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
- 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 UKs 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 Cooks statement no. WS 270).
- This was an inaccurate claim for many reasons. It is particularly ironic in the light of
Dr Andrews statement that the UKs 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 UKs 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, OKeefe 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 Eires 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 Taskers Statement [WS273] does not
specify that they are relating to phosmet as an individual compound when it cites
Eires 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%
Warble Fly Treatment was never compulsory (Mr Cooks 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 wasnt
compulsory?(see my Inquiry Statement WS 23 paragraphs 3 and 4) Mr Cooks
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
Compulsory Warble Fly Zones only existed in tiny pockets in SW
England and Wales in the 1980s (Mr Cooks statement paragraph 47 WS 270)
- This is painting a totally inaccurate picture. As depicted in MAFFs 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 Cooks
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
- 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 UKs 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 NOAHS STATEMENT; THE ALLEGED LINK
BETWEEN OPS AND BSE (WS 270)
Background (paragraphs 12 to 15 of Mr Cooks statement)
- I made it quite clear in the mid 1980s that my reasons for challenging MAFFs
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 PrPs 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 Cooks 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, NOAHs 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 Wilesmiths
- 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, NOAHs 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.
- 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
- 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 OKeefe 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, NOAHs 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 Andrews statement to the Inquiry claims that the UK sales
figures for phosmet have been lost (WS 269A paragraph 45), which in my view
undermines NOAHs statement where they state that phosmet was used equally in
- However, A H Andrews 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 Andrews 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 phosmets
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 Cooks 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.
- NOAH in Mr Cooks 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 cows 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 COWs back as a mature larvae.
- Thus NOAHs 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 Jerseys 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 Cooks 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.
- 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 phosmets 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) didnt 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 NOAHs 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.
Noahs Summary (paragraphs 47 to 50 of WS 270)
- NOAHs 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. MAFFs 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
- 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
- Whilst I take Mr Taskers 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 Youngs 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 OKeefes 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
OKeefe 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
- 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 phosmets 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
- 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 phosmets oxon metabolite. Thus the pathology induced
by phosmet intoxication, plus phosmets disturbance of vitamin C and DNA-RNA
exchange, does indeed suggest that some of phosmets 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 brains 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
- 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
- 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
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