed in this country.
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1 MR PURDEY: (Nods)
2 MR WALKER: Do you recollect him making that point to you in
3 the past?
4 MR PURDEY: Yes, I did. But I think he is taking the
5 involvement that I was hypothesising with citrus pulp
6 out of context. This was one avenue of potential
7 organophosphate toxicity. I have research papers backing
8 -- giving evidence that OPs were found to be present as
9 residues in citrus pulp. I think this whole response
10 from the Ministry, I felt very let down that they were
11 trying to sidetrack the whole issue of my theory on to
12 one aspect of it, which was citrus pulp, rather than
13 taking a holistic sort of perspective of my work. For
14 instance, there was no mention of warble fly liquids,
15 which were after all the mainstay of my theory and the
16 backbone of what I was really saying. The statement he
17 made about there being no evidence that uncontaminated
18 pulp was toxic to ruminant, this is an obvious
19 statement. I was talking about contaminated pulp. This
20 was, you know, what I was talking about.
21 MR WALKER: By this stage, I think your article in the
22 Journal of Nutritional Medicine had appeared. Indeed,
23 I think that Mr Eddy says that they have now seen it.
24 I thought perhaps I should take you to it. If we can
25 just keep this bundle on the table for the moment? We
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1 need to return to the loose document we were looking at
2 earlier. I think it is somewhere on the table there.
3 This was what was described as a special article in the
4 Journal of Nutritional Medicine in 1994. We talked a
5 little bit about this article with Professor Lacey. Can
6 I just tell you what Professor Lacey said about it? It
7 is in our transcripts for Day 5 at page 73. What
8 Professor Lacey said was:
9 "The paper produced by Mark Purdey proposing the
10 organophosphorous cause for BSE was published in the
11 Journal of Nutritional Medicine of which I am on the
12 editorial board, and I refereed it."
13 He then refers to another paper he refereed. He
14 said:
15 "Both of those papers, in my capacity as referee
16 and editor, I said to the editor 'reject'. My main
17 criticism of Mark Purdey's paper was that he had shown,
18 rightly, a statistical association between BSE and the
19 use of organophosphorous chemicals -- that is right --
20 and he had also pointed out that BSE was very rare in
21 organic beef herds where OPs were not used. That is
22 correct. But the interpretation that OPs caused BSE is
23 wrong for these two reasons."
24 Then he gave the Committee two reasons. The first
25 was:
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1 "[in] the great majority of organic beef herds,
2 the animals are slaughtered before they are aged two and
3 half years, there only being 80 confirmed cases I know
4 of in these young animals. Therefore, the age of the
5 animal guards against BSE, not the lack of use of OPs.
6 "Of course ...", I think this is the second
7 reason, "... with dairy herds, he had not provided any
8 evidence looking at the association of OPs in other
9 countries and the lack of BSE. In the dairy herds, the
10 apparent association of OPs and BSE was a common factor,
11 the cow. So, true, the cows were having OPs, the cows
12 were suffering from BSE, and also did not explain the
13 epidemiology because OPs had been used for some years.
14 The editor overruled my objections by saying, I suppose
15 with some reason, that everyone had the right to express
16 a hypothesis. But I do not accept it."
17 Were you aware at the time that Professor Lacey
18 had turned it down?
19 MR PURDEY: No, I mean, I actually read his peer review.
20 He made a very intelligent critique of my theory. I was
21 quite -- you know he had obviously read through the
22 entire paper in detail. I must say, a lot of
23 peer-reviewers -- often you get the gist that they
24 probably have not read through the paper, but he did say
25 categorically that he recommended it for publication.
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1 And the previous paper in The Ecologist he did the
2 same. Yes, I mean, I found his critique quite helpful.
3 He said at the end that this is making an important
4 advancement into the science of transmissible spongiform
5 encephalopathies, and should be published, and words to
6 that effect. In answer to his criticisms to the
7 Inquiry, I cannot understand his assertion that --
8 because organic cattle live a lot longer than cattle on
9 conventional farms, because the whole point is that on
10 organic farms cattle are not forced, they are not given
11 growth hormones, et cetera, so they would die older than
12 cattle on inorganic farms.
13 So whilst I agree that killing an animal in the
14 two to three year bracket might mask animals that are
15 already incubating BSE, I think on organic farms cattle
16 can be killed around the three, three to four year mark,
17 which is an area where I think a lot of the cases of BSE
18 would already have shown up. I do not really agree with
19 his criticism at all there. In fact, that is the other
20 way round.
21 The other critique he levied at me was about
22 taking no bearing on organophosphate use in other
23 countries around the world. I think he again
24 misrepresented my theory by looking at OPs in general,
25 instead of focusing into the systematic aspect of my
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1 theory; systematic being relevant in the fact that the
2 chemical goes through the skin and penetrates the
3 central nerves, which is the route of this disease. In
4 fact, the chemical had to be poured along the spinal
5 column, which is just millimetres from the actual
6 proteins damaged in the disease. The chemical in this
7 form of systemic delivery bypasses the liver and goes
8 straight in, so it is not detoxified.
9 I think he really misrepresented the detail of
10 what I was saying in my theory in relation to
11 organophosphate compounds. Certainly, more recently,
12 I have published journals that have looked at the use of
13 phosmet in countries all around the world, particularly
14 in the European perspective.
15 SIR NICHOLAS PHILLIPS: How have you obtained that data?
16 MR PURDEY: I have been travelling to countries around the
17 world that have had clusters of the disease, and I have
18 visited farms and done surveys in Switzerland and
19 France. I have been to Colorado looking at the deer
20 disease. This year I am going to the High Tatra
21 mountains in Czechoslovakia to look at a cluster of CJD
22 in farm workers; and I am going to Iceland to look at
23 scrapie in the north part of the island.
24 SIR NICHOLAS PHILLIPS: Have you done any research into
25 farms abroad which have not experienced BSE to see
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1 whether they nonetheless have been using
2 organophosphates in a systemic matter?
3 MR PURDEY: No. I have not been to any farms that did not
4 have BSE, which, again, I agree, is an inadequacy in my
5 work. It was time factors. I had to sort of get away
6 from the farm for a quick week, and go to survey --
7 I found the Swiss Government very cooperative; they put
8 me in touch with a lot of farms that had had BSE. I had
9 a fascinating time going to questionnaire the farmers
10 there. I found a correlation between organophosphate
11 use on the farms that had BSE. As you say, I should
12 have gone to look at the farms that did not, in an ideal
13 world, yes.
14 MR WALKER: What I was proposing to do, rather than to take
15 you through the detail of this article, was to take you
16 to some of the things you have said in your later
17 article in 1996 in Medical Hypotheses, which I think are
18 a development of what you were putting in the 1994
19 article.
20 MR PURDEY: Yes.
21 MR WALKER: I was also proposing, if I may, to just ask you
22 to remind yourself of what you said in paragraph 15 of
23 your statement about the latter part of 1994.
24 MR PURDEY: Which section?
25 MR WALKER: Paragraph 15 of your statement.
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1 MR PURDEY: Right, yes.
2 MR WALKER: And you describe there some of the
3 correspondence that you had in the second half of 1994
4 on the citrus pulp aspect --
5 MR PURDEY: Yes.
6 MR WALKER: -- and on the attitude of the Ministry. I was
7 not proposing to take you to the detail of those
8 letters, unless there is something in particular that
9 you want me to raise right now. If it is convenient to
10 you, I would like to move on, if I may, to the
11 submission of the articles for Medical Hypotheses.
12 Those two articles we have in our Purdey references
13 bundle at tab 1. If you could be provided with that
14 again? Now, I think what we have at tab 1 is both
15 articles. Part 1 is entitled "Mechanisms for a
16 Clinically Induced Pathogenesis Transmissibility".
17 MR PURDEY: Yes.
18 MR WALKER: This was eventually published in 1996, but as
19 stated here, it was submitted in April 1995 and accepted
20 in May 1995. The thesis put forward in part 1 is
21 described in the abstract. If I can just quote from it:
22 "Multi-site binding organophosphate toxic
23 metabolites penetrate the fetus, covalently binding
24 with, phosphorylating and ageing serine, tyrosine or
25 histidine active sites on fetal central nervous system
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1 prion protein. An abnormal negative charge corrupts
2 prion protein molecular surface, which blocks both
3 proteases and chaperones from accessing their
4 cleavage/bonding sites. This impairs normal degradation
5 and folding of prion protein respectively. Once the
6 abnormally phosphorylated abnormal prion protein isoform
7 agent is initiated, any stress event ensuing in adult
8 life induces a nerve growth factor-mediated synthesis of
9 normal cellular prion protein isoform, thereby becoming
10 infected or transformed into the same; due to the
11 vicious circle of positive feedback invoked by the
12 blocking of a prion protein-specific kinase. Prion
13 protein could therefore serve as a hitherto unrecognised
14 critical link in a chain of delayed neuroexcitotoxic
15 proteins that are triggered off by chronic exposure to
16 specific classes of chemical or metal that hit and run
17 during the vulnerable in utero period, producing
18 spongiform encephalopathy disease years later."
19 Doing the best I can, going through the article,
20 that did seem to me to be a fair summary of the points
21 that you were making?
22 MR PURDEY: Yes.
23 MR WALKER: I wanted to take you on, if I might, to the
24 second part, the epidemiological perspective. It may be
25 that there are points that you would like to come back
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1 to in the light of the epidemiological perspective. If
2 we go on to page 445, the abstract there tells us first:
3 "The paper elucidates the flaws in the official
4 hypothesis that BSE originated from alterations in the
5 way that scrapie-contaminated cattle feeds were
6 manufactured."
7 And you have an alternative hypothesis in the
8 second paragraph. You say:
9 "Both the timing, distribution and dynamics of
10 usage of these specific organophosphates correlates with
11 the epidemiology of BSE as well as accounting for the
12 23,000 cattle that have developed the disease yet were
13 born after the 1988 ban on scrapie-contaminated cattle
14 feed."
15 If I could, I would like to take you to page 446,
16 where you deal with the flaws in the Ministry theory.
17 In the right-hand column of page 446, at the top, what
18 you say about the Ministry theory is that:
19 "It was a safe bet hypothesis --
20 MR PURDEY: Yes.
21 MR WALKER: -- in that virtually every brand of cattle
22 concentrate feed manufactured during the 1980s contained
23 the incriminated MBM ingredient with virtually every cow
24 in the UK ingesting it."
25 Then you go on to say about the born-after-the-ban
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1 cases that:
2 "Not only are farmers witnessing BSE cattle that
3 never ate the incriminated animal protein, but
4 approximately 16,500 of 17,000 born after the ban cattle
5 were also born out of mothers who had never exhibited
6 the outward symptoms of BSE. This may rule out
7 possibilities that the majority of these BABs cases are
8 due to a spread of the disease through vertical
9 transmission."
10 MR PURDEY: Yes.
11 MR WALKER: Also in this section, you refer to the MAFF
12 experimental farm at Exmoor, which I think you mentioned
13 earlier.
14 MR PURDEY: Yes.
15 MR WALKER: In the next section, on page 448, you describe
16 the epidemiology of organophosphate-induced BSE.
17 SIR NICHOLAS PHILLIPS: Just before we get there though, if
18 one was going to take this epidemiological consideration
19 to its conclusion, one would want to do the positive as
20 well as the negative, and to explore whether the born
21 after the ban cattle, which are also cattle born after
22 organophosphates were being reduced, as you have pointed
23 out, but nonetheless been subjected to organophosphates.
24 That, of course, is a major operation which, presumably,
25 you would not have been able to undertake?
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1 MR PURDEY: No, that is right. But I have done sort of
2 anecdotal with farmers who I know.
3 SIR NICHOLAS PHILLIPS: Yes.
4 MR WALKER: Then, in the section that begins on page 448, I
5 have noticed that there was a heading on the next page
6 "compulsory high dose phthalimide containing
7 organophosphate warble fly insecticides."
8 In that section, in the right-hand column on page
9 449, you refer to the compulsory twice annual OP
10 treatment that MAFF had required.
11 MR PURDEY: Yes.
12 MR WALKER: You also say that:
13 "Low springtime levels of magnesium probably
14 explain why a significantly greater number of acute
15 poisonings of cattle following warble fly treatment were
16 reported."
17 You go on to say that:
18 "Epidemiological research into the month of birth
19 of those cattle that develop BSE indicates that there is
20 a ten-fold increase of BSE frequency in cattle that are
21 born in the autumn over those that were spring-born."
22 MR PURDEY: Yes.
23 MR WALKER: And I think that the reference for that is the
24 article by Hoinville in the Veterinary Record in 1994.
25 MR PURDEY: Yes.
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1 MR WALKER: At the foot of page 449, you refer to:
2 "Some of the toxicological 'unknowns' surrounding
3 the OP warblecide phosmet and its phthalimide
4 ingredient, has led to an extremely cautious approach
5 being adopted by various establishments."
6 You mention the Bureau of Standards at Prague and
7 the World Health Organisation.
8 MR PURDEY: Yes.
9 MR WALKER: In the last sentence on that page, you say:
10 "MAFF have surprisingly granted approval for its
11 veterinary use, but refrained from approving its use on
12 arable crops."
13 MR PURDEY: Yes.
14 MR WALKER: Are you offering an explanation for that?
15 MR PURDEY: No. I found this rather strange because
16 phosmet is used as a non-systemic pesticide in arable
17 farming. I would not perceive that as deadly, using it
18 as a systemic formulation applied directly to animals.
19 Phosmet, once it is in the open environment, does
20 actually degrade quite rapidly. It is when it gets
21 conjugated on to fat that it tends to remain more stable
22 in its systemic formulation.
23 I was also surprised, looking at the Russians, who
24 have rightly or wrongly been recognised to have a very
25 cavalier approach to pesticide licensing. They used
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1 phosmet in Russia as an animal pesticide, yet they
2 refused to allow women, at any stage during their life,
3 to have contact with the pesticide at all. They only
4 allowed men between the ages of 20 and 40 to have
5 contact with phosmet. This was when they wore an
6 aspirator mask that was getting rid of the chemical
7 through filters.
8 This seemed bizarre, very incongruous with the way
9 that, surprisingly, the British authorities seem to have
10 been very lax with this particular chemical in relation
11 to the Russians, because usually, as track records show,
12 it was the other way round.
13 MR WALKER: Can I draw your attention now to page 450 and
14 your Figure 2? This is the distribution of confirmed
15 cases of BSE by month of birth, compared to the
16 estimated dynamics of OP phosmet usage.
17 MR PURDEY: Yes.
18 MR WALKER: Could you explain that a little?
19 MR PURDEY: In relation to ...?
20 MR WALKER: What does this figure demonstrate?
21 MR PURDEY: Sorry, the ...
22 MR WALKER: What we have are some bars. Are we looking at
23 the same figure, Figure 2 on page 450?
24 MR PURDEY: Yes.
25 MR WALKER: We have bars along the horizontal axis. We have
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1 months of birth, then we have bars for the number of BSE
2 cases, presumably that were born in that month?
3 MR PURDEY: In the particular month, yes.
4 MR WALKER: We see a high point in 1988.
5 MR PURDEY: Yes.
6 MR WALKER: Now the line that we see going across in 1989 --
7 it is a little bit of the way up the vertical axis, what
8 is that?
9 MR PURDEY: Yes, the publishers made the mistake. The line
10 did not go to zero because phosmet was still in use, so
11 I crossed out -- it should have tailed off where I have
12 drawn in the line on to the diagram. Whilst three
13 brands of phosmet were withdrawn around this time, there
14 were still, I think, three or four brands on the market
15 and they continued in use at a very low level. It is
16 still on farm shop shelves today. I saw it a few days
17 ago in our local farmer's store.
18 MR WALKER: I wanted to ask you about that line. As
19 I understand it, the line is your estimate of phosmet
20 use?
21 MR PURDEY: That is right.
22 MR WALKER: How does that correlate with the vertical axis?
23 Is that the number of cattle you believe were subject to
24 phosmet use?
25 MR PURDEY: No, it was a rather cavalier line which was
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1 drawn just to -- there was a double up in usage in that,
2 when the period when Fenthion -- Fenthion was very
3 popular. This was the lower dose, the 5 milligrammes
4 per kilogramme body weight organophosphate, and it was
5 very popular that was taken out -- it was not actually
6 taken out, there were restrictions put on its use where
7 you have to throw the milk away for five days if you
8 wanted to use the chemical.
9 Therefore, every farmer immediately plumbed for
10 phosmet, because you only had to discard milk for six
11 hours, which meant that you would never actually have to
12 throw it away. So all farmers took on the use of
13 phosmet from the middle of 1985 onwards. I think
14 Fenthion just quickly disappeared off the market in this
15 country after that.
16 MR WALKER: Also on that page, you make a point about
17 Northern Ireland. You say that it first took up high
18 dose phosmet in 1978, and that correlates with the first
19 reported case of BSE in Northern Ireland in 1989.
20 MR PURDEY: Yes, the warble fly programme in Ireland, they
21 would run their warble fly programmes at the same time
22 with the south and the north working in tandem together,
23 but in the north of Ireland, they abided by the UK sort
24 of requirements under the Warble Fly Order, which was
25 the twice a year treatment; whereas, in the south of
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1 Ireland, they used a once a year treatment, and in the
2 case of phosmet, it seemed to be going out at a much
3 lower dose of 6 milligrammes per kilogramme body weight
4 in the south of Ireland. Southern Ireland ironically
5 eradicated their warbles using this low dose treatment
6 before the north of Ireland.
7 MR WALKER: The other thing I wanted to draw attention to
8 was your next paragraph where you have asserted that:
9 "A strong correlation can be drawn between warble
10 fly zones in Britain where farmers were compelled to
11 treat their cattle annually and zones with the highest
12 incidence of BSE".
13 You refer there to Figure 3, where I think you
14 have two diagrams, two maps showing this account
15 effectively?
16 MR PURDEY: Yes.
17 MR WALKER: There are then sections on organophosphate
18 residues and cattle concentrate feeds, and on
19 organophosphate sheep dip. I wanted to take you on, if
20 I may, to the concluding two paragraphs where you say:
21 "It seems possible that the withdrawal from the UK
22 market between 1989 and 1991 of three out of four of the
23 high-dose phosmets which corresponds with the virtual
24 eradication of the warble fly in the UK, plus the advent
25 of the passport system on OP grain treatments in the
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1 early 1990s, coupled to the recent depletion of the UK
2 'grain mountain' intervention stores, plus the
3 abolition of compulsory twice-annual sheep dipping with
4 OPs in 1992, is perhaps accountable for the recent
5 substantial downturn in the incidence rate of BSE in
6 1994.
7 "This downturn of BSE incidence could also be
8 partially ascribable to the fact that family lines of
9 cattle carrying greater susceptibility to TSE on their
10 PrP or liver detoxification enzyme genes have already
11 been eradicated by the disease. Thus, the
12 BSE-susceptible genotypes have largely become
13 annihilated from the UK cattle herd".
14 Is there anything more you would like to say about
15 that paper?
16 MR PURDEY: Not really, no. Obviously, I have extended
17 aspects and evolved in other ways, as one does with a
18 scientific theory. I still very much hold to -- perhaps
19 in the light of the research done at the Institute of
20 Psychiatry the actual biochemical mechanism, you know,
21 once you have experimental evidence that then acts as a
22 pointer. Before you are floating in space, devising
23 hypothesis which are academic and all very intriguing
24 and exciting. Until you have evidence of what is going
25 on you do not have a pointer which -- I think now it
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1 would be easier for me to focus, now we have some
2 evidence to focus into specific avenues of the way that
3 the biochemistry is working.
4 MR WALKER: On that, can I say that the Committee has heard
5 evidence from, as you may know, Dr Whatley and that I
6 anticipate as further work is done over the course of
7 the next year the Committee will be kept informed of the
8 results of that work.
9 MR WALKER: I am getting a little bit concerned about the
10 time, because I have another 15 minutes of questions
11 that I wanted to ask you about. I am conscious that we
12 are approaching 1.30.
13 MR PURDEY: Well, let us go through it quickly.
14 MR WALKER: I do not want to rush you. Would it be
15 acceptable if I was going to continue questioning until
16 about 1.45?
17 SIR NICHOLAS PHILLIPS: Yes.
18 MR WALKER: Thank you. I wanted now to turn to paragraph 19
19 of your statement. You are dealing there with some
20 arrangements that were made for some testing by the
21 MRC. I think the first thing I would like to do is to
22 take you to a fax which we have in our year book for
23 1995. If the bundle for 1994 can be put away. I think
24 we can put away the Purdey references bundle as well,
25 for the time being.
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1 In the bundle for 1995, just after divider 3, we
2 have a fax that Dr Ray sent to Lauderdale Productions.
3 In that fax Dr Ray says that -- Dr Ray, I should add, is
4 at the Medical Research Council in Leicester?
5 MR PURDEY: Yes.
6 MR WALKER: In that fax what Dr Ray says is that the topics
7 of organophosphate toxicity and organophosphate protein
8 interactions are certainly of interest, and that he had
9 spoken to you about your hypothesis. Is that right?
10 MR PURDEY: Yes. He had phoned me up and asked if I would
11 give their department a lecture on my theory.
12 MR WALKER: Did you go to give the department a lecture?
13 MR PURDEY: Yes, I did.
14 MR WALKER: Did you talk about the proposed test that
15 Lauderdale Productions had in mind?
16 MR PURDEY: Yes, that came secondary to me being invited to
17 give a lecture. This was being organised at the time,
18 I believe.
19 MR WALKER: The fax from Dr Ray suggested two problems with
20 the suggested experiments. The first was the practical
21 toxicology. He said:
22 "Many commercial pesticides were in a thion
23 compound, which, within the body, needed to be
24 transformed to an active oxon form." The oxon form, that
25 is phosphorous double bounded to an oxygen molecule?
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1 MR PURDEY: Yes. That is right, yes.
2 MR WALKER: In relation to that he said one would have to
3 test these oxon forms as well, instead of the pesticides
4 themselves; but:
5 "That is not an insurmountable problem, as we have
6 a number of pure oxons. They are rarely commercially
7 available however."
8 As I understand it, the chemical DFP that was
9 actually used for the test is a chemical which is a pure
10 oxon form?
11 MR PURDEY: I must say, until today I did not realise
12 that. I thought that DFP had to be metabolised like the
13 organophosphates to yield the oxon form. I take David
14 Ray's point that oxon was tested in this particular
15 test. I still have grievances about that there are
16 other breakdown compounds relating to phosmet, the
17 chemical, notably the phthalimide which, I feel, was
18 very relevant to this test.
19 Those are circumstances in which I was pressured
20 into accepting this test, linked to trying to get this
21 film off the ground. They were desperate to get the
22 film commissioned. It all hinged on the going on of
23 these tests. I had a gun at my head that the film would
24 not go ahead unless I accepted these quick tests that
25 had been proposed by David Ray.
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1 MR WALKER: What David Ray then said, having described
2 various other problems, at the foot of page 2 of this
3 fax was that he did not have the funds or the staff to
4 do a lengthy test, but that he would be prepared to do a
5 preliminary test with DFP and, if that proved positive,
6 to then undertake further studies. So that in the fax
7 is described the way on which it was put?
8 MR PURDEY: Yes.
9 MR WALKER: Does that accord with your recollection at the
10 time, that so far as Dr Ray was concerned the first
11 stage would have to be doing the test with DFP, and if
12 that was positive then you might be able to go on
13 further?
14 MR PURDEY: Yes; but I made it quite clear that I felt that
15 phosmet, the actual chemical used on farms, would be a
16 far more relevant test to do than using DFP because that
17 would be nearer to the reality of what was happening on
18 farms.
19 MR WALKER: Another aspect to what happened in relation to
20 these tests is the question of exactly what it was that
21 was kept secret from you?
22 MR PURDEY: Yes.
23 MR WALKER: As I understand it, again this is from Dr Ray,
24 he believed it was the results of the test that were to
25 be kept secret from you at least for some period of the
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1 time but that the protocols for the testing were
2 protocols that were agreed with you. Is that right?
3 MR PURDEY: Yes, I was told that if there was any
4 interaction with the prion protein and the
5 organophosphate then they would do a challenge for
6 protease resistance which is establishing whether we
7 have the putative BSE agent. Basically, I was kept in
8 the -- the reasons for the secrecy was linked to the
9 Channel 4 film, where the film wanted a surprise element
10 from me, so I would react to the result, you know,
11 genuinely as the first time I had heard it.
12 MR WALKER: Yes.
13 MR PURDEY: You know, I remember Dr Ray telling me that he
14 thought it was very unfair that I suddenly had had these
15 results sprung on me with the camera running. Really,
16 I had no idea exactly what had happened in the test,
17 what procedures had and had not been used. I had to
18 interpret four documents in two minutes and interpret
19 the data and make my comments. Here he said to me he
20 thought it was very unfair that this is what had
21 happened. So I was kept in the dark for that reason of
22 surprise element on film, which I could accept, you
23 know, that it would make a better film if I was not
24 acting.
25 MR WALKER: There is another aspect that you have raised in
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1 paragraph 19 which is concerning the question of whether
2 the protein with the glycolipid anchor was to be
3 examined?
4 MR PURDEY: Yes.
5 MR WALKER: You say yourself in paragraph 19 that you knew
6 that would not be the case, that it would be a --?
7 MR PURDEY: Yes, I mean this was another reservation that
8 I had about the test that I discussed with David Ray.
9 I felt a glycolipid anchor should be attached because
10 I hypothesised in my Medical Hypotheses article that we
11 had open that there was a potential binding sight where
12 the glycolipid anchor joins to the main body of the
13 prion protein, that it was a potential serine binding
14 sight, which serine sights are the sights that
15 organophosphates generally target. But, having said
16 that, there are other amino acids sights, such as the
17 tyrosine and histidine sights which can also be targeted
18 by organophosphates, as well as other sights with
19 different interactions that organophosphates cause; but
20 this was the main avenue that I thought would be
21 essential to test, as a first stage, to look at whether
22 organophosphates interact with the serine sight. The
23 fact the there was a potential serine sight where the
24 glycolipid anchor joins to the prion protein, concerned
25 me at the absence of the glycolipid anchor.
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1 David Ray had quite correctly pointed out that
2 they had not yet got the technology to produce this
3 recombinant prion protein without its glycolipid
4 anchor.
5 I think one of my other grievances was that when
6 you are trying to test to see whether a chemical, a
7 protein, is folding in the wrong way, how can you do
8 with that with a recombinant protein? You need a living
9 protein, which is going through all the different stages
10 of protein folding with the presence of organophosphate
11 to establish a misfolding possibility. To use a static
12 recombinant protein was, in a sense, not a very good
13 test. I was surprised it was never proposed to me, the
14 tissue culture process which has been done at the
15 Institute of Psychiatry.
16 MR WALKER: The other aspect of this that I need to mention
17 to you is the question of somebody saying that MAFF
18 owned this work, which is the last point you make in
19 paragraph 19?
20 MR PURDEY: Yes, there were a lot of rumours that were
21 going about at this time. Initially, Channel 4 had
22 commissioned this research. I know that for a fact, I
23 have seen the letters. Then when Channel 4 came to pay
24 for the work, after it had been completed, they actually
25 received a letter from David Ray saying the work had
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1 already been paid for and there was no need.
2 I was aware that the Ministry were aware of the
3 results, certainly before I was; and it seems possible
4 that they were aware of the results before Channel 4
5 Television were aware of them. There were also a lot of
6 other people involved in the work other than David Ray.
7 Christopher Bostock at what was the AFRC at Compton in
8 Berkshire was also jointly involved in this trial. He
9 has much closer associations with MAFF, so I believe,
10 than they do at Leicester at the MRC Toxicology
11 Department. There could have been some link up here
12 with the Compton laboratory as opposed to the MRC labs.
13 But there was a lot of hearsay, a lot of rumours,
14 because I had been kept in the dark over the whole thing
15 because of the secrecy aspect for the film I was, you
16 know, mystified by what had been going on.
17 MR WALKER: Yes. What Mr Ray has told us is that he did not
18 say that MAFF owned the work. I do not think you have
19 suggested that he said that?
20 MR PURDEY: No. I have not, no.
21 MR WALKER: He has also said that payment for the work came
22 from his own MRC funds?
23 MR PURDEY: Right. Well, I was not told that before. Yes.
24 MR WALKER: I would like now then to come on to paragraph 20
25 of your statement, where you deal with Mrs Browning's
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1 letter and her written answer to Parliament. I do not
2 think that I need take you to the documents in
3 question. You make the point that she relied on the
4 conclusion of Dr Ray as the basis for saying that your
5 ideas were unsubstantiated?
6 MR PURDEY: Yes. Yes.
7 MR WALKER: Then in paragraph 21 you describe subsequent
8 correspondence both with Mrs Browning and with Mr King?
9 MR PURDEY: Yes.
10 MR WALKER: Mr King, having received a letter from the then
11 Minister of Agriculture, Mr Hogg, saying that in the
12 light of this MRC work it would not be appropriate or
13 justifiable to use public funds to carry out further
14 research to test your ideas.
15 We have heard from Dr Whatley that nevertheless
16 funding was made available for his work at the
17 Maldsley. Were you involved with that funding?
18 MR PURDEY: I am unaware of this.
19 MR WALKER: You do not know where he got it from.
20 MR PURDEY: This is the work in relation to my theory.
21 MR WALKER: Yes, in relation to your theory?
22 MR PURDEY: The funds were raised by various different sort
23 of small groups and individuals. I collected a lot of
24 money via several newspaper articles. Money came from a
25 group called the Independent Research Fund that funds
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1 this type of work, and was collected from a range of
2 concerned individuals. So this all came from individual
3 members of the public. Yes, we payed I think £14,000 in
4 all to run this trial, which was the trial which
5 I always wanted to do because I felt it was the most
6 representative of my theory because it involved a living
7 cell.
8 MR WALKER: I think the actual trial brings us to beyond the
9 period of 20th March 1996, which is the cut off date for
10 the review of facts by the Committee. They have
11 nevertheless heard evidence about the work that was done
12 by Dr Whatley. We are hoping that we will hear further
13 as further work is done.
14 MR PURDEY: Yes.
15 MR WALKER: I think that, for my part, that brings me to an
16 end to the questions I wanted to ask you today. There
17 may be other matters we need to write to you about as
18 our work proceeds. There is one question, which I ask
19 almost all the witnesses who come, which is: Have you
20 changed your diet at all since learning about BSE?
21 MR PURDEY: No. No. No. I think, you know where there is
22 a risk involved, I would tend to eat, you know, organic
23 produce. For me, you know, I feel safe eating organic
24 beef. So it has perhaps strengthened my commitment,
25 certainly as regards my family and children, to having
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1 organic produce.
2 MR WALKER: The Committee may have some questions.
3 PROFESSOR FERGUSON-SMITH: It would help me very much if
4 you would clarify for me just when you brought the prion
5 hypothesis into your -- from some of the comments that
6 we have had just this morning it has been a little
7 confusing. I would like to know. Because at one point
8 you did not accept the prion hypothesis, you felt it was
9 all organophosphates. Then at a particular point you,
10 before you provided these two important papers, you
11 obviously changed your mind.
12 MR PURDEY: Yes. It was when I became aware of Prusiner's
13 work and his associates that that is what made me
14 realise that perhaps there was an association between
15 organophosphate.
16 PROFESSOR FERGUSON-SMITH: Would that be in about 1990 or
17 something like that?
18 MR PURDEY: Yes, something like that.
19 PROFESSOR FERGUSON-SMITH: Probably the transgenic work ...
20 MR PURDEY: I was interested in the conformational change
21 to the prion protein, because organophosphates are known
22 to produce a similar conformational change to other
23 brain proteins, like acetyl cholinesterase and
24 neurotoxic --
25 PROFESSOR FERGUSON-SMITH: Yes.
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1 MR PURDEY: Then I integrated my theory. I think there
2 were so many of these theories, and I think they all can
3 actually be linked up in a very positive way. There is
4 almost room for all of them. This is a very complex
5 disease as you know.
6 PROFESSOR FERGUSON-SMITH: It will clearly need more
7 research.
8 MR PURDEY: Yes.
9 PROFESSOR FERGUSON-SMITH: One very small point that arose
10 very early in your evidence, something that I had
11 missed, was that you mentioned something about meat and
12 bonemeal being made in Australia and New Zealand.
13 MR PURDEY: Yes.
14 PROFESSOR FERGUSON-SMITH: Do you actually know whether it
15 was imported? We can find this out I am sure. Was
16 there imported meat and bonemeal from United Kingdom?
17 MR PURDEY: No. No. They exported virtually all of their
18 meat and bonemeal. I think it went to China.
19 PROFESSOR FERGUSON-SMITH: So that if the origin was not
20 scrapie and in fact was derived from bovine ...
21 MR PURDEY: Yes, that would stand. They have only had
22 scrapie on an island of New Zealand.
23 PROFESSOR FERGUSON-SMITH: And they slaughtered it ...
24 MR PURDEY: Yes, that is right.
25 SIR NICHOLAS PHILLIPS: I have no questions. Thank you
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1 very much for coming to help us. Could I just make one
2 thing plain? I have made it plain before that this is
3 not a scientific Tribunal of Inquiry. We are really
4 looking at the way the BSE emergence was handled. We
5 have been asked to review the history, which we shall
6 do. What I have made plain is that we are not in a
7 position ourselves to evaluate conflicting scientific
8 theory.
9 MR PURDEY: Yes, I understand.
10 SIR NICHOLAS PHILLIPS: If there are people who are hoping
11 that we are going to be able to say: "Having read
12 Mr Purdey's latest paper we are persuaded it is
13 scientifically correct" or "incorrect", I fear they may
14 be disappointed. Thank you very much.
15 MR PURDEY: Thank you very much.
16 PROFESSOR FERGUSON-SMITH: Perhaps I should say, on a
17 personal level, I think certainly more research is
18 required on several of these aspects.
19 MR WALKER: I think that Mr Purdey's evidence concludes our
20 Stage 2 for the time being. Stage 3 of the evidence is
21 now scheduled to resume on 27th April at 9.30.
22 SIR NICHOLAS PHILLIPS: Before which we have quite a lot of
23 work to do, if anybody thinks we are going to have a
24 long Easter break.
25 MR WALKER: No, we will be very busy.
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1 (1.45 pm)
2 (Hearing adjourned until 9.30 am on 27th April 1998)