La strana storia di Mark Purdey e la mucca pazza

The BSE Inquiry / Statement No 23A (supplementary)
Mr Mark Purdey Issued 07/06/1999
(not scheduled to give oral evidence)

THE BSE INQUIRY
SUPPLEMENTARY STATEMENT BY MARK PURDEY
GENERAL COMMENTS

My concerns with Phase 1 of the BSE Inquiry surround what I believe to be the inaccuracies and misleading statements made in several of the written documents and hearings involving the various critics of my Organo-phosphate/BSE thesis.
I take issue with the core of the arguments propounded during the hearings of November 5 1998 (Day 5). This session hosted the various representatives/advisors of the organisations opposed to my thesis – Mr Roger Cook (NOAH), Dr Tony Andrews (formerly at the Veterinary Department of the MLC), Dr Tim Marrs (senior medical officer, Joint Food Standards and Safety Group) and Mr John Tasker (Grampian Pharmaceuticals).
Understandably, these people all share an interest in defending their past decision making skills and/or their commercial products against the potential threat that my thesis on the UK’s overuse of the systemic OP phosmet presents to their professional reputations and/or financial interests.
All of these individuals had generally utilised the same lines of argument to counter my thesis. Consequently, in my view, their various statements are all flawed in the same way, so I can largely address all of their statements via a single attack.
I refer to what I consider to be the most obvious flaws; in paragraph 6 to 16 below.
Equal Amounts of the warblecide, Phosmet were applied each year in Eire, UK and France (paragraph 28 Mr Cook’s statement no. WS 270).
This was an inaccurate claim for many reasons. It is particularly ironic in the light of Dr Andrew’s statement that the UK’s sales figures for phosmet usage had been lost! (Dr Andrews supplementary statement no. WS 269A para 45). How could they arrive at such an assumption if the UK’s sales figures were genuinely lost?
Furthermore the French body INRA have confirmed to me in writing that only 150,000 doses of phosmet were used per year in France during the mid 1980s only. (I hold a 1996 fax from Mr Roger Cook of NOAH to the French ‘Ecology Party’ which demonstrates that NOAH were aware of this French sales data).
In Eire, O’Keefe et al state that phosmet was first taken up at the end of their warble campaign in 1978 where it was only used once a year in certain regions. We are told that the Dovea region only ever used phosmet (Dr Andrews’ statement WS 269A paragraph 49), but if Dovea had conformed to Eire’s eradication campaign that was initiated in the 1960s, , then other types of OP warblecide must have been used there prior to the introduction of phosmet in 1978.
It should also be pointed out that Mr Tasker’s Statement [WS273] does not specify that they are relating to phosmet as an individual compound when it cites Eire’s warblecide usage figures for 1978-1980 (Annex 1 paragraph 7 of WS 273). This should be clarified, because these same figures, also cited in a letter I hold from the NFU chairman, Ben Gill, would appear to relate to all types of OP warblecide such as fenthion and famphur which were more widely used in Eire than phosmet at that time.
However in the UK, phosmet use steadily increased from 1975 until 1985, when it became the only type of systemic OP left on the market – at a time when it was compulsory to apply warblecide twice a year in the warble infested zones at 20mg/kg dose employing a 20% concentration fluid.

Warble Fly Treatment was never compulsory (Mr Cook’s statement paragraph 39 WS 270)
It was compulsory from 1982 onwards; whereby treatment was required 2 times a year in various sized zones all over the country. One must question why I needed to take out a High Court action to debar the compulsory treatment of my cows in 1984 if it wasn’t compulsory?(see my Inquiry Statement WS 23 paragraphs 3 and 4) Mr Cook’s statement is contradicted for example by Dr Andrews (WS 269A paragraph 43) where he refers to "the notifiable period of the disease when Mr Purdey did not wish to treat his cattle."
Compulsory Warble Fly Zones only existed in tiny pockets in SW England and Wales in the 1980s (Mr Cook’s statement paragraph 47 WS 270)
This is painting a totally inaccurate picture. As depicted in MAFF’s Annual Animal Health Reports for this period, warble fly zones were declared all over the UK. Although it is true that the majority of warble outbreaks did occur in the South, this generally reflects the geographical distribution of BSE incidence.
The Warble dose rate for Phosmet was set at the same 20mg/kg dose rate in all of the nine countries where Phosmet was licensed and marketed (Mr Cook’s statement paragraph 27 WS 270)
This is a true statement in itself but is misleading. For in real terms, it presents a flawed and irrelevant argument against my theory because the UK, Ireland and France (NB BSE endemic countries) were the only countries to have licensed phosmet and actually applied it at its warble fly dose rate.
Warble flies have simply never existed in countries such as Australia and New Zealand where phosmet has only been licensed for use at the lower10mg/kg lice dose rate. This is analogous to purchasing an American made Combine Harvester in the UK, where its universal instruction manual would naturally give you the different settings for all types of combinable crops such as soya beans, even although soya is not actually grown in this country.
I believe that my thesis on the use of phosmet and its unique practice of ‘overdosing’ in the UK still holds. Phosmet is unique amongst systemic OPs in that it contains a phythalimido moiety which belongs to the family of chemicals to which thalidomide belongs. It was the unique compulsory twice annual usage of a systemic pour-on formulation of the OP phosmet in the UK – used at a 20mg/kg bodyweight dose employing a 20% concentrated warblecide – which initiated the UK’s BSE epidemic.
Once solvent extraction ceased in the rendering process in the early 1980s, the tallow fraction of MBM became responsible for the spread and bioacumulation of both phosmet and its ‘prion’ products up the farm animal foodchain.
THE STATEMENT OF MR COOK, DIRECTOR OF NOAH (NATIONAL OFFICE OF ANIMAL HEALTH) A DETAILED RESPONSE TO NOAH’S STATEMENT; ‘THE ALLEGED LINK BETWEEN OPS AND BSE’ (WS 270)

Background (paragraphs 12 to 15 of Mr Cook’s statement)
I made it quite clear in the mid 1980s that my reasons for challenging MAFF’s Warble Order stemmed from my fears surrounding the delayed neuro-psychiatric and mutagenic aberrations resulting from exposure to ‘systemic’ types of ‘pour-on’ OP insecticides. I pointed this out directly to Roger Cook of NOAH via a public letter to Farmers Weekly of 10/5/1985. Had I not had grounds for extreme concern, then I obviously would not have bothered to go to the extent of mounting a High Court Action, etc, which naturally incurred an intense amount of stress and personal loss.
I was concerned about;

the risks to the consumer of the meat and milk from OP treated cows;
the risks to the farmer applicator who applied the insecticides; and
the long term, delayed risks posed to the central nervous system of the OP treated cattle, mediated via a neurotoxic or mutagenic effect of the chemical itself.

I expressed my fears that an epidemic of bovine neurodegenerative disease would ensue in cattle, and I was quoted saying this in my newspaper articles, news media at that time, plus I expressed this fear in letters to numerous MPs, MAFF officials. The fact that many of the MAFF/HSE letters (held by the Inquiry) in response to those of mine all state that my claims, on the long term, delayed neurological/psychiatric effects of OPs were at variance with expert medical opinion, clearly demonstrated that I must have been raising this issue in the first instance. However, there were numerous papers published in journals at that time which clearly depicted that my ‘views’ were not actually at variance with informed expert opinion and that these types of neurotoxic sequelae to certain types of OP intoxication were indeed widely recognised.
The moment BSE became officially recognised I wrote to the Farmers Weekly and pointed out that this disease was the direct result of the warble fly campaign (see paragraph 6 of my Inquiry statement WS 23)
Both NOAH, Dr Andrews, the Government and the majority of my critics have repeatedly alleged that I "keep on changing my theory over the years… each time it is rejected, etc", but in reality it is only they who are changing my theory.
The fact that I have not changed the cornerstones of my theory is clearly witnessed by my 1987 letter to the Farmers Weekly where I refer to a small survey that I had carried out on farms affected with BSE and how that had indicated that it was the ‘phosmet’ brand of warblecide that had (theoretically at that time) caused a delayed neurodegenerative condition in cattle manifesting as ‘BSE’. In this letter I also inferred that these OPs would be concentrating in the meat and bone derived from those treated cattle, and therefore getting back into cattle via the feed route too. Essentially, I am still saying exactly this today, but one has to exercise an open minded and lateral approach when formulating and developing any scientific hypothesis. A rigid dogmatic approach is no good for anyone. So it is inevitable that ‘extensions’, ‘updates’ and greater detail will become incorporated into the evolution of any hypothesis that it gaining momentum whenever fresh pieces of evidence come to light.
The Inquiry Secretariat, told me that "many people are saying that I change my theory", pointing specifically to one ‘alleged’ change where I am hypothesising that OPs are interacting with the glycolipid anchor. I have consistently been focusing on PrP’s glycolipid anchor as a potential OP interaction site as highlighted in all of my papers since 1993. I referred to this glycolipid site as ‘the surface of PrPc’ in my 1994 J. Nutri. Med. Article [J/NUM/4/43], then again (more up front) as ‘the all important serine 231 site on PrP’ on p436-437 of my 1996 Med. Hypotheses article [J/MH/46/429], then finally as ‘the glycolipid anchor’ in my Med. Hypotheses 1998 article [J/MH/50/91]. As the Institute of Psychiatry tissue culture study has demonstrated a protracted retention of PrP on the membrane surface in phosmet treated cells, then one explanation for this abnormality could infer that a conformational change had indeed occurred at this precise serine 231 site – this could cause an impairment of cleavage by phospholipase C at this site, thus delaying the release of PrP from the membrane which is one of the a characteristic features of TSE pathogenesis.
The experiments of Shaw I [J/NST/1993/50] et al and Ray D [WS68] et al both involved the exposure of recombinant PrP to OPs. Because Recombinant PrP lacks the PI anchor conjugate then these experiments did not cover the main candidate site of OP interaction according to my theory, let alone cover other candidate mechanisms that I have proposed such as a phosmet invoked free radical interaction with the copper domain on prion protein, or with side chains etc, etc.
I have consistently proposed that it is an ‘in utero’ intoxication which heralds the ‘initiating’ event of BSE pathogenesis (for phosmet concentrates in the fetus), plus the fact that I have also proposed that phosmet needs to bio-concentrate up through the bovine foodchain (via the tallow fraction of MBM) as a contributory means towards achieving the endpoint whereby the ‘threshold level of toxic tolerance’ to phosmet is exceeded, and then BSE erupts. I contend that the OP-BSE theory does indeed cater for the delayed lag that exists between the time when phosmet use really took off and when the first cases of BSE erupted, etc. So the timing of systemic phosmet use in the UK in relation to my proposed mechanisms of phosmet bioaccumulation (via tallow, etc) does indeed correlate with the spatio-temporal epidemiological facts surrounding BSE.
From the onset, my work has clearly striven to pinpoint some ‘unique’ facet of OP usage in the UK in order to address the virtual exclusivity of the BSE outbreak to the UK. This is why I focused on ‘phosmet’ as the most likely hypothetical candidate for BSE initiation, simply because the UK was the only country in the world to compel its 2 times annual usage as a ‘systemic, pour-on’ 20mg/kg dose of a 20% concentrated formulation within certain zones of the UK.
MY DETAILED RESPONSE TO THE NOAH REPORT
NOAH quite correctly set the scene by depicting the distribution of BSE cases internationally (paragraph 16 of Mr Cook’s statement WS 270).
But it should be born in mind that since Ireland, Switzerland, France and Portugal adopted a more ‘over the top’ policy of BSE control than applied in the UK – eg. slaughter of the entire herd following the emergence of the first case of BSE – then this would have masked a considerable number of further cases of BSE that would have emerged in these countries had entire herds not been slaughtered following diagnosis of their first BSE case.
It should also be noted that it is only the UK, Ireland, Switzerland, France, Portugal and Holland that have hosted endemic BSE in their native cattle – so the various criteria of the particular pesticide / feed policies relating to those countries must be able to satisfy the prerequisites of the OP hypothesis, whereas the respective policies of the remaining endemic BSE-free countries must fail to match the OP Hypothesis.
However the remaining countries on the BSE list involved BSE cattle that had been imported in from the UK whilst incubating the disease. NOAH go on to address the widespread use of OPs around the world-particularly in the arable sector (paragraph 20 of statement WS 270). I regard this as irrelevant to my theory that focusses on the use of ‘systemically’ acting phosmet warblecides on farm animals.
However, NOAH’s table 2 (page 3 of WS 270) provides an interesting insight into the relatively excessive use of OPs in 1987 on food animals in Western Europe – the area which NOAH correctly cites as the global region that suffers an exclusive BSE problem. Of particular interest is the near 20 fold less usage of OP by monetary value in BSE-free North America as compared to Western Europe; NB, Both USA and Europe share a similar monetary value for OPs.
NOAH then state that in their experience there is no single use of OPs, or specific OPs, which is unique to the UK(paragraph 21 of WS 270). I agree with this, but my theory focuses on the overall annual dosage rate and frequency of application of a specific type of ‘systemic’ pour-on OP, phosmet, whose usage, albeit less intensive, also had to be linked to the other countries suffering a much smaller incidence of endemic BSE.
The dose rate and frequency of dosing of any chemical is very important when gauging the specific toxicological effect of a given chemical. Eminent neurologist Peter Spencer states in his paper ‘recognising neurotoxic disease’ that multiple types of syndrome can develop from the same toxic substance. He states that "exposure to different levels of the same substance may result in a dramatically different clinical picture. This fundamental principle of toxicology is frequently overlooked in the haste to simplify a puzzling clinical picture." This is why, according to my theory, BSE will only erupt in a country once a certain profile of repeated, high dose usage of phosmet and its residual contaminant in tallow is adhered to.
NOAH then quite correctly state that animal by-products have been fed for over a century (paragraph 24 of WS 270), but ignore the fact that tallow has been extracted from this feed for over 60 years – via the solvent extraction method – right up until the early 1980s when solvent extraction was dropped once the rendering process was revolutionised, adopting the ‘continuous flow system’ (See Wilesmith’s papers).
NOAH further make generalised statements that OPs have been in use on farm animals internationally since the 1950s (paragraph 24 of WS 270). But I would like to point out that we must be aware that very little OP was used in ‘systemic’ formulations, if at all, in those early days; NB; ‘systemic’ infers that the OP has to be in a ‘fat soluble’ formulation and capable of penetrating through to the central nerves and therefore relevant to the basic mechanics of my theory. Most OPs were more widely used as non-systemic ‘contact’ aqueous based liquid formulations for use in dip baths, spray-ons and ‘back rubs’ or as powders in the early days. In fact, most of the OP products are still applied in the third world countries and in the USA/Australia are still formulated as non systemic products.
Furthermore, NOAH’s statements at this point fail to encompass the basic prerequisite of my theory that it is the ‘phythalimido’ type of OP formulation – phosmet – that fits the BSE facts and its use did not take off in the UK until the mid 1970s.
Phosmet
At paragraph 26 of [WS270] NOAH now begin to address my correct theory – ‘phosmet’ as the causal agent of BSE. But I consider their response is too generalised.
For instance NOAH state that phosmet is licensed for use in most of the major livestock producing countries (paragraph 26 of WS 270) without stating which countries, at what dose rates, whether applied for warbles, lice, mange etc, whether as a ‘systemic’ or ‘non systemic’ formulation, etc?
The only country which has compelled the use of phosmet in its ‘systemic’ pour-on type of 20% concentration formulation (and that does not mean the ‘spot on’ or ‘spray on’ types) for warbles at 20mg/kg dose is the UK; please see the chart of global phosmet usage in relation to the global distribution of BSE on page 101. The only other countries that have used systemic pour-on phosmet on cattle for warble control were Ireland and France; interestingly these countries make up the majority of other countries afflicted with endemic BSE, albeit suffering a relatively much smaller incidence than the UK. Ireland did not introduce phosmet until 1978 – at the end of its warble campaign – and even then, although hardly used, it was used as a 6mg/kg dose as a once annual dressing (see O’Keefe paper for dose of active ingredient used) in competition with three other types of OP warblecide – fenthion, famphur and cruformate. However, after the warble campaign ended in Ireland, the dose of phosmet was increased to a 10mg/kg bodyweight dose to include a fourteen day repeat treatment for any farmer who wanted to use the product (however many times a year) for controlling lice on a voluntary basis – I believe that this explains the sudden increase in BSE incidence in Ireland over the last four years – as a delayed lag response to the increased dose rate of phosmet.
Again, France only used phosmet on a voluntary basis over a short period in the 1980s when only 150,000 doses were used per year according to the enclosed letter from the French authorities. Phosmet use was minimal in relation to the much more intensive use of its popular competing compounds – fenthion, neguvon and Ivermectin. For instance, Neguvon was used in France at 800,000 doses in 1991. Phosmet is also used systemically at a 20mg/kg dose for controlling ectoparasites in pigs in France, as well as in Switzerland, and the fat soluble residues of this chemical could have entered cattle via the tallow ingredient of feedingstuffs – used intensively in these countries.
In view of the aforementioned, NOAH’s statement that "significant and similar levels of use of phosmet for warbles took place in UK, Ireland and France" (paragraph 28 of WS 270) is incorrect.I have never been able to obtain any details of doses of phosmet used in the UK (see enclosed correspondence but, its usage in the UK must have risen once its competing OP warblecides – fenthion and famphur – were withdrawn from use in 1985. Dr Andrew’s statement to the Inquiry claims that the UK sales figures for phosmet have been lost (WS 269A paragraph 45), which in my view undermines NOAH’s statement where they state that phosmet was used equally in Eire/UK/France.
However, A H Andrew’s paper on abnormal reactions to OP warblecides [M54 Tab11 page 25] indicates that 8,560,000 doses of warblecides were used in the UK over the four year period of his survey (1975 – 1978). This suggests that 2,140,000 doses of OP warblecide were being used in the UK each year, prior to treatment becoming compulsory over entire zones in the early 1980s. Considering that Tony Andrew’s paper indicates that 11 brands of OP warblecide were being employed at that time – 4 of which were phosmet brands, then one can estimate that approximately 778,000 doses of phosmet were annually used in the UK from the mid 1970s up until the advent of the 2 times annual compulsory treatment measures introduced in 1982, and then the removal of phosmet’s competing brands of OP in 1985. Thus one can argue that the use of systemic phosmet for warble control in the UK was several magnitudes greater in the late 1970s-early 1980s over a far longer duration in comparison to the relative insignificant usage of phosmet in France and Ireland.
Contrary to the picture that NOAH has painted in Mr Cook’s statement, the actual timing, distribution and intensity of phosmet usage and tallow consumption does indeed correlate with the spatio temporal epidemiology of BSE in Europe. The correlation involves a delayed lag period due to the prerequisite that phosmet must bio-accumulate in the bovine foodchain to assist in the overall concentration of phosmet exceeding the threshold of toxic tolerance in the cow – coupled to the fact that I have hypothesised that the toxicological initiation of the conformational change in the prion protein is an ‘in utero’ event, which subsequently requires several years of incubation period prior to the eruption of the outward symptoms of the disease.
Geography
NOAH in Mr Cook’s statement do not mention the fact that the various warblecides on the market employ different modes of application (eg spray on, spot on or pour-on) and different types of carrier medium (oil or water based, etc) which are designed to assist the active ingredient in performing its specific task once it has been delivered onto/into the cow. Essentially my BSE thesis centres on the ‘systemic’ oil based pour-on warblecides which are delivered along the entire length of the cow’s spine (just millimetres from the prion protein!) and the base of its brain. Furthermore these types of chemical are deliberately designed to penetrate through the skin to exterminate warbles whilst inside the cow. These chemicals even had to kill those warble larvae that had congregated in the fatty tissues of the spinal cord.
I believe that the ‘spot on’ and ‘spray on’ types of contact warblecide – used in countries such as Hungary, Poland, Denmark, Holland, USA, etc wisely employed far less total active ingredient per animal and were delivered directly onto the warble larvae itself at the stage of its life cycle when the creature popped out through the skin of the COW’s back as a mature larvae.
Thus NOAH’s generalised chart of the different countries employing or about to employ warble fly policies (WS 270 paragraph 31) is irrelevant to my theory. For instance, I refer to a letter from the German Pesticide licensing authorities that declares that they have never permitted the use of ‘systemic’ type treatments on cattle in Germany. And again, Denmark did not employ systemic pour-on phosmet, they used spot-on fenthion. This explains why Germany and Denmark, etc, do not have an endemic BSE problem. NOAH incorrectly state that Jersey farmers had treated their cattle against warbles. A letter from Jersey’s Chief Veterinarian published in "Farming News" has already pointed this error out to NOAH.
The point that I would make in relation to Jersey and Guernsey is that the same systemic phosmet warble fly liquids were used intensively for controlling lice at a double 10mg/kg dose – for lice pose a significant problem in the warm, mild climate of the Channel Islands. Also tallow and ‘protected fat’ were feddingstuff ingredients that were in strong demand with Jersey and Guernsey cattle breeders who bred cows to produce milk with a very high butterfat.
Guernsey suffered more BSE than Jersey simply because the soils of Guernsey are very deficient in copper and selenium in relation to Jersey. The results of my own global field surveys of isolated clusters of spongiform disease have consistently demonstrated that both selenium and copper deficiency is a crucial prerequisite that must be fulfilled before any type of sporadic spongiform disease can erupt. Copper and selenium deficient areas of the BSE affected countries – such as Hampshire, Norfolk, Guernsey, Brittany, etc, - have all hosted the highest intensities of BSE outbreak relative to the overall BSE rates of their particular country. This is simply due to the fact that copper and selenium are essential co factors for several enzyme systems that are crucial for scavenging free radicals; thus, once copper and selenium are in short supply, the body is not so well equipped to mop up these highly lethal radicals. Thus, when free radical chain reactions are initiated in the CNS membranes following exposure to the systemic types of high dose OP, then the radicals that are generated as a direct consequence will be free to react with proteins like the prion protein in any animal that is already environmentally predisposed to a deficiency of radical scavenging enzymes. It is these radicals that can cause protein deformation, which, in turn, kicks off the pathogenesis of TSE.
Again, NOAH generalises by referring to intense usage of OPs on cattle in both Africa and South America (Mr Cook’s statement WS 270 paragraphs 33 and 34), but cannot say whether these OPs were in systemic formulation or indicate the dose rate applied, the type of OP, or whether permitted for use on ‘pregnant’ cattle. Once again, the context of OP use in Africa and South America, according to my research, falls a long way short of fulfilling the prerequisites of my OP-BSE theory.
Timing
There is a very strong relationship between the spatio temporal dynamics of systemic phosmet use in the UK and the spatio temporal epidemiology of BSE incidence. Whilst there is a delayed lag period of approximately six years, this can be explained by the need for phosmet to have bio-accumulated in cattle to critical levels as a result of the recycling back of residues (plus the ‘infectious’ oxidative potential of the prion itself) via the tallow fraction of MBM. Also it has to be born in mind that the intoxication event responsible for initiating TSE pathogenesis probably occurred in the womb, several years before the outward symptoms of the disease started to manifest itself. Furthermore if a phosmet induced mutation event was involved, (one mechanism I suggested in my J Nutritional Medicine paper 1994 [J/NUM/4/43]) – then TSE may not have emerged until several years later in succeeding generations.
The reason that the first cases of ‘officially’ recorded BSE were largely born after 1982 is probably due to the fact that solvent extraction mainly ceased (plus a drop in temperature) in the rendering factories in the early 1980s, thus permitting the tallow fraction of MBM, phosmet residues and prions all inclusive, to remain in the feed. Having said that, all vets, farmers and slaughterers that I have spoken to are adamant that several cases of BSE were trickling through the system in the late 1970s/early 1980s before the disease was officially recognised.
Warble treatment did not become a compulsory treatment for whole herds in declared zones until the early 1980s. Coupled to the fact that MAFF were writing to all UK farmers each year urging them to treat throughout the 1980s (and even as late as 1995, then one can assume that phosmet was used at higher levels in the 1980s than in the later half of the 1970s – particularly since phosmet’s competing brands of OP were virtually all removed by 1985.
I should also point out that many types of highly neurotoxic impurities have been associated with various types of OP technical grades that have been on the market – phosmet being one of those OPs that could be contaminated in this way. As different chemical processes can be employed for manufacturing the same type of OP and some of those processes could predispose more favourably for the formation of unwanted ‘impurities’, then research should be executed to see if any such changes were implemented in the manufacturing process of phosmet at any time during the warble campaign. Conditions of storage of phosmet can also considerably influence the toxic potency of the chemical.
It should be pointed out that Northern Ireland did not take up the use of phosmet until a long time after 1969 – when Northern Ireland first kicked off its warble campaign.
Whilst it is true to say that the UK warble fly campaign initially only encouraged farmers to treat their cattle in the late 1970s, it is totally untrue to say that it was never compulsory to treat all of the herd (paragraph 39 of WS 270). Compulsory treatment of entire herds was introduced in the 1980s which gave rise to my court case in 1984. As NOAH pointed out earlier (paragraph 12 of WS 270), I had broken the law by refusing to comply with this compulsory requirement to treat my cows. But in truth, the verdict of my court case indicated that MAFF had actually been working outside of the law by compelling treatment with a chemical dressing. The Animal Diseases Act only empowered MAFF to compel treatment with a vaccine or a serum (paragraph 4 of my InquiryWS23).
Such an introduction of compulsory treatment of all cattle in designated zones around the UK in the early 1980s indicates that the use of phosmet would have increased considerably at this time, particularly as all of its competing compounds were removed off the list by 1985. Surely this supports my theory and explains why BSE really got underway by the end of the 1980s.
Again, NOAH are considerably exaggerating their position when they suggest that the warble fly campaign was nearly wrapped up by 1981 (paragraphs 45 and 46 of WS 270). Working as a farmer throughout this entire period myself, I (plus other organically orientated dissidents) didn’t come into confrontation with this government Warble Order [L9 Tabs 1-5] until 1982, 1984, etc. We were hardly aware of the existence of such an Order before that time. If we had a warble infestation in our cattle prior to 1982, we simply used derris powder which was officially sanctioned up until that time.
Furthermore, during the 1980s all farmers outside of the compulsory zones received letters from MAFF urging them to treat all of their cattle on a voluntary basis as an extra insurance. All farmers received such pamphlets from the 1980s up until 1995, but I should point out that we did not receive pamphlets urging voluntary treatment during the 1970s at all.
NOAH does not mention that the new ‘non OP’ warblecide, ‘Ivermectin’, could not be used on milking cows for economic reasons; for the licensing criteria stipulated that the milk had to be thrown away for 28 days after treatment. Consequently, Ivermectin was widely taken up by beef farmers and not dairy farmers, which answers NOAH’s next point about the beef-dairy differential surrounding BSE incidence (paragraph 44 of WS 270)– where a considerably higher incidence of BSE exists in dairy cows as opposed to beef cattle.
Thus, the explanation for this BSE differential in beef and dairy cattle partly lies in the fact that beef cattle received ivermectin post 1981 instead of OP warblecides. Furthermore, most beef cattle do not live long enough to develop the outward symptoms of BSE, plus beef cattle receive nowhere near as much tallow based feed. Most beef stock are farmed under a less intensive management strategy than dairy herds and therefore do not receive much feed or milk from a concentrate/artificial source – particularly the young calves who derive their nourishment from suckling milk from their mothers. Beef suckler herds are also largely based in the moorland areas of Britain/Scotland which were largely never designated as warble fly compulsory zones. And, pertinent to the prerequisites of my theory, beef calves are largely born in the spring and were therefore at their most ‘chemically vulnerable’ early stages of embryonic development during the summer months. Eg, at a time when warble fly treatments were not applied. Please note that there is a 10 fold greater incidence of BSE in cattle that were born in the autumn. As twice as many cattle are born in the autumn in comparison to those born in the spring, then there is a five fold greater risk of contracting BSE in cattle that were in their vulnerable embryonic stages during the compulsory ‘springtime’ warble treatment period in March. This highly significant seasonal fluctuation of BSE susceptibility – whether it relates to any ‘in utero’ connection or not – has been totally ignored.
Noah’s Summary (paragraphs 47 to 50 of WS 270)
NOAH’s summary is irrelevant to my theory as it focuses on the use of warblecides as a general group – and not the systemic pour-on phosmet brands.
Thus if we correctly insert ‘phosmet’ into the hypothetical template, then we can see that significant usage of the chemical got underway in the later half of the 1970s, peaking after the imposition of 2 times annual compulsory treatment measures in 1982, and then gradually tailing off right up until the early 1990s, leaving a situation today where limited treatment is still occasionally carried out in very small pockets and on imported cattle, as well as in a voluntary capacity for lice control. NB, I should also add that zones for warble treatment were declared all over the southerly/mid areas of the UK in the 1980s (eg Kent, Yorkshire, etc) and not only in the SW and Wales as NOAH suggests. MAFF’s annual animal health publications depict this.
If PHOSMET were the cause of BSE, then the pattern of BSE should look like this – which it does!

much greater intensity of BSE in dairy cattle as opposed to beef cattle;
emerging in the first half of the 1980s;
peaking in the early 1990s;
steadily tailing off, with cases occurring all over the UK but with a greater concentration in the South West and Wales; and
prevalent to a much lesser degree in countries which employed systemic phosmet at the 20mg/kg warble doses as a voluntary treatment over much shorter period – eg France, Eire, Channel Islands, etc (includes the double 10mg/kg lice dose, but BSE free Australia and New Zealand only licensed it for the single lice dose)

REPONSE TO THE HEARING ON 5/11/98 AT THE BSE INQUIRY (DAY 78)

Page 24 (line 12) Tony Andrews states that the OP warblecides containing famphur as an active ingredient would have been disappearing at the time when the warble fly eradication came in.
This is incorrect. Famphur products were for sale in farm stores – thus competing against phosmet brands – right up until 1985. This is pointed out in a House of Commons reply to Sir Richard Body in 1985.
Page 25 line 2 to page 26 line 14 Mr Tasker explains the sales chronology of the different phosmet formulations. The marketed brands progressively increased their concentration of active ingredient (5% to 10% to 13.3% to 20%) from the 1970s until present day.
Whilst I take Mr Tasker’s point about the relative drop in the total volume of fluid applied as the concentration of formulation increased, he does then go on to explain how the delivery system for the pour-on pesticide became more precise (eg, there was less wastage and displaced chemical (Dr Andrews explains this p 27 line 7) which would imply that a fluid of 20% concentration of phosmet (albeit less in total volume) instead of a 13.3% or 5% concentration is going to have to soak through the spinal cord/base of the brain before it permeates the circulatory system and the main batteries of detox enzymes in the liver where chemical degradation begins.
Fundamental toxicological principles would suggest that exposure to a given volume of a toxic chemical at 20% concentration would be more likely to exceed toxicological thresholds and initiate a pathogenic disturbance in biological systems, than in the context of an exposure to a relatively higher volume of a 13.3% or a 5% concentration of that same chemical.
It is interesting that the UK is the only country in the world to have employed the 20% concentration phosmet brand for warble fly control – eg at the 20mg/kg dose rate. As the 20% concentration brands largely came into use in the early to mid 1980s after France and Eire had finished employing phosmet for warbles, then this may hypothetically explain both the timing and the virtual uniqueness of the BSE epidemic to the UK.
Page 28 (line 5) Mr Tasker. I agree with Mr Tasker that systemic phosmet is "applied along the backline" where it is "attracted to and dissolves in fat." He confirms a large chunk of my thesis that phosmet will concentrate in fat. Others have tried to deny the lipophilic properties of systemic warblecides. Indeed, Professor Prusiner has pointed out that the prion protein is found in these same fatty regions of the CNS – the regions over which the OP pour-ons are delivered. PrP is found conjugated onto the phospholipids in the liposome structures of these regions.
Page 30 (line 21). Mr Tasker. I thought that ivermectin had a 28 withdrawal period for milk and not 2 days. It was certainly a 28 day withdrawal period during the 1980s.
Page 33 (line 1). Mr Tasker. According to the package label for the Young’s phosmet pour-on that was registered in Australia in 1995, there is no advice or recommendation given for a 14 day repeat treatment of the 10mg/kg lice treatment.
Page 34 (line 5) Mr Tasker. I find it hard to accept that O’Keefe’s study has applied phosmet onto cattle at such a markedly different dose rate to that employed in the real life context. After all, this whole study was designed to safeguard public health in Eire by applying all of the different types of systemic OP warblecides onto milking cattle at their prescribed Eire dose rates, and then measuring the various residual contaminants in the milk resulting from those OP treatments for several days after the treatment. These O’Keefe studies tested fenthion, famphur and crufomate warblecides at the dose rates prescribed in Eire, so it would seem unlikely that phosmet was suddenly tested at an irrelevant dose rate in these trials.
Page 37 (line 17) Mr Tasker. It looks as though Mr Tasker is correct in pointing out that I have made a ten fold mistake in the calculation of the actual dose rate of the phosmet pour-on for pigs. The different authorities had merely supplied me with the concentration of formulation and amounts of the fluid poured-on to pigs.
However, the 10 times higher dose rate of phosmet for pigs actually improves the viability of my theory and demonstrates that the tallow fraction of cattle feed in countries such as Switzerland/France (which utilised large amounts of systemic phosmet for pigs) would have contained higher levels of residues of phosmet which would infer greater toxicological significance.
Whilst pigs have been recorded to suffer from the more conventional OP induced delayed neuropathy in the literature, pigs are not susceptible to prion disease as a species. Furthermore, pigs are routinely fortified with large doses of copper, which would occupy and thus safeguard the histidine sites at the copper domain on the prion protein against modification by OPs. When copper is in short supply in the CNS however, the histidine residues on PrP become ‘vacant’ and therefore vulnerable to occupation or interaction with competitive organic foreign chemicals or metals.
Page 38 (line 5) Mr Walker. Phosmet was not permitted for use upon milking cows in the USA because of the US pesticide authorities tougher line taken on the health problems posed by phosmet’s residues appearing in the milk. Consequently, phosmet use was very limited in the USA, being used largely as the ‘non systemic’ water based spray-on (at 2mg/kg dose), pour-on, back rub, etc I have some usage figures for Colorado-Wyoming states that indicate very low use of phosmet in relation to other OPs.
Page 48 (lines 4 and 23) Dr Marrs. Dr Marrs himself cites one study ‘Good J et al, J Neurol. Neurosurg. Psychiatry 1993 56 290-294’ in his JMPR 1994 report which highlights ultrastructural abnormalities in the motor endplates of a human exposed to sub acute doses of phosmet. So I am surprised that he is ruling out structural changes in the peripheral and/or central nervous system that might lead one to expect that phosmet induces anything other than an anti-acetylcholinesterase mediated effect on nervous tissue.
It is well recognised that phosmet induces cerebral edema with gliosis in exposed victims (hydrocephalus in exposed fetuses) which is largely disrelated from the anti-cholinesterase effects of phosmet’s oxon metabolite. Thus the pathology induced by phosmet intoxication, plus phosmet’s disturbance of vitamin C and DNA-RNA exchange, does indeed suggest that some of phosmet’s effects are disrelated to its cholinergic effects. In fact, these disturbances probably reflect the well recognised impact of chain reactions of various free radical species that are generated by phosmet intoxications. The free thiol radicals associated with the phthalimido-N-methyl mercaptan metabolite group of phosmet could well interact with sulphur amino acids in proteins causing conformational changes. Furthermore, this mercaptan group serves as a copper chelator forming a tightly bonded ring with copper – explaining the spongiosis pathology that is invoked by phosmet. This would deprive the copper domain of PrP of a copper supply, leading to a breakdown in CNS activity of superoxide dismutase activity and in the brain’s resistance against superoxide radical induced oxidative stress. Such free radical disturbances would also exert knock-on effects on the signal transduction cycle and protein kinase mediated phosphorylation within intoxicated cells.
Phosmet has also been shown to increase the turn over of glutamate oxaloacetate transaminase, demonstrating another non-cholinergic effect which resembles the pharmacokinetic characteristics of other members of the phthalimide family such as thalidomide.
The non-cholinergic neurotoxic effects of impurities, such as chloromethylphthalimide, which have been commonly associated with the technical grades of phosmet used in the field, should also be recognised as potential influences in the pathogenic consequences of phosmet intoxications.
Page 86. (line 9) Mr Cook. It should be pointed out once more that the 28 day withdrawal period of milk following treatment with ivermectin resulted in a zero use of ivermectin upon milking cows for warble control. Ivermectin was used on beef cattle for warble control however, perhaps explaining why BSE largely affected dairy cattle (which only received OPs) and remained at a low level in the beef suckler cattle.
Page 86. (line 19) Mr Walker. My comment on the work carried out by Professor Shaw is that, once again, the test protocol fails to test the key prerequisities of my theory because it employs a recombinant PrP model that is totally divorced from the ‘in vivo’ context of PrP as a living protein, interacting with its cellular environment, etc. The recombinant PrP does not contain the glycolipid anchor, nor does it contain copper (which bonds to the histidine residues of the octapeptide repeat region of PrP) or side chains that are crucial components required for the putative mechanisms of PrP conversion that I have proposed in my various publications. For instance, outside of the cellular context it is impossible to initiate any free radical generated impact of chronic phosmet intoxication using recombinant PrP. There is no cell membrane where lipid peroxidation could be initiated, and no copper ions for the resulting peroxides to interact with. The resulting formation of the hydroxyl and Cu 111 radicals would also require the presence of side chains, other proteins and free transition metals to exert their pathogenic impact.

[Secretariat Note: An annex to this statement will be published in due course which will give the BSE Inquiry references to documents referred to in the statement]

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