BSE Inquiry / Statement No 23B Mr Mark Purdey
Issued 12/01/2000

SECOND SUPPLEMENTARY STATEMENT OF MARK PURDEY

 

  1.   This statement is made in response to the supplementary witness statement of Mr Roger Cook

    PARAGRAPH 3

  2.   I reiterate that the overall rate of active ingredient used to treat warbles (20mg/kg) is not the same as the rate employed for lice (10mg/kg). This is clearly stated on all of the packages representing the different brands of pour-on phosmet employed in agriculture – package labels which have been supplied/shown by me to the Inquiry Secretariat in 1998.
  3.   However, whilst I understand that NOAH say that a 14 day repeat treatment of the 10mg/kg lice rate of phosmet could be used for lice control if the problem of infestation persisted (eg; the two separate applications adding up to a total dose of 20mg/kg), I should point out that a 14 day repeat treatment was also recommended following use of phosmet at its 20mg/kg warble fly dose rate (producing a total dose of 30mg/kg).
  4.   However, it should also be pointed out that toxicological effects can be markedly different when a 20mg/kg dose of a given substance is applied to a mammal on a single occasion, as opposed to a treatment strategy which involves two separate lower dose applications of 10mg/kg of the same substance 14 days apart. (See; Professor Dayan’s toxicological briefing to the BSE Inquiry which outlines this most basic toxicological principle (IA Vol.1 Tab 19)).
  5.   What I am saying is that the prion protein will be rendered susceptible to its initial conversion into an ‘infectious’ BSE misfolded isoform once concentrations of phosmet in brain cells exceed a threshold level that results from treatments at the 20 mg/kg warble dose rate.
  6.   I have also supplied the Inquiry with labels of the phosmet lice fluid currently being applied exclusively as a 10mg/kg dose in Australia and New Zealand. The wording on these labels does not state the need or recommendation for a 14 day repeat treatment.
  7.   Mr Cook also states that “European type, phosmet based warblecides were used in South America without BSE developing”. Again, I must stress that warbles have never existed in South America, indicating that phosmet can only have ever been used at its lice dose rate of 10mg/kg – presumably to control the skin parasite, dermatobia, which is cited by NOAH in paragraph 33 of their initial statement 270 (WS 270).
  8.   However, I must state that the South American pesticide registration authorities did not imply that they have utilised ‘phosmet’ when they responded to the survey that I circulated around various countries respective pesticide licensing authorities in 1996.
  9.   They did however indicate that they have been utilising ‘fenthion’ and ‘trichlorphon’ types of OP pour on at the 10mg/kg dose rate. This is confirmed in para 14 of Bayer’s submission to the 5/11/98 hearing of the Inquiry (WS 274).
  10.   The use of Phosmet at the non-warble dose of 10mg/kg would virtually debar the possibility of BSE arising. Furthermore, putting aside the status of phosmet usage in S America, other aetiological prerequisites would have to be simultaneously fulfilled before one could predict whether BSE would be likely to emerge or not.

    PARAGRAPH 5

  11.   Even if I had changed my theory as Mr Cook suggests, the number of times that it has been changed is totally irrelevant to the issue at stake – the reality of whether or whether not phosmet plays an actual role in the aetiology of BSE.
  12.   Mr Cook suggests I am changing my theory by isolating and listing select aspects of my multifactorial thesis which infers that I am simultaneously presenting several different pathogenic mechanisms, each of which contradicts the viability of the other.
  13.   However all of the different aspects that Mr Cook has listed do in fact mesh together to form a unified, homogenous hypothesis.
  14.   Since no proper extensive research programme has ever been commissioned into investigating my theory, then in the interests of sound lateral scientific thinking it has been necessary to propose various optional pathogenic mechanisms over the years whereby phosmet could feasibly play a role in BSE aetiology.

    PARAGRAPH 6

  15.   The tiny errors in my supplementary statement (WS 023A) surrounding letter dates, whether Roger Cook represented UKASTA or NOAH at a given time, or whether a particular communication was a fax or letter do not hold any relevance whatsoever to the science of the putative role that phosmet may have played in BSE aetiology.

 

  Issued on behalf of the witness by:
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