Case No: 1996-S-No-6
 
IN THE HIGH COURT OF JUSTICE
QUEEN’S BENCH DIVISION

Heard at the Royal Courts of Justice
Strand, London, WC2A 2LL
Handed Down at Liverpool Crown Court.

Date: 9th November 2001

B e f o r e :

THE HONOURABLE MR JUSTICE MORLAND 

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	Herbert George Snell and Others	Claimants	
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	Robert Young & Co Ltd and Others	Defendants	

(Organophosphate Group Litigation - Part 24 Applications)
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Mr John Melville Williams Q.C. and Mr John Bates (instructed by Gabb & Co for the Claimants with the exception of Mrs Eaglestone (By Thompsons) Mrs Jones (By Mustoe Shorter) and Mr Tyrer (By Alexander Harris)
Mr Jeremy Stuart-Smith Q.C. and Mr Neil Block (instructed by Messrs Beachcroft Wansboroughs for the Defendants Turneys and John Turner Ltd And (instructed by Cartwrights Insurance Partners on behalf of Gloucester County Council)
Mr Shaun Ferris (instructed by Kennedys on behalf of Ciba Geigy Plc and Novartis Ltd.
Mr James Medd (instructed by CMS Cameron McKenna) on behalf of SP Vetinary Ltd and Mallinckrodt/Coopers Animal Health.
Mr Julian Matthews (instructed by Messrs Vizards Staples & Bannisters) on behalf of Robert Young & Co Ltd, Young’s Animal Health Ltd, Youngs Pharmaceuticals Ltd, Grampian Pharmaceuticals Ltd.
Mr Charles Gibson Q.C. (instructed by Davies Arnold Cooper) on behalf of the second Defendants Bayer Plc.
Ms Anna Guggenheim Q.C. (instructed by Elborne Mitchell) on behalf of the fifth Defendant, The Wellcome Foundation Ltd
Mr Charles Feeny (instructed by Berrymans Lace Mawer) on behalf of Clwyd County Council.

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I direct that pursuant to C.P.R. PD 39A PARA 6.1 no official shorthand note shall be taken of this Judgment and that copies of this version as handed down may be treated as authentic.

The Honourable Mr Justice Morland.
JUDGMENT: APPROVED BY THE COURT FOR HANDING DOWN (SUBJECT TO  EDITORIAL CORRECTIONS)
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Mr Justice Morland: The Organophosphate Group Litigation.  Further Reasons for Judgment given on 31st July 2001.
Introduction
1.	This judgment is to be read with the judgment given on the 31st July 2001.  I do not propose to repeat what I said in that judgment. Further detailed reading and rereading of upwards of thirty ring-binders and transcripts of oral submissions have fortified my general conclusion that on the evidence as it now stands the claimants’ claims are unviable, the group action would fail and that it would be unjust and oppressive to the defendants to allow it to continue in the hope that at some indefinite date in the future the claimants would be able to put their house in order and adduce sufficiently adequate evidence on the all-important issue of causation from experts with the relevant expertise.
The History of the Inception and Progress of the Litigation.
2.	In order to put the defendants’ applications in context it is necessary to set out in some detail the chronology of progress in the litigation.
3.	In the early days it was envisaged that many hundreds of people connected with farming would be making claims alleging injury attributable to organophosphate exposure.  In the event that did not occur.  By the time the applications were heard by me in July 2001 the number of claimants resisting the defendants’ applications had been reduced to only eleven.  Others had fallen by the wayside over the years and others had accepted the conclusion that their claims were unviable.  I was told by Mr Melville Williams Q.C. that there were upwards of thirty live legal aid certificates giving leave to issue but not serve writs and that there may be about seventy potential claimants who awaited the outcome of the defendants’ applications.
4.	A general chronology is to be found in File 2 p1-6A.  This shows that the defendants or many of them have been facing litigation or the threat of litigation for upwards of eight years.  Because the claimants have so far achieved little in the advancement of their case, even assuming that the claimants were able to obtain sufficient evidence to forward their case on causation, several more years would elapse before the Group Litigation came to trial.  The defendants must already have spent several hundreds of thousands of pounds. If the defendants were eventually successful, they would have incurred a huge expenditure of costs of which they would have no hope of recovery.
5.	It was on the 30th January 1997 that the Legal Aid Board formally awarded the generic contract to Dawbarns  It was at a meeting on the 25th April 1997 attended by Organophosphate generic Solicitors, Counsel and the Legal Aid Board that it was decided to carry out a medical pilot study to seek to establish a causative link between organophosphate exposure and the medical conditions suffered by all claimants benefiting from a legal aid certificate.
6.	On the 21st December 1998 Lord Bingham C.J. issued a Practice Direction (File 24 p.1.) in which he nominated Master Miller to be the assigned Master.
7.	On the 14th June 1999 Master Miller made an order giving important directions (File 24 p.2-16).  He ordered at 6.1(e) each claimant to serve “a medical report substantiating the claimant’s alleged injuries complying with the CPR Part 16 Practice Direction 4.3” and at 6.1.(f) “complete data relating to the individual claimant generated as a result of the Pilot Study”.  These orders were not complied with by the claimants or at least were not fully complied with.
8.	The Pilot Study did not come up to expectations and was at best inconclusive.
9.	The medical reports served purportedly in compliance with Order 6.1.(e) came from a G.P. with a special interest in the effects of exposure to organophosphates,  Dr Myhill.  Master Miller in a judgment dated the 1st February 2000 held that the reports of Dr Myhill did not comply with Order 6.1(e) saying (File 2 p.64):-
"I am satisfied that Dr Myhill is not qualified to give or to make such statements in terms of a medical report: she is not an expert in such matters.  Clearly, she can give expert evidence within her experience as a general practitioner, but her expertise does not lie in the realms of attribution and causation. Accordingly, and bearing in mind that it is a medical report in the nature of evidence, those reports must be treated as silent on matters of causation or attribution."
10.	Master Miller ordered (File 24 p.21):-
"3.5.	For the avoidance of doubt in respect of the medical reports referred to in 3.4 above each claimant shall serve medical reports that will address the issue of attribution as well as report on the injuries.
 3.6	The reports of Dr Myhill and the report of Dr Weardon in their present form are to be excluded as evidence in the case"
11.	There has been no appeal against the judgment or order of Master Miller
12.	Applications to strike out the Group Action and individual claims were made in August 2000.  The claimants’ legal teams announced in December 2000 that the applications could not be defended and legal aid was withdrawn
13.	Every citizen has a right of access to the Courts and to sue a defendant but the Court has the power and indeed the duty to prevent the exercise of those rights becoming oppressive to defendants and causing them injustice.
14.	Those principles accord with Article 6 of the European Convention on Human Rights which speaks of a “fair” hearing “within a reasonable time,” not it should be noted a “full” hearing.  What is a “fair” hearing will depend upon all the circumstances of the case.  Fairness comprehends fairness to both claimant and defendant.
15.	Those principles also accord with the “overriding objective”, CPR 1.1(1) and (2) in dealing with a case justly.
16.	See also A.B. and Others v. John Wyeth [1994] P.I.Q.R 109 (The benzodiazepine group litigation) per Stuart-Smith L.J. at p.113.
"The Court is concerned to see that its proceedings are not used in any way that is oppressive and vexatious to the other party or which involves serious injustice to him.  If the court is satisfied that the proceedings do have that effect, it has power to strike out on the grounds that they are vexatious and an abuse of process"
17.	The defendants are entitled to rely upon the facts that after the applications to strike out had been made the very experienced Leading Counsel in this field (Mr Stephen Irwin Q.C.), had a series of meetings with experts and concluded that the strike-out actions could not be defended and that the Legal Services Commission, no doubt after careful consideration having invested over £1.1 million in the litigation, withdrew funding.
18.	I do not think that there is any likely prospect of the group action or indeed individual claims being progressed without funding and I think that there is no reasonable prospect of that funding being forthcoming.
19.	The defendants’ conduct throughout has been co-operative over extensions of time and complaisant towards failures to comply on the part of the claimants to orders of the court.  Viewing the matter overall it would not be equitable to allow the group action to proceed even allowing for the fact that the slow pace of progress of the claims has in part probably been due to limited funding and in part due to the unsatisfactory manner in which the Pilot Study was conducted and the meagre results it produced.  In my judgment the defendants are fully entitled to call it a day and limit their liability for their own almost unrecoverable costs already exceeding £½M.
Group Action
20.	Master Miller and indeed the defendants have given the claimants all reasonable opportunities to advance their case to a stage of viability.
21.	Among the matters which Mr Melville Williams Q.C. for the claimants submitted were required was Toxicological evidence.  He stated that Donald J. Ecobichon, a renowned Canadian Toxicologist, was prepared to be a Court or Joint Expert.  Presumably he would require funding.  In his book “Pesticides and Neurological Diseases” Ecobichon has a chapter on Organophosphones and other insecticides tables 4 and 5 (file 4 p.396) setting out signs and symptoms manifested by those poisoned by organophosphates.  These signs and symptoms are manifested by many litigants in these proceedings.
22.	Mr Melville Williams also submitted that disclosure from the defendants in particular with regard to the chemical composition of the various products was required before claims could be accurately formulated.
23.	Mr Melville Williams also submitted that a report from a clinical toxicologist would be required for each claimant.
24.	Dealing with the tests carried out by Dr Jamel and the Pilot Study Mr Melville Williams submitted that evidence was required from a neurologist or physician saying in relation to each claimant that his signs and symptoms “are more consistent with organophosphate poisoning than with anything else”
25.	Mrs Charles, the claimants’ Solicitor in her statement (File 1.p.13 - 35) makes the point after conceding:-
"I take the view that the set up of the Medical Pilot to “provide definitive evidence” was wholly unrealistic and I agree it has resulted in a significant waste of time and costs.  As a consequence of the way it was organised many individual reports prepared for it are not available to individual claimants”
“There is a large amount of raw data in the medical pilot relating to these cases which show that there are abnormalities in relation to the general population which appear to be significant.  At the moment we do not have funding to have this data properly analysed but hope to do so in the future.
If these reports are somewhat limited then it must be remembered that at this stage the funding available to us is severely limited and has to cover the costs of defending all the part 24 applications incurred by several solicitors.  By way of example, it has not yet been possible to obtain a report from a toxicologist for each client although we are advised by Counsel that it would be very helpful"
26.	All this illustrates how much had to be done to make the group litigation viable.  I consider that it was unrealistic to suggest that the Group Action could have been made viable and ready for trial in less than two years by which time many more hundreds of thousands of pounds would have been spent with still a very uncertain prospect of any success.
27.	The claimants rely very substantially on neuro psychological evidence.  In my judgment such evidence is of very limited value towards the proof of causation.
28.	In her statement of the 9th of April 2001 Sarah Mackenzie Ross explains the role of the neuropsychologist (File 1 p.37-43).  She can provide an opinion as to the existence and extent of a psychological disorder or cognitive impairment and whether the apparent deficits are acquired brain injury or psychiatric disorder but in my judgment she is not competent to give an opinion as to the cause of those deficits because it is not within her expertise to make a diagnosis of neurological disease, brain injury or psychiatric disorder.  The making of such a diagnosis is within the expertise of the neurologist or psychiatrist.
29.	Because the COT report is unable to say whether prolonged low level exposure by organophosphates can cause chronic ill-health, the neuropsychologist is unable to state whether the deficits found by her in a particular claimant are attributable to prolonged low-level exposure.
30.	Impressive and conscientious as the reports of Sarah Mackenzie Ross and Julia Clark are they do not repair the weakness in the claimants’ cases which is the lack of evidence of causation from authoritative neurologists and psychiatrists.
31.	A major difficulty facing the claimants is the conclusions albeit not definitive of the COT report published on the 26th November 1999.
32.	The high-powered membership of the Working Group on organo-phosphates is listed in File 5 p.786.
33.	I quote from chapter 7 of the COT report (File 5 p.606
"Various types of chronic illness have been reported in individuals who have been exposed to Ops, and these illnesses are suspected to occur as a result of toxic effect of such exposure. However, the fact that in some individuals an illness develops following exposure to Ops does not in itself establish that Ops have caused the condition.  Before it can be concluded that there is a causal link there is a need for the following:
	*	reliable evidence that the illness is more common in people who have been exposed to Ops and that this excess is unlikely to be explained by other known causes of the illness:
	*	a plausible toxic mechanism through which Ops could give rise to the illness.
27 reports that the Working Party considered to be the most informative with regard to the potential toxicity of low-level exposure to Ops.  These reports are summarised in Appendix 4 with a discussion of their individual strengths and limitations.  Some of them concern the late sequelae of acute poisoning episodes, rather than low-level exposure as defined by the Working Group.  However, they are relevant either because they identify long-term health effects that might also be associated with lower exposures, or because  they indicate that the frequency of certain health outcomes does not appear to be elevated even after episodes of acute toxicity.  The absence of any increased incidence of an illness in subjects with exposure to Ops sufficient to cause overt acute toxicity makes it less likely that such effects would occur from low-level exposure, although there remains the possibility of cumulative effects occurring after prolonged low-level exposure."
34.	The Executive Summary of the COT report illustrates that at present there is no or no substantial evidence that prolonged low-level exposure to organophosphates does cause physical or mental injury.  Further research over an indefinite period of years may result in findings indicating that it does.  In my judgment it would not be justifiable to keep the Group Action alive indefinitely in the hope that such evidence might emerge particularly as only eleven individual claims remain extant.  To do so would be unfairly oppressive to the defendants who have been facing claims for over 8 years.
35.	After dealing with the long-term sequelae of acute poisoning the Executive Summary deals with prolonged low-level exposure:-
"1.17	In comparison with the positive neurological and neuropsychological findings following recognised poisoning incidents, the evidence relating to chronic low-level exposure to Ops, insufficient to cause overt acute toxicity, is less convincing.
Neuropsychological outcomes
1.18	Although some studies suggest impairment in the same tests that are affected after acute poisoning others do not.  The balance of evidence does not support the existence of clinically significant effects on performance in neuropsychological tests from low-level exposures to Ops.  If such effects do occur, they must either be relatively uncommon or so small that they are not consistently detectable by standard methods of testing.
Peripheral neuropathy
1.19	The balance of evidence indicates that low-level exposure to Ops does not cause peripheral neuropathy.  If effects on peripheral nerve function sufficient to cause severe disability do occur, they must be rare.
Psychiatric illness
1.20	The available data indicate that exposure to OP sheep dips is not a major factor in the excess mortality from suicide among British farmers.  However, in general, the evidence relating psychiatric illness to Ops is insufficient to allow useful conclusions.
Acute exposure to Ops at a lower dose than causes frank toxicity.
1.21	No studies have examined the long-term effects of a single exposure to Ops insufficient to cause acute toxicity.  However, the findings in individuals with prolonged and repeated low-dose exposures, and in those who have suffered recognised acute poisoning, together indicate that any risk of serious health effects from such limited exposure must be small."
36.	It went on to refer to:-
"Outstanding issues.
1.24	In addition to drawing the above conclusions the Working Group identified outstanding issues, which need to be addressed by further research.
1.25	The major gap in current knowledge relates to the possibility that Ops cause disabling neurological or neuropsychiatric disease in a small sub-group of exposed persons.  Most research has focused on people who were in work at the time of the investigation, and therefore by definition were sufficiently fit for employment. Moreover, the available published studies have generally been designed to look for effects on the mean level of quantitative health indices in the exposed population, rather than exploring the possibility that only a small proportion of subjects may be at increased risk of clinically significant disease.  Thus, although the substantial body of evidence that has now accumulated gives little support to the hypothesis that low-level exposure to Ops can cause chronic disease of the nervous system, it does not exclude the possibility that at least some of the illnesses that were described to the Working Group as following such exposure are indeed a manifestation of toxicity.
1.26	Further investigation, using suitably designed studies, is needed to establish whether the risk of more severe neurological or neuropsychiatric disease is increased by low-level exposure to Ops.
1.27	In view of the widespread public concern about Ops, evident from the response to the Working Group’s inquiry, there is an urgent need for further research targeted at the issues set out above.
Recommendations for further research
1.28	The Working Group recommended further research to address the outstanding issues.  These were grouped around the following questions, the answers to which would help to clarify the remaining uncertainties:
	What are the most common patterns of exposure, clinical presentation and subsequent clinical course among people in the United Kingdom with chronic illnesses that they attribute to Ops?
	How common is dipper’s flu, and what causes it?
	Does low-level exposure to Ops cause disabling neurological or psychiatric disease in a small subgroup of exposed persons?
	Do people with chronic disabling illness that is suspected of being related to Ops differ metabolically from the general population?
	Other than acetycholinesterase inhibition, what mechanisms play an important role in the causation of adverse health effects by OPs?"
37.	That shows how much work on the issue of causation remains to be done.  Nevertheless a CIBA - Geigy Agriculture Health and Safety Data Sheet for Topclip Gold Shield on organophosphorus compound dated the 3rd February 1989 (File 5 -p.789 - 794) stated:-
"Repeated absorption of small doses, as may occur from saturated clothing, has cumulative effects resulting in progressive inhibition of nervous tissue cholinesterase. This happens when the repeat exposures occur within the cholinesterase recovery period.  Further small exposure may then precipitate the classical condition of OP poisoning.
Regular surveillance is desirable for anything more than occasional exposure to OP compounds, e.g. garden use.  An effective programme for screening workers regularly exposed to OP compounds would include:
(a)	pre-exposure measurement of both plasma and erythrocyte enzymes.  There should be a minimum of 60 days without exposure.
(b)	regular monitoring of plasma cholinesterase levels in repeatedly exposed subjects, e.g. Sheep Dipping Contractors."
38.	However, the report of Dr Hodges, the hepatologist, (File 1 p.46-47) although raising the possibility of causation is insufficient to make the claimants claim viable.
"I am satisfied that a significant subset of the group of farmers for whom I hold bone density data demonstrate thinning of bone, this being most evident, indeed a statistically significant difference - compared to control subjects, at the proximal femur.
After applying stringent study exclusion criteria to both farmers and controls (in order to reduce factors known to influence bone metabolism), given the farmers exposure to organophosphate insecticides through occupational exposure and the results of the in vitro studies,  I believe it is possible that the bone loss that I have demonstrated in the farmer cohort could have been, at least in part, caused by their exposure to organophosphate insecticides 
39.	However this should be read with his Lancet Article:-
"These results demonstrate significantly lower cancellous bone area and bone formation at cellular and tissue level in agricultural workers with long-term exposure to organophosphates compared with healthy age-matched controls.  The increase in eroded perimeter may reflect increased resorption or a failure by osteoblasts to fill in previously resorbed cavities: the presence only of occasional osteoclasts suggests that the latter is the most likely explanation.  The controls were closely matched for age but were predominantly from an urban population.  Lifestyle differences are, however, unlikely to account for the highly significant differences between the groups.
The clinical significance of these findings is unclear.  Bone mineral density in the spine and proximal femur was within 2 SD of the reference mean value for age and sex in all but one of the agricultural workers, and only one had a history of fragility fracture.  Low bone turnover results in an increase in bone age, which may have adverse effects on the mechanical strength of bone, possibly increasing fracture risk in later years.  The cause of the reduced bone formation in these agricultural workers also remains to be established in particular, we cannot distinguish between direct and indirect effects of organophosphates, the latter occurring possibly as a result of changes in physical activity and general health induced by organophosphate exposure.  With the exception of one volunteer, who was confined to a wheelchair.  The agricultural workers in this study had normal amounts of physical activity, although a reduction from previously higher physical activity cannot be excluded as a contributory cause"
Bruce’s Claim.
40.	This is an employer’s liability claim.  Bruce was employed by Turney for an exceedingly short time after a lifetime spent working on farms and being exposed to innumerable chemicals over very many years (See “Factual Details”- File 23 p.173-183 and chemicals listed File 23 p.30-33).
41.	Bruce was employed by Turney from the 18th November 1991 until about the 13th January 1992 at East Ayton Farm on the Isle of Wight.  In the Statement of Claim (File 23 p.16-21) allegations of breach of statutory duty and negligence are made in relations to two matters.  On the 6th January 1992 a spray tank containing Actellic D which includes an organophosphate compound was drained.  Bruce pleads that he worked on that draining.  It is not disputed that the tank was drained on the 6th January 1992 but is disputed that Bruce assisted in the draining of the tank.  However it is not disputed that over the next seven days that he assisted another employee of Turney in cleaning out a farmyard drain.  Thereafter he became ill and has not worked since.
42.	In my judgment Bruce faces an insurmountable hurdle in establishing causation and has no realistic prospect of success.
43.	His Statement of Claim was supported by a medical report (File 23 p.30-34) from Dr Julian Kenyon of the Centre for the Study of Complementary Medicine at Southampton who wrote in a letter (File 23 p.29) dated the 23rd September 1994:-
"I would think that from Mr. Bruce’s history that the vast majority of his problem is in fact due to chemical poisoning.  This in turn would lead to a depressed immune system which then would make it more likely for him to have a persistent virus such as the coxsackie B virus.
The symptoms one might expect from a persistent virus are basically those of immuno-depression which is exactly the sort of symptom picture you see in chronic chemical poisoning.  However, in Mr Bruce’s case he has evidence of poisoning in every body system i.e., heart, nerves, circulatory system, lungs, kidneys and the gastrointestinal system.  On the basis of this my considered opinion is that the vast majority of his problem is actually due to chemical poisoning.  However, it does mean that what the Guy’s Hospital people said is medically correct in that one needs to be aware that coxsackie B is also a possibility, but a lesser possibility on clinical grounds in my view."
44.	Dr Myhill, whose evidence has been rejected by Master Miller, in her report of 20th October 1999 (File 23 p.35-52), sets out Bruce’s dire physical condition and complaints.  She states on page 51:-
"Mr Bruce’s clinical history and symptoms are typical of chronic OP poisoning.  This needs substantiating with tests"
45.	Bruce was not a subject of the Pilot Study.  His case on causation entirely depends upon fringe medical opinion.  The evidence against him is weighty.
46.	Dr David Williams, a consultant chemist, in his report dated the 12th January 1999. (File 23 p.189) said at page 197:-
"As the information stands, I am of the view that Mr Bruce has not had exposure to organophosphates as pleaded, this view arising primarily because of the chemistry of the compounds in question.  In addition, there is no or no substantial and congruent evidence in the literature that these particular organophosphates are capable of causing the alleged conditions suffered by Mr Bruce.  To my mind, his case does not bear scientific scrutiny on the basis of lack of a causative factor."
47.	Bruce was investigated at Guys Hospital in 1993.  On serology (File 23 p.262)
"The only positive finding was a positive coxsackie B IgM,  this is consistent either with a recent entroviral infection or persistent entroviral infection"
48.	On the 22nd December 1993 the Registrar wrote to Bruce’s G.P. (File 23 p.265):-
"Based on our current findings and present data available we do not think that the long term chronic symptoms of this patient is due to organophosphate exposure although we have stressed that the acute symptoms secondary to acute exposure were certainly consistent, both the patient and his wife are in fact very distressed and disappointed at our diagnosis.  We did however stress that all these conclusions that we have come to are based on current research and data available"
49.	In his report (File 23 p.205-230) dated the 30th January 1996 Dr Frew wrote at page 208:-
"It will be clear from the above that the acute illness experienced by Mr Bruce in January 1992, and the subsequent chronic symptoms are compatible with the known clinical features of coxsackie B virus infection.  In my opinion Mr Bruce has been suffering from chronic fatigue syndrome (Ref 9) and it is much more probable that this was as a result of him becoming infected with the coxsackie B virus than from any exposure to organophosphates.  There is no evidence that Mr Bruce has been immunodepressed or that he has had any clinical condition which would render him more susceptible to a coxsackie B infection than any other normal individual."
50.	Mr Bates in making his oral submissions on behalf of Bruce accepted that his case was exceedingly weak but should not be deprived of his legitimate expectation that his claim should come to trial.  He should be allowed to instruct his own chemist to re-evaluate the conclusions of Dr David Williams.
51.	His Solicitors have contended that Bruce’s claim can still be advanced on the “exclusionary basis”.  In my judgment in view of the medical evidence such an approach would have no realistic prospect of success.
52.	I would not have complied with the overriding objective if I had not struck out Bruce’s claim.
Forbes’s Claim.
53.	Forbes who is now aged 52, a chartered accountant by profession, suffered no exposure to agricultural chemicals during his various employments.  His father being a farmer and having been brought up on the family farm until he went to University, in 1981 he bought his own farm as a sideline.
54.	He sues three manufacturers.  In Paragraph 3 of his Particulars of Claim are listed their products and the periods of use of the Sheep Dips (see File 18 p.2)
55.	It was in 1986 that he began to suffer symptoms which he attributes to sheep dip.  Those symptoms included severe headaches, sore muscles and a flu like feeling after dipping (See his statement File 17 p.11).  He has not worked since the 21st January 1991.
56.	Dr Julia Clark, the neuropsychologist, in an impressive report following an interview and formal psychometric assessment of Forbes on the 3rd March 2001 (File 18 p.23-56) reached on an exclusionary basis this conclusion:-
"Given the nature of symptoms, medical history and the timing of onset of symptoms following exposure to organophosphates the balance of probabilities points to the fact that these were the causative agent.  I have considered a variety of agents that might produce similar symptomatology but in all cases these have been discounted.
In my opinion organophosphate poisoning is the only reasonable explanation for the symptom cluster and development of a chronic but non progressive condition"
57.	However, I consider that it can be cogently argued that this conclusion is only reached by Dr Julia Clark going outside and beyond her special expertise, however distinguished she may be as a neuropsychologist she gives opinions on matters which are within the province and expertise of the neurologist and physician.  For example:-
"Mr Forbes has similar but more extreme symptomatology than that described in CFS patients.  The involvement of the same neural pathways in the brain would suggest that the causative agent in his case affected the same mechanisms but in a more extreme fashion.
Mr Forbes suffered from a viral infection in 1988 which was so severe he has to receive hospital treatment.  The infection was identified as Coxsackie B virus
In my opinion it is most unlikely that Coxsackie B virus is responsible for the cognitive deficits demonstrated in Mr Forbes."
58.	Dr M.J. Campbell, the neurologist, in his report dated the 4th October 2000 (File 18 p.57-73) was much less convinced of causation.  He wrote:-
"There is no overt general medical problem.  Psychologically he appeared normal today and there was no evident impairment of memory or intellect.  The subjective mild impairment of pinprick sensation over the fingers and palms is in a rather odd distribution, and mainly in peripheral median nerve territory.  There is no significant subjective impairment of sensation over the feet.  Reflexes are a little sluggish but do not support any suggestion of a polyneuropathy.  There is no evidence of any other neurological disease
There is a history of recurrent chest infections and/or flu like illness since February 1982.  Some such episodes have occurred in April or October/November of various years at times of sheep dipping activity, but this is not invariable.  I have little doubt that the weekend hobby of sheep farming including the physical activity of dipping up to 2,000 in a day is a very physically exhausting activity by itself, irrespective of the exposure to the toxic fumes from the organophosphate compounds but that should not give specific chest symptoms
At the present time Mr Forbes main complaint is of an almost constant left chest pain which appears to be a non specific musculo-skeletal problem and unrelated to any possible toxic exposure.  His long-standing complaints of sensory disturbance over his hands and feet do not have any supporting examination features of a polyneuropathy.  I note that his was a consistent complaint from May 1995 onwards, that is more than 5 years after the last exposure to OP chemicals, and hence probably unrelated.  It is possible that repeated exposure to organophosphates between 1988 and October 1990 has exacerbated the PVFS but it is difficult to prove this.  He has rather non specific complaints of fatigue, poor concentration and retentive memory disturbance occasionally with stress headaches which are fairly typical of a chronic fatigue syndrome, and are fully compatible with a post-viral illness syndrome.  They are not indicative of any specific chronic organophosphate poisoning syndrome."
59.	Although there was force in Mr Ferris’s oral argument for the defendants pointing at the weaknesses in Forbes’s case; Dr Campbell was Forbes’s expert neurologist; there is substantial inadequacy of temporal correlation between exposure to organo-phosphates and Forbes’s ill health; and Forbes will have substantial difficulty in proving attribution, that is linking a particular product to a manufacturer he has sued causing his ill health; I am unable to say that Forbes has no realistic prospect of success having regard to Dr Julia Clark’s report.
60.	In his oral argument for Forbes Mr Bates submitted:-
"Mr Forbes is right not to ask the Court to rely on Dr Campbell’s report and that his case should go forward for further examination"
61.	Such a plea has been a feature of both individual claims and the Group Action convincing me that the Group Action should be brought to an end.  Forbes ceased working in January 1991 allegedly through ill health caused by organophosphate exposure.  That is approaching eleven years ago.  His case is too weak to proceed now.  Will it ever be strong enough?
Ford’s Claim.
62.	Ford who is now aged 50 worked on his fathers’s farm until 1978 when he and his wife bought their own farm.  Over the years they had various farms.  Rearing sheep was a substantial part of their business.  Inevitably this entailed twice or thrice annual dipping.  After 1978 the dip used was a Young’s product.  Ford became significantly unwell in 1994 and in the following year retired.
63.	He sues Young’s Animal Health Ltd.  He was granted legal aid on the 3rd January 1998, the writ being issued on the 30th March 1998.  The Particulars of Claim which allege breach of Consumer Protection Act 1987 and negligence was served on the 19th April 2000 (File 10 p.3-73)
64.	In his statement (File 9 p.8-17) Ford says:-
"At the end of a days dipping, I would feel shattered.  My limbs would also ache.  Initially I attributed this to the physical effort of handling sheep.  However with hindsight I am convinced that these and many other symptoms have in fact been caused by the dip itself
It was in the Autumn of 1994 that I started feeling unwell.  I was suffering from a bad arm and chest pains, dizziness, feelings and faintness and passing out.  I visited Casualty in Lynton twice.  Looking back I can see that I tended to feel rather unwell at dipping time generally."
65.	The medical records of Ford are in File 10 -p.158-161.  In 1994 there is recorded:-
"25 March 1994	Headaches and mild dizziness one 			week
18 November 1994	Palpitations
8 December 1994	All normal. Palpitations seem 				more awareness than rapidity.				Depressed. Weeps. No energy "
66.	Letters from Ford’s G.P. state:-
"14 November 1994	Letter from General Practitioner. 			Had been seen on 11 November 			with a fluttering sensation and 				tightness in the chest - radiating 			into the back. Felt dizzy. Pulse 			104.  Blood pressure 155/95. ECG 			normal.  Said to be under pressure 			with business.  Naturally anxious 			person.
	22 February 1995	Further letter from GP.  Had 			experienced more chest pain with 		radiation to the left arm"
		“He tells me that he has been lacking energy and has been unable to do a full days work for six months because he feels tired”  The symptoms warrant further investigation”
67.	The first mention of sheep dip is on 25th August 1995 when Ford was referred to Dr D.R. Davies, the Psychiatrist who wrote on the 2nd November 1995 (File 9. p.26):-
"Thank you for asking me to see this man who gives a history of classic organophosphate neurotoxic symptoms.  He developed an episode of depression lasting 4-5 months during which time he experienced intensive episodes of suicidal thinking though, mercifully, did not act on these.  This has largely resolved though he still gets episodes where he feels low for brief periods and also becomes irritable which is a change from his former personality.  He has considerable difficulty in concentrating and also complains of a degree of memory loss.  From time to time he gets sentences backwards and his wife confirms this tendency to word reversal.  He has become sensitive to a number of odours and when recently at market and in the vicinity of dipped sheep, became quite ill overnight and for the next couple of days"
68.	Dr Davies’s alleged expertise was rejected by Mrs Justice Smith in Hill v. William Tomkins Ltd (See pages 27 and 28 of her judgment) where she said:-
"Dr Davies very frankly accepted that this was not a sophisticated piece of research.  It was not a controlled study.  His patients were usually referred to him by their general practitioners.  His method of interviewing was not well controlled.  Sometimes symptoms would be described spontaneously; at other times, they emerged in response to direct or leading questions from the doctor.  The patient’s description of his symptoms were relied upon and no objective tests were carried  out
Dr Davies readily accepted that his work could not stand up to scientific scrutiny.  However, he said that many medical discoveries began from modest beginnings and he thinks he may be on the track of something useful.  He may be.  However, I could not rely upon his work as anything other than a collection of cases of anecdotal interest."
69.	On the 18th October 1996 Renée McCarter, neuropsychologist wrote:-
"In summary.  Mr Ford presented as a man of average intelligence with preservation of intellectual and executive functioning, mild impairment of concentration and psychomotor speed and severe impairment in recent memory. There was no indications of malingering and the neuropsychological profile is suggestive of an organic disorder."
70.	He was referred to a number of consultants.  On the 30th October 1996, Dr Hogg, neurophysiologist wrote:-
"In summary this is a 45 year old man with a confusing history of unilateral motor and sensory symptoms for which we can find no neurophysiological cause."
71.	On the 6th February 1997 Dr J.M. Bird, neuropsychiatrist, wrote:-
"I saw Mr Ford as an out-patient on 17 December.  He came along with his wife.  There has been no change at all in his clinical situation, indeed he may have a little more problem with his right leg now and seems to have difficulty standing.  I reviewed the nerve conduction studies which were carried out in October and they demonstrate that nerve conduction in both upper and lower limbs was within the normal range.  We therefore do not have any explanation for these problems."
72.	On the 12th May 1997 Dr M.J. Campbell, neurologist, wrote:-
"In summary I believe that his left limb symptoms are a psychogenic disturbance and do not have a focal brain cause.  This could of course be a psychogenic reaction to some diffuse neuropsychlogical dysfunction.  However, I notice that formal testing showed no evident cognitive deficit although poor concentration and memory recall.  There are also delayed cortical evoked potentials on cognitive testing and some very doubtful profusion disturbances on SPECT.  In view of this I will arrange for a repeat MRI brain scan although the previous one in January 1996 was normal."
73.	On the 8th August 1997 Dr Campbell again wrote:-
"As promised I write with the results of the MRI brain scan performed on the 28th July and I am very happy to report that his was entirely normal with no evidence of any brain abnormality to account for your continued symptoms.  I find it very difficult to advise any specific treatment for your condition but perhaps Dr Bird or Dr Davies may be able to offer you more help in this respect. "
74.	Ford places reliance on the report of Sara Mackenzie Ross, the neuropsychologist, of the 10th March 2000 (File 10 p.74-92) who concluded:-
"Mr Ford’s performance was consistent and his pattern of deficits is similar to that seen in other individuals with a history of exposure to OP’s.  Therefore, it is my opinion that on balance of probabilities, Mr Ford’s cognitive deficits are more likely to be due to the cumulative effects of exposure to OP’s than mood disorder."
75.	Dr Stuart Turner the psychiatrist, in his report of the 22nd May 2000, (File 10 p.93-113) is  more guarded in his opinion on causation saying:-
"The neuropsychological assessments undertaken by two clinical psychologists are reported as consistent with an underlying organic condition.  Dr Mackenzie Ross goes further and attributes the abnormalities on the balance of probabilities, to organophosphate toxicity.
If this is correct, then it may be that the depression is in some way directly bound up with organophosphate exposure or it may be, as Mr Ford himself indicates, that it was his state of being unwell and the impact on his ability to work which through psychological mechanisms led to him becoming depressed.  In either case (based on the evidence of the first paragraph of this section) the cause of his depression would be related to an organic disorder and, if Dr Mackenzie Ross is correct, to organophosphates.
The results of my investigation are consistent with such a relationship, but I cannot confirm this causation on the basis of my psychiatric examination."
76.	Professor Langton Hewer, the neurologist, in his report dated the 28th June 2000 (File 10 - p.121-164) asks two questions:-
"What is the diagnosis?
i)	It should be stated initially that there is no clear cut evidence of neurological disturbance here.  There is definitely no evidence of peripheral nervous system damage.  There is no evidence of any damage to the right side of the brain and I do not think that the pain and possibly impaired function in the left arm and leg has a structural basis. I am uncertain as to the significance of the neuropsychological findings.  I would be reluctant to dismiss these but I have to say that I do not think that it has been conclusively proved that this man has a structural brain disease.  The matter might well need further assessment.  At the present it is, perhaps, sufficient to point out that cognitive functioning appears to be adequate for farming duties.  The findings of the Department of Health Working Party are noted (see earlier in this report).  I would not regard these findings as being “the last word” on the subject but the Working Party did have the advantage of being able to review all the published evidence
ii)	Heart disease.  As far as I can ascertain - there is no evidence of heart disease here.
iii)	Chronic fatigue syndrome.  This is a case in which fatigue and lethargy do not see to me to be prominent symptoms although they have certainly been mentioned from time to time.  I am doubtful about this diagnosis.
iv)	Multiple chemical sensitivity.  Doctor Myhill suggested that Mr Ford may be suffering with multiple chemical sensitivity but I am not aware of any clear cut evidence to support this contention.
v)	Involvement of other organs.  As far as I can ascertain - there is no evidence of involvement of the liver, lungs, endocrine system, or other organs.
Does Mr Ford suffer with chronic OP poisoning?
i)	This is a case in which there does seem to be significant exposure to OP’s over a long period of time.  However, no conclusive physical abnormalities have been found and investigations have been largely negative.
ii)	There is no doubt, in my mind, that many of this man’s symptoms cannot be explained on the basis of OP poisoning (e.g. the left limb symptoms).  However, the possibility does exist that some of the other symptoms might be due to this although I am personally unconvinced
iii)	The neuropsychological findings have been discussed above.  I think that these require further evaluation.  Brain scanning may be required.
iv)	I found it difficult to decide whether this man should be put into the uncertain or the unlikely group.  I eventually decided that the uncertain group would be most appropriate - at this stage."
77.	Although appreciating that Professor Langton Hewer does not specifically mention the test of “balance of probabilities”,  I categorise Ford’s case as weak.  Maybe with more testing and examinations it could be strengthened.  It certainly cannot be said that his claim has no realistic prospect of success.  Although much would depend on the reliability of Ford’s evidence, having reviewed the case I consider that there is much cogency in the argument of Mr Matthews for Young’s Animal Health Ltd that there is a absence of clear cut evidence of a temporal connection between exposure to organophosphates and ill health. 
Evan Jones’s Claim.
78.	Jones who is now 57 became the Director of Dyfed Rural Council in 1981.  At about the same time he bought a small farm Bryngwddil where he ran on a part time basis a business of rearing and selling sheep.  He did not dip sheep because he bought them after the autumn dip and sold them with their lambs.
79.	On the 4th June 1983 he was admitted to hospital with chest pain and hypertension after visiting a barn in which there were about a hundred dipped sheep (See File 13. p.23)
80.	He decided to give up his office job and take up full-time farming buying a 230 acre farm at Briwnant in 1985 with a flock of about 1100 ewes.  Sheep dipping was compulsory and approved MAFF dips all of which contained organophosphates had to be used.  When dipping Jones used protective clothing which exceeded the maximum recommended by leaflets from manufacturers and MAFF.
81.	Over the years his farming business expanded considerably and involved the sale of both organic and non-organic meat on a substantial scale.  However in 1992 his health collapsed completely and the farm was sold in 1995.
82.	By a writ issued in 1996 Jones sues a number of manufacturers of organophosphate based sheep dips and government departments (See the Particulars of Claim File 14 pages 1-93).
83.	The problem he faces as with other claimants is proof of causation.
84.	Professor Langton Hewer in his report dated the 28th June 2000 (File 14 p.142) poses the question:-
"Does he suffer with chronic OP poisoning?
i)	The outstanding features in this case appear to be the relative normality until the late 1980’s, his previous success as a business man, and the rather sudden development of fatigue and other symptoms in 1991 to 1993.
ii)	There appears to be reasonably good evidence of significant exposure to OP’s.
iii)	The symptoms have, on the whole, been rather non-specific.  The symptom of smell hypersensitivity, however, seems to be rather characteristic of the chronic OP group.
iv)	As things stand at the moment. - I am uncertain as to the significance of the neuropsychological findings and whether or not he was cognitively disturbed in any  major way in the early 1990’s.  There seems to be some evidence that this was, indeed, the case.
v)	There can clearly be no certainty about the relationship between OP’s and the subsequent development of symptoms.  After much thought - I placed him in the uncertain group."
85.	Dr Stuart Turner, a psychiatrist, in his report of the 25th April 2000, says this about causation (File 14 p.181):-
"I have already indicated that I do not regard the possible depressive symptoms in 1983 as of particular relevance.  This is a man with an organic pattern of symptoms and this pattern has been confirmed on neuropsychological assessment.  He has also been assessed in detail by a consultant neurologist.  I am aware that there have been other investigations undertaken as part of this legal action - the results of which I have not seen.  As a psychiatrist, I would point to the need to find an organic explanation.  This explanation rests on the results of these physical investigations, including that of his neurological state.  Causation is likely, in my opinion, therefore to be determined by the results of these investigations in full.  I am aware that this is a legal action to do with organophosphates in sheep dip.  I have no reason to believe that these are not responsible, but would point to the role of the other experts in taking this statement further."
86.	Dr Julia Clark, the neuropsychologist, in her report of the 27th September 1999 gives these opinions (File 14 p.194-5)
"Mr Jones was exposed to organophosphate containing compounds for a number of years when he was involved in farming and later in his wholesale business.  The physiological and cognitive symptoms he reports resemble the cluster of long term effects documented regarding OP exposure.
In Mr Evan’s (sic Jones) case attentional problems and psychomotor slowing (plus the variability in these) are probably linked to the spread of EEG irregularities.  However the language problem reflects the permanent underlying organic damage.  These symptoms were first identified following increased OP exposure in 1990"
87.	Doubts are raised on causation by the variance in results in the Pilot Studies of the 13th October 1994 and the 6th June 1998 (See File 14 p.101 and 102) and the report of Dr Scammell of the University of Nottingham dated the 26th January 1999 who states (File 14. p.105):-
"SUMMARY FROM THE RESULTS OBTAINED THUS FAR.
Mr Jones has no previous history of metabolic bone disease and neither have we found any evidence of this.  He does not, as yet, have any biochemical evidence of any disease processes that may explain his current ailments.  These ailments may or may not be attributable to his organophosphate exposure, but this cannot be proven with the tests thus far carried out.
FURTHER ANALYSES TO BE CARRIED OUT.
1.	Spinal morphometry
2.	Urine analysis
3.	specific serum bone marker analysis
4.	enzyme analysis
5.	Bone histomorphometry (from trans-iliac bone biopsy 	specimen
6.	Sex hormone binding globulin
NB	The above tests will not be carried out until all our other subjects with similar exposures have been seen and specimens taken to avoid inter-batch error with certain assay reagents."
88.	In my judgment it cannot be said that Jones has no reasonable prospect of success.  To make that prospect a good one further tests would be required.  I consider that it would be quite wrong to strike out Jones’s claim as an individual claim although the defendants could validly argue that Jones’s ill health is scarcely if at all correlated temporally with organophosphate exposure.  The tin lid incident in the autumn of 1990 and the onset of broncho-pheumonia in April 1991 is an example.  Moreover much would depend on the accuracy of Jones’s recollection of events of long ago between 1985 and 1992.  His claim is not one that could be advanced on a purely exclusionary basis.
Layton’s Claim.
89.	Layton is nearly 22 years old and is taking a business course at the City of Bath College.  He appears to have been reasonably intelligent and still is.  He was also physically active enjoying football and scuba diving.  He also played the tenor horn.
90.	He was brought up on the family farm.  Although he was not allowed to help in the actual dipping of sheep, with his brothers he watched at a distance away.  However he helped to bring in the sheep from the fields and drive them back after dipping.
91.	From the age of 12 he had his own small flock of sheep which he looked after entirely himself, when he was fit and well, except for dipping but when they had dried off after dipping he would handle them frequently.
92.	He fell ill in January 1993 since when his education has been severely disrupted.
93.	The evidence on causation is sketchy and as it presently stands Layton’s claim must be categorised as weak.
94.	Mr Bates for Layton recognised the difficulties in his oral submissions saying that there was a reasonable prospect of evidence being available at the trial and that children may be more adversely affected by organophosphates particularly if it comes in contact with the skin.  He accepted that there was no acute precipitating event.  He suggested that there was a plausible mechanism that of organophosphates adversely affecting Layton’s cholinesterase and thereby triggering particular symptoms of organophosphate poisoning.
95.	However the medical evidence remains in an amorphous state
96.	Dr Jamal, the neurophysiologist, states in his report of 22nd October 1998 (File 16 p.307-318):-
"Joseph was extensively investigated at Hereford Hospital including metabolic screen, haematologic screen and virological tests, all of which were entirely normal.  He had a lumbar puncture which was reported as showing a slight increase in intracranial pressure at 23cms but this was dismissed later on by the consultant paediatrician as probably being spurious.  A CT scan of the head was normal.  He was also investigated at the Victoria Eye Hospital but extensive visual investigations including visual field, colour vision, and fundi were also found to be normal.  A cervical X-Ray was normal.  The consultant paediatrician (Dr Butterfill) has diagnosed Joseph initially as having benign intracranial hypertension based on the slight increase in CSF pressure but later this was thought unlikely.  Later on, he diagnosed Joseph confidently as chronic fatigue syndrome.  This was also thought to be the case by Dr Williams who used the label post viral fatigue syndrome.  Joseph was eventually referred to a consultant paediatric neurologist Dr S Green, who did an MRI scan of the head which was reported as normal.  Dr Green concluded that the symptoms may be non-organic but mainly depended this conclusion on the back of a diagnosis.  Joseph’s physical symptoms persisted and he continued to have profound fatigue, constant neck and head pain and recurrent sore throat.  He is currently on no medication and had a course of physiotherapy with no major benefits.
There remains the explanation of the mild peripheral neuropathic changes which had improved in subsequent testing and the non-specific autonomic changes seen on the second assessment.  It is difficult to explain these with certainty but it is likely that the former be related to some sort of viral infection and there has been some report describing some neurogenic changes in patients with post viral fatigue.  The autonomic changes, though interesting do not direct us to specific area and it s is conceivable that they may be a part of the chronic fatigue syndrome.  It is possible that the current changes are due to his exposure to Ops but this is less likely than the alternative explanation in light of the overall picture and in any case extremely difficult to prove."
97.	Dr Stuart Turner, the psychiatrist, states in his report of the 17th May 2000 (File 16 p.319-336)
"The history which he outlines, and which is extracted from his medical notes, is, in my opinion, consistent with a diagnosis of Chronic Fatigue Syndrome.  There is no evidence of any other specific functional psychiatric disorder - either now or in the past.  However, this diagnosis rests upon the absence of another organic explanation for his symptoms.  I am aware that Dr Jamal has put forward evidence indicating a link between these symptoms and organophosphates.  I am aware that Dr Myhill has found evidence linking these symptoms with multiple chemical sensitivity secondary to OP exposure. It is beyond my expertise to comment further on these potential organic or neurotoxic explanations for his symptomotology  but, based on this evidence, it seems likely that his fatigue symptoms are associated with an underlying physical disorder (although I cannot confirm this directly on my assessment)"
98.	However Sarah Mackenzie Ross, the clinical neuropsychologist, is more specific in her report of the 14th April 2000 (File 16 p.209-225) giving this opinion:-
"Joseph Layton has been exposed to organophosphate containing compounds during childhood whilst handling sheep  which had been dipped. Organophosphates (OP’s) can be absorbed rapidly through the skin, lungs, gastrointestinal tract and conjunctiva.  Once absorbed their principle action is to inhibit acetylcholinesterase which can result in changes in peripheral, autonomic and central nervous system function (cholinergic crisis).  The immediate effects of OP poisoning which occur within hours of exposure have been well documented.  Joseph Layton’s mother reported that he suffered episodes of flu-like symptoms sheep had been dipped on the farm and these symptoms are consistent with those reported by other individuals who have been exposed to toxic levels of OP’s.  It suggests that Joseph Layton suffered episodes of mild acute poisoning.  Whilst it is possible to recover from an acute cholinergic crisis and for levels of the enzyme acetylcholinesterase to return to normal, recent research suggests there may be long-term changes in nervous system function following cessation of he cholinergic effect.  The mechanism for this is unclear.  OP’s may permanently damage synaptic receptors and membranes.  They are lipophilic and can remain in tissue for a long period of time, and they are thought to affect other enzymes and neurotransmitters, apart from the cholinergic system e.g. serotonin.  As a result, the clinical course of organophosphate poisoning may show prolonged and relapsing episodes.  Evidence is emerging that children may be particularly vulnerable to the effects of organophosphates.
Less is known about the effects of repeated exposure to low doses of OP’s which do not cause an acute cholinergic crisis.  Attentional deficits, psychomotor slowing, impaired information-processing speed, memory impairment, language deficits and greater vulnerability to psychiatric disorder (particularly anxiety and depression) have been found in individuals with a history of chronic exposure.  Joseph Layton is showing evidence of impaired verbal memory, verbal fluency and psychomotor speed.  I was unable to identify any other factors in his background, apart from exposure to organophosphates, which might otherwise account for his results.  Therefore it is my opinion that on balance of probabilities, Joseph Layton’s cognitive deficits are likely to be due to the cumulative effects of exposure to OP’s."
99.	In view of that opinion despite the overall weakness of Layton’s claim it would not be right to strike out his claim on an individual basis.
Sayce’s Claim.
100.	Sayce was born on the 1st November 1947.  He was brought up on his father’s mixed farm in Herefordshire.  As a boy he took part in a variety of farming activities including sheep dipping and crop management.  When his father retired in 1970 he and his brother took over running the farm in partnership until 1993.
101.	On the 5th June 1995 he was told by Dr Myhill that his health problems were attributable to exposure to organophosphates.
102.	On the 4th June 1998 he issued a writ suing twelve manufacturers of agricultural chemicals (File 20, p.3-5)
103.	Over the years he was exposed to 130 chemical products listed in File 20. at p.126.
104.	The dates of purchase and the usage of about 23 different organophosphate products are listed in File 20 at p.123-125.  Usage included sheep dipping, cattle treatment and crop treatment.
105.	In File 20 p.128-149 there is a schedule giving details of the purpose for which the organophosphate product was used, the period of exposure, the dates of purchase and the protective clothing or equipment used by Sayce.
106.	By his Particulars of Claim dated the 18th April 2000 he proceeded against only two manufacturers of organophosphate products, Bayer, manufacturer of Metasystox used for crop spraying, and the Wellcome Foundation, manufacturer of Cooper’s Winter Fly Dip and Coopers BHC Fly Dip both used as sheep dips.
107.	The immense complexity of the litigation is exemplified by a reading of the Particulars of Claim that with annexes runs to 44 pages (File 20 p.6.80).
108.	An adverse consequence to Sayce from discontinuing against other manufacturers is that the costs of three manufacturers against whom he has discontinued would be set off against any damages or costs to which Sayce might be entitled.  (See the Order dated the 29th August 2000 - File 19 p.96).
109.	The inability of Sayce to progress his claim without public funding is shown in the letter of his Solicitors, Gabb & Co dated the 17th October 2000 which stated (File 19 p.101A):-
"We are proposing to apply to have Mr Sayce’s claim removed from the group action and it follows that if that is done, directions concerning this case ought not to be included in the group action directions summons.  However, as you will also know, the Legal Services Commission have threatened to withdraw the claimant’s public funding.  If that happens, unless alternative funding can be found, he will not be able to continue with his claim."
110.	The extensive entries in Sayce’s  medical records are set out on pages 30 to 37 of File 19.  It should be noted that from 1976 onwards there are frequent references to lethargy, listlessness, general weakness, no energy, tiredness and such like.  There is no entry indicating any possible acute exposure to organophosphate poisoning and no clear pattern of temporability; that is exposure to organophosphates and consequent illness.  In his statement dated the 5th April 2001 (File 19 p.71-84) Sayce said:-
"I recall feeling a bit queasy after dipping.  I cannot explain exactly how I felt, just off colour, but I thought it was due to the hard work involved and did not associate my feeling ill with the dip mix.  I would often be splashed by the diluted dip, mainly when the sheep went into the dip rather than when they came out.  It was hot, heavy work and the sheep were all struggling not to go into the dip and would splash you when they came out.
When I had been using Coopers products, I found that towards the end after use, I suffered from flu-like symptoms.  I had dizziness and weakness, I was lethargic, had aches and pains, felt nauseous, was trembling and had a headache.  This would last for a few days.  I did not go to the doctor about my symptoms for two reasons: I thought that the problems arose from having overdone it with the amount of work; and because it took too long to go to see the G.P.  Thinking it was probably flu it had to run its course.
Of all the pesticides I used for crop spraying the ones that affected me most were the aphicides which contained demeton-s-methyl, and in particular Metasystox.
The product came in an aluminium container which was well sealed and which poured out well.  There was little spillage or splashing while mixing the product, but the smell was very strong.  Towards the end of the time that I was spraying with Metasystox, I began to feel queasy, a bit sick and would be starting a headache which became very bad and which, even after taking paracetamol would not clear up.  I would have a dull headache for some time, often four to five days, and feel very weak and sweating although my feet remained cold. I also found that up to three or possibly even four days afterwards, if I took a deep breath and breathed out through my nose, I could still smell the chemical.
Although it made me feel ill, I continued to use it, because it was a good product.  It was a 100% kill on aphids.  Although I had mentioned how I felt when using OP’s, my doctor had said they could make you ill for a few days but there were no long-term effects and I did not suspect that I could be harming myself by continuing to use the products.
I did a tiny amount of contract work in late 1994/early 1995, and was feeling a good deal better.  In May 1995, I helped do some potato planting which required me to use Phorate in the planter.  I became progressively more ill as I was doing the potato planting and my symptoms seemed to be linked to ME.
My wife mentioned that there was to be a talk given by the ME Association at Hay-on-Wye by Dr. Myhill.  I went to the meeting.  At the time, I was feeling particularly ill having just been using Phorate.  I passed out during that meeting for the only time in my life.
I bought Dr Myhill’s book which listed symptoms, all of which seemed to relate to the symptoms I was suffering from.  I spoke to my doctor and asked if he would mind my seeing Dr Myhill and he confirmed that he would not, and on 5th June 1995 I saw Dr. Myhill who told me that she thought all of my problems were linked to my exposure to organophosphates.
Having seen Dr. Myhill, and realising that having had a spell away from organophosphates and feeling better, and then suddenly coming into contact with them again and feeling worse, I became convinced that my problems were linked to organophosphate poisoning.  Dr Myhill made recommendations to my doctor for treatment, which have left me feeling considerably improved."
111.	Clearly Sayce fortified by the views of Dr Myhill believes that his ill health is caused by exposure to organophosphates
112.	In my judgment the belief of Sayce is not supported by reliable medical evidence.
113.	Dr Hallstrom, a consultant psychiatrist at the Charing Cross Hospital says in his report of the 9th May 2000 (File 20 p.81-95):-
"Of course he has never been treated effectively with antidepressants and he does now have significant depressive symptoms, although he does not fulfil the diagnostic criteria for a major depression and depression itself has been notably absent from his complaints throughout the years.
The question of brucellosis diagnosed in 1974 remains uncertain, but the general view is that he did not actually suffer brucellosis then and certainly the titres have been negative.  If he had brucellosis, this might account for some of his chronic fatigue symptoms, although I think it unlikely his symptoms would persist for 25 years.
He himself notes that he gets better when not in contact with organophosphates, but when he smells the chemicals his symptoms recur.  This might mean some association with chemicals.
Mr Sayce appears to have a Chronic Fatigue Syndrome of unknown cause.  It seems to be cyclical.  In the absence of a cause, organophosphate poisoning remains a possibility."
114.	The report of Dr Julia Stewart Clark, the neuropsychologist, I found difficult to accept at face value but on a strike out application I must be careful not to conduct a mini-trial.  In particular I found her conclusion that Sayce has a pre-morbid IQ of 145 unconvincing.
115.	In her report of 28th September 1999 (File 20 p.96-110) Dr Clark said:-
"Mr Sayce had pre-morbid ability in the very superior range.  Ability at present is reduced to the higher average range.  As original ability was so extremely high it is difficult to demonstrate accurately the degree of deficit (sensitivity is poor at the extremes of the test range).  Despite this the degree of difficulty is statistically significant.  There is evidence of both attentional problems and psychomotor slowing.  The language deficits identified compromise the verbal memory tests such that it is difficult to separate the effects of language and memory.  The end result is that verbal material will be poorly and inaccurately remembered.  Frontal lobe function in general has been adversely affected and the variability in test results indicates an underlying mood disorder despite Mr Sayce response to an anxiety and depression screening tool"
116.	In her letter of the 7th July 2000 (File 20 p.111) she said:-
"You are correct in interpreting my opinion to be that in the balance of probabilities, Mr Sayce’s cognitive deficits are likely to be due to the effects of exposure to organophosphate chemicals"
117.	In my judgment Dr Clark is not qualified to give an expert opinion as to the cause of cognitive deficits.  That is a matter for a medical clinician.  Her expertise is in the field of the extent of the reduction of cognitive abilities.
118.	However, very significantly although Sayce has been examined by Professor Langton Hewer, his report has not been disclosed.  The inference must be that it does not support Sayce’s case.  The best the Pilot Study could do for Sayce was to award him a question mark.
119.	Sayce’s case against both Bayer and the Welcome Foundation is based solely in negligence.  As I said in my Introductory Judgment it has no realistic prospect of success.
Snell’s Claim.
120.	Snell who is aged 61 has lived all his life at Tor Down Farm near Barnstaple.  Until his father’s death on the 16th November 1991 he ran it in partnership with his father.  It is a mixed farm of 133 acres with sheep, cattle and crops which involves the use of a range of agricultural chemicals, sheep dips, treatment for warble fly and crop sprays.  However, according to Snell except for one occasion when a Young’s warble fly product made him violently ill the only products which he used containing organophosphates were sheep dips from the late 1970’s.  On average there were between about 400 and 500 ewes and lambs on the farm.
121.	Snell describes the dipping procedures, the precautions which he took and protective clothing that he wore in detail in his statement (File 7 p.11 -14).  According to Snell the first that he knew about the potential hazards of organophosphates was when his G.P. mentioned it.
122.	Snell says that the first time that he became particularly ill was after the Autumn dip in 1990 when he used a Young’s product, Ectomort.  He says that he suffered flu like symptoms.  He says that he was again particularly ill after using Ectomort in July 1991 or 1992.
123.	Snell was granted Legal Aid on the 12th April 1994 but the writ was not issued until the 19th January 1996 nor the Particulars of Claim (File 8 p.3-90) served until April 2000.
124.	Snell’s case is supported by the report of Dr Jamal dated the 14th November 1995. (File 8 p.98-103):-
"It is therefore highly likely that Mr Snell has had repeated attacks of mild-moderate poisoning due to exposure to relatively small sub-lethal quantities of organophosphorus compounds contained in the sheep dip during the course of his occupation.
Both the clinical picture and the results of the fully objective neurophysiological studies and quantitative sensory testings, indicate that Mr Snell suffers from damage of the peripheral nerves"
125.	However this conclusion is undermined because in the Pilot Study when Snell was retested on the 6th June 1998 Doctors Jamal and Julu listed him among the claims that could not be supported (See File 8 p.105)
126.	Snell’s claim is also endorsed although not in an unqualified manner by the report of Sarah Mackenzie Ross, the neuropsychologist dated the 4th March 1999 (File 8 p.106-117) who said:-
"The fact that Mr Snell failed a test designed to detect functional complaints and/or malingering indicates that his mood state may have had some affect on his performance on psychometric tests.  However, his pattern of results is not typical of that seen in depressed/anxious patients.  Depressed/anxious patients often show a pattern of global impairment characterised by inconsistencies in performance between tasks, over time and between subjective reports and actual performance.
It is my opinion that on balance of probabilities, Mr Snell’s cognitive deficits are more likely to be related to the cumulative effects of OP exposure than mood disorder"
127.	In a follow-up letter Sara Mackenzie Ross dated the 26th June 2000 (File 8 p.118-119):-
"It is my opinion that, on balance, Mr Snell is more likely to have failed Rey’s test because of significant cognitive impairment and not because he was malingering.”

128.	Dr Hallstrom, the psychiatrist, in his report dated the 9th May 2000 (File 8 p.120-133) wrote:-
"Mr Snell has symptoms of depression and chronic fatigue which could well be caused by chronic organophosphate exposure "
129.	In the face of this evidence clearly his claim could not be struck out on an individual basis albeit that it is arguable that Snell’s ill health is more related to depression following his father’s death than to exposure to organophosphates as the medical records do not support a temporal correlation between the sheep dipping in the Autumn of 1990 and July 1991 or 1992 and that Professor Langton Hewer, the neurologist, is unconvinced on causation in his report of the 28th June 200 (File 8 p.134-174) where he says:-
"Diagnostic possibilities.
Many of the OP Claimants have been diagnosed as having chronic fatigue syndrome.  Mr Snell does have some apparently diminished tolerance(e.g. having to come in every 1¼ hours during the day for a rest).  There is no clear cut evidence of chronic fatigue syndrome here however.
Does he suffer with chronic OP poisoning?
i)	There is reasonably good evidence of exposure to OP’s over a long period of time.
ii)	The symptoms appear to have come on quite rapidly in the early 1990’s
iii)	The symptoms are somewhat non-specific and do not really implicate any particular organ or organ systems.  The possibility of cerebral and peripheral nerve damage has been mentioned above.
iv)	I find it difficult to come to a definite conclusion about this case.  As things stand at the moment - I put him in the uncertain category."
Stoker’s Claim
130.	Stoker who was born on the 16th April 1957 sues John Turner Ltd who were his employers for a short period during the summer of 1982 and again from the summer of 1983 until October 1985.  He brings his claim in negligence and breach of statutory duty (see his Particulars of Claim File 22 p.21-27)  He alleges that he was exposed to organophosphates when spraying chemicals from a tractor onto fields.  He alleges that as a result he has been ill since 1985 and is now confined to a wheelchair.
131.	His employment history (File 22 p.226-227) shows that he has frequently worked in the farming industry.  His statement dated the 3rd April 2001 (File 22 p.215-225) disclose that he was first exposed to organophosphates at his parents’ farm in 1975.  This exposure continued on occasions of sheep dipping until 1984.  He was also exposed to organophosphates when helping his father to apply warble fly treatment to cattle and when spraying insecticides when working at a farm in Pembrokeshire between 1975 and 1977.  However he contends that he did not feel ill until he worked for John Turner Ltd.
132.	In October 1985 Stoker was suffering from an abscess in the mouth.  He was treated with Carbamazipine which has many potential adverse side-effects which are listed in the statement of Mr Montgomery (File 22 p.281-232).
133.	Stoker was a subject in the Pilot Study but was rated non causative?  On the all important issue of causation Stoker obtains limited support from the inadmissible evidence of Dr Myhill who stated (File 22 p.57)
"These symptoms are consistent with a chronic fatigue syndrome, damage to the central, peripheral and autonomic nervous systems, and damage to the immune system.  Other symptoms are typical of multiple chemical sensitivity"
134.	And, from Dr Julia Clark, the clinical neuropsychologist, who in her letter dated 7th July 2000 wrote:-
"On the balance of probabilities I am of the opinion that the profile of symptoms exhibited by Mr. Stoker was caused by exposure to OP’s"
135.	In her report (File 22 p.76) gave this opinion:-
"Opinion.
Mr Stoker was exposed to a variety of chemical sprays used in arable farming from childhood onwards.
His profile is suggestive of a depressive condition in that both short-term memory and psychomotor retardation are present.  In common with other depressed patients he shows a global lowering of ability of approximately one standard deviation.  It is however uncommon for depression to involve lateralised impairment.  In Mr Stoker’s case, he shows specifically language related difficulties of a variety of types.  Despite this there is maintenance of many frontal lobe functions at premorbid levels.  The lowering of the Verbal IQ from 127 to 103 since 1989 would indicate that this difficulty has its origin after this date either as a newly acquired injury or by exacerbation of an existing injury because of co-existence of a depressive condition.  I am not able to define the cause of the underlying language dysfunction."
136.	These opinions of Dr Myhill and Dr Clark do not attribute Stoker’s malaise specifically to exposure to organophosphates when he was employed by John Turner Ltd.
137.	Other more cogent evidence in my judgment shows that Stoker’s claim is ill-founded and has no realistic prospect of success.  I have struck it out.
138.	Dr Ferner, consultant physician, clinical pharmacologist, and senior lecturer in medicine at the University of Birmingham gave this opinion (File 22 p.119-121):-
"Mr Stoker has some exposure to agricultural chemicals as a teenager and after dipping sheep on his father’s farm; and at one time sprayed arable crops, though the nature of the sprays is unknown to him.
At no time did Mr Stoker experience symptoms consistent with acute poisoning with organophosphates.
The onset of “paralysis” in his lower limbs, described as being unable to move but still being able to stand, is inconsistent with loss of power in the legs, since those with no power in the legs are unable to stand.
Extensive investigations after the onset of Mr Stoker’s disability rendering him unable to walk, have failed to find any physical cause for that inability.
It is most unlikely that Mr Stoker has suffered harm from organophosphates chemicals because:
There is no history of sufficient exposure.
There is no evidence that he ever developed a characteristic syndrome of organophosphate poisoning, or indeed a poisoning by other organic agents; and his illness is not characteristic of any chemical poisoning."
139.	Dr Frew, head of University Medicine at Southampton, reached this conclusion (File 22 p.158-159:-
"Mr Stoker was exposed to diluted organophosphate insecticides between 1975 and 1985.  The bulk of this exposure will have taken place in the course of sheep dipping on his parents farm between 1975 and 1983. At no stage did he experience any episodes of acute OP poisoning.  He has developed a bizarre disability which does not appear to have any neurological basis and is now confined to a wheelchair.  A diagnosis of multiple chemical sensitivity has been suggested by an non-specialist but no supporting evidence has been provided and Mr Stoker himself did not put this forward as a description illness.  On the basis of the information provided to me and my meeting with Mr Stoker I do not think there is any organic illness present.  It seems unlikely that he was exposed to significant quantities of OP and there is no obvious connection between any of his current symptoms and the known effects of OP."
140.	Professor Swash, neurologist of St Bartholomew’s, concludes (File 22 p.250-251):-
"Conclusions.
1.	Mr Stoker presented with an acute illness, consisting of unsteadiness, for which no organic cause could be found, in the context of dental abscess in 1985.  No underlying personal or social conflicts have been recognised and the case notes are silent on any enquiries that may have been institute in relation to possible causative psychiatric factors.
2.	He subsequently developed weakness of the legs, at first occurring intermittently, and then as a permanent phenomenon.  Extensive investigation has failed to reveal any neurological cause for this feature.
3.	There is agreement that the paralysis in the legs is not due to neurological disease but is psychologically determined.  It has been felt due to hysteria, simulation, and malingering.  No underlying pschodynamic basis has been discerned.  One observer felt that Mr Stoker seemed to enjoy presenting the enigma of his weak legs to the medical profession.
4.	My clinical assessment revealed many features consistent with “functional weakness”, that is weakness not due to organic disease, including the absence of features of organic disease, preservation of the sphincter functions, preservation of sensation, a non-organic sensory level on the trunk, give-way weakness in the arms, depressed, but bland affect, fluctuation in the degree of deficit with inconsistency in the signs and the reported degree of weakness and observed strength of varying degree in the legs during tasks taken under direct observation, for example undressing in the wheelchair.
5.	There is no evidence of peripheral neuropathy, of autonomic disorder of dementia, of neuropsychiatric disturbance other than depression or of motor neuron disease.
6.	There have been no features consistent with acute OP poisoning.
7.	The development of the “Neurological disorder” has not occurred in a time course commensurate with OP exposure, or with the recognised delayed complications of OP poisoning."
141.	Mr Melville Williams Q.C. for Stoker recognised the problems in oral argument saying:-
"I think the highest I can put it is that it is a case in which there should be further investigation”"
142.	He suggests that for Stoker to receive justice a clinical toxicologist should be retained and a thorough psychiatric investigation carried out.
Taylor’s Claim.
143.	Taylor who is now aged 37 has spent a life time in farming.  He grew up and helped on his father’s small-holding.  He first actually dipped sheep in about 1985.  He became a self-employed sheep shearer and dipper.  In about 1988 he was registered with M.A.F.F. for treatment of sheep scab.  At its peak he was dipping on a contract basis about 20,000 sheep annually.
144.	Annexed to the Particulars of Claim are schedules (File 12 p.92-97) setting out the dates and places of dipping both his own sheep and the names of farmers whose sheep he dipped with the numbers of sheep dipped from August 1984 until December 1993.
145.	It should be noted from his statement (File 12 p.100-104) that, while he usually used Young’s dips when dipping, on others’ farms he might use whatever dip the farmer provided.  This raises the difficulty of establishing if organphosphate exposure is established of attributing an exposure to a product manufactured by a sued defendant.
146.	Taylor describes the onset of his symptoms:-
"Pretty soon after I started dipping found that I started to feel headachey(sic) and washed out.  It was a very hot, sweaty business and the first couple of times, having got hot and then cold, and being wet I thought I might have had a chill or picked up something such as a cold or flu.
As I continued to do the dipping, I found that I was becoming ill for longer periods of time.  In about April 1993, I recall that this was the first occasion that I felt really ill.  I had chests pains, very bad headache and my eyes were sore and bloodshot.  I thought it was a bad bout of flu or a virus but I did not know what it was."
147.	He was referred to Dr Davies who attributed his symptoms to organophosphates.
148.	Mr Matthews for the defendants in oral argument conceded that there was some evidence suggesting that the onset of some of Taylor’s symptoms followed dipping.
149.	Taylor relies on reports from Dr Jamal and Dr Julu who were substantially discredited in Hill .v. Tomkins Ltd.  However, in their reassessment of the Pilot Study on the 21st March 1998 (See File 12 p.120) they were unable to advance the claim of Taylor.
150.	Sarah Mackenzie Ross, the neuropsychologist, in a well-reasoned report based on an interview and formal psychometric assessment of Taylor on the 9th March 2000 (File 12 p.121-138) concluded:-
"Mr Taylor’s pattern of deficits is consistent with that seen in other individuals with a history of exposure to OP’s.  Therefore, it is my opinion that on balance of probabilities,  Mr Taylor’s cognitive deficits are more likely to be due to the cumulative effects of exposure to OP’s than mood disorder."
151.	Dr Stuart Turner, the psychiatrist, in his report dated the 17th May 2000, (File p.139-152) does not assist on the issue of causation.
"It is beyond my expertise to comment on the evidence for potential organic or neurotoxic causes, but based on the evidence available to me (including that of Dr Jamal and Dr Myhill) it seems likely that there are chronic fatigue symptoms which are associated with an underlying physical disorder (although I cannot confirm this directly on my assessment)."
152.	Professor Langton Hewer, the neurologist, in a typically careful and balanced report dated the 28th June 2000, is unable to come off the fence but as in other cases suggests the need for further investigation, effectively nearly 8 years after Taylor ceased dipping.  In his report (File 12 p.153-197 he said:-
"What diagnoses are considered and does he suffer with chronic OP poisoning?
i)	The major symptoms seem to be tiredness and lethargy.  This obviously raises the possibility that he may suffer with chronic fatigue syndrome.  It has been suggested that there may be an immunological disorder.  There are really no obvious clinical features of this but I note the reported abnormalities (eg. presence of antinuclear antibodies).  I think that it has to be concluded that he does not suffer with an autoimmune disorder
ii)	Doctor Myhill has suggested multiple chemical sensitivity.  This is not a diagnosis which is generally accepted in medicine and I am not aware that there is any evidence for such a disorder in this case.
iii)	? OP poisoning.
	a)	This is a case in which there is reasonably good evidence of exposure to OP’s.
	b)	The symptoms seem to have developed insidiously during the early 1990’s.  There appears to be a gap between the maximum exposure and the first development of significant symptoms.
	c)	It is possible that there may have been some episodes of flu like symptoms - “Dippers flu”
	d)	The clinical symptomatology is very much in keeping with many of the other Claimants.  The symptoms of lethargy, headache, and skeletal pains are non-specific but reasonably constant in this group  I am quite impressed with the frequency of smell hypersensitivity.
	e)	I was also impressed with Mr Taylor as a person.  He was not someone who appeared to me to embellish his problems and indeed was somewhat reluctant to talk about them.
	f)	I would place him in the uncertain category on the above basis.  This assessment might need to be reviewed if further neuro-psychological data and scanning becomes available."
153.	I consider that Taylor certainly has a arguable case viewed individually.
Tyrer’s Claim.
154.	Tyrer who is now aged 54 sues the Clwyd County Council who employed him as an Assistant Trading Standards Officer from about July 1983 until September 1992 when as part of his work he was in contact with livestock and exposed to organophosphates.  Outside this period he was never exposed to organophosphates.
155.	As Assistant Trading Standards Officer his duties included attending 5 livestock auctions weekly, visiting farms, agricultural shows and abattoirs, and supervising sheep dipping.
156.	He had to check the movements of animals.  Cattle had to have their ear tags checked and had to be checked for warble fly which was done by running the hands along the backs of cattle.  Warble fly was treated with organophosphate products.Thus physical contact could occur between Tyrer’s hands and organophosphate.
157.	Sheep dipping was of two kinds; a full witness dip and a part witness dip.  Full witness dip involved the dipping of a whole flock which Tyrer had to supervise.  Frequently he would be splashed with dip which contained organophosphates.
158.	Between 1983 and 1990 Ministry of Agriculture officials took fleece samples from sheep.  The sheep had been recently dipped.  Tyrer had to hold the sheep while the officials took the samples.  Thus again Tyrer was in physical contact with products containing organophosphates.
159.	Until 1987 Tyrer did not feel unwell but thereafter until his retirement due to ill health he was frequently unwell (See File 27 Tab 4 p.8-1-)
160.	Tyrer now suffers from a spectrum of symptoms which are set out in File 27 Tab 4 p.15-16.
161.	Tyrer’s claim faces overwhelming obstacles.
162.	On the 26th May 1989, highly able Junior Counsel settled Particulars of Claim in the Mold County Court, alleging that Tyrer had been negligently exposed by the Clwyd County Council to organophosphorus poisoning with consequent symptoms.  (See File 26) Supplemental Documents.  That claim was supported by a medical report from Dr Gatley, a consultant occupational physician, dated the 4th February 1989 who said:-
"Since I saw him in 1987 he has remained very well with no symptoms whatever.  His only medical problem during this period was an attack of sciatica in 1988 from which he made a full recovery in about 3 weeks.  He returned to work in the Autumn of 1987 but was not inspecting sheep dipping until 1988 when he did his normal duties.  Changes had been made when he returned to this type of work.  For the first time he was supplied with a comprehensive kit of protective clothing which included overalls, goggles and face mask (later changed to a full face visor) and substantial gauntlet type gloves.  Mr Tyrer brought me a set of photographs which illustrated these changes.  He was also provided with a stop watch so that he could time the dipping process without the need to lift his sleeve and risk contamination on looking at his watch.
Blood tests were carried out before starting the work and repeated once at two to three weeks into the first dipping period but not thereafter.  He believes that the results of these were normal.  During the second dipping period no blood tests were performed but a duplicate set of protective clothing was provided and the employing authority issued a new Code of Practice for the work.  I have not seen this but understand from Mr Tyrer that they reinforce the need to leave the job if any symptoms develop and to report to the doctor.
I have no doubt that when I saw Mr Tyrer in September 1987 he was suffering from mild organic phosphorus poisoning as a result of exposure to pesticides (sheep dips) in the course of his work.  The normal levels of cholinesterase which were recorded at that time do not alter my opinion as the symptoms complained of, and, in particular, the observations of his wife about the state of his pupils, were absolutely typical of the condition.  I believe that, had these tests been carried out earlier while he was still at work, his cholinesterase levels would have been shown to have fallen.  Neither his working conditions nor the medical surveillance provided at that time came up to the standards recommended by the Health and Safety Executive.
Since the episode the working conditions have been improved to the standard expected although he is still not having regular blood tests.  He has had no recurrence of the problem since the original attack in 1987 and has made a full recovery.
The attack was mild and there will be no permanent sequelae as a result of it."
163.	Dr Gatley saw Tyrer again on the 25th August 1994 when he reported:-
"It is difficult to relate this man’s condition to exposure to pesticides.  When I saw him the past he had undoubtedly had symptoms of organic phosphorus toxicity but it was very-mild.  I do not think that this would lead to long term central nervous system toxicity.  I wondered at first whether some of his symptoms were psychosomatic but he has definite abnormal objective signs.
I cannot make a definitive diagnosis and think that he requires a thorough neurological assessment.  His blood pressure also needs attention.  If, after this, the question of possible toxic effects of chemicals arises, I would be happy to try to help further."
164.	The Clwyd County Council paid into court without admission of liability the sum of £500 which was accepted by Tyrer.  Not surprisingly in these proceedings the Clwyd County Council plead an accord and satisfaction.
165.	In my judgment the effect of the accord and satisfaction is that Tyrer cannot now recover damages (if any) caused by pre-1989 exposure.  Any claim would be limited to any medical condition arising post - 1989 caused by post - 1989 exposure to organophosphate resulting from negligence or breach of duty on the part of the Clwyd County Council superimposed on Tyrer rendered more vulnerable by pre - 1989 exposure.  Tyrer’s claim on this basis is factually skeletal in the extreme and in my judgment has no realistic prospect of success.
166.	The factual weakness of Tyrer’s claim is exemplified by the report of Dr Julia Clark, the neuropsychologist, of the 13th September 1999.  This is the evidence upon which Tyrer principally relies.  Dr Clark says (File 27 Tab 2):-
"Despite the high level of symptomatology there was a divergence of clinical opinion.  On one hand neurophsyiological findings concluded that he had evidence of distal sensory motor axonal neuropathy.  An alternative view was that Mr Tyrer was a high complainer with poor tolerance of pain and a tendency to overuse of painkillers.
As Mr Tyrer suffered a head injury in 1974 with a blow to the left frontal area of the brain it is possible that he suffered a degree of damage at that time
Mr Tyrer’s cognitive difficulties are consistent with what is known about the effects of exposure to OP’s.  Although Mr Tyrer suffered a head injury in the past this is not thought to have produced this cluster of symptoms.  It is not however possible to rule out the possibility that this may have rendered the brain more vulnerable to the effect of toxic organophosphate compounds."
167.	It can be seen that Dr Clark does not deal with the problems of pre and post 1989 exposure.
168.	Tyrer also relies on reports of Dr Jamal, the neurophysiologist, who was discredited in Hill .v. William Tomkins Ltd (17th October 1987).  In her judgment Smith J. said (Transcript p.86):-
"I am driven to the conclusion that, for some reason, Dr Jamal reported test results which appeared to demonstrate phenomena and abnormalities which I am satisfied were not present.  This may have been due to some fault of technique.  It may have been due to over-enthusiasm and a willingness to find the result which would support the theory; in other words lack of objectivity.  I do not know the explanation.  Further I am satisfied that when the plaintiff complained of pins and needles and numbness in a glove and stocking distribution in December 1995 and September 1995, he was describing symptoms which did not exist."
169.	In his report dated the 17th October 1995 Dr Jamal concluded:-
"There is therefore a reasonable degree of clinical certainty in my opinion that the previous and current complaints of Mr Tyrer are due to his repeated exposure to organophosphate compounds contained in the sheep dip during the course of his occupation"
170.	Again Dr Jamal does not deal with the problem of pre and post 1989 exposure
171.	Tyrer makes wholly extravagant claim for damages of nearly £450,000 which ignores the fact that he became unemployable because of an unrelated back condition.  See the summary to the report of Mr David Carden, orthopaedic surgeon, dated the 12th October 2000.
"Mr Tyrer has been assessed and medical records reviewed.  It is confirmed that the reason for Mr Tyrer medical retirement in 1993 was back pain secondary to degenerative lumbar disease.  It is noted that this condition is separate and discreet from any effects which may or may not be present due to organophosphate poisoning.  It is accepted that Mr Tyrer’s back condition has improved since he has been able to restrict physical activities having retired from work.  It is considered that at this stage he is fit for light work and it is noted that such an assessment was made when Mr Tyrer retired from work, the reason for his retirement from work was that he was not fit for the position he was holding at that stage and there was no other suitable employment available.  It is also confirmed that there is not considered to be any association between degenerative back pain and the effects of organophosphate poisoning."
172.	The weakness of Tyrer’s claim is further exemplified in the reports of Dr Andrew Bowden of 5th September 1994, 22nd November 1994 and 27th February 1995 in File 28 Tab 1.  Who said:-
"I doubt that there is an organic neurological disorder here and I doubt that his present disability can be related to OP poisoning"
173.	Tyrer faced further difficulty on Limitation.  He issued his writ on the 15th October 1998.  Yet in December 1993 he made a claim to the D.S.S. for Industrial Injury Benefit based on the contention that he was suffering from an industrial disease because of organophosphate poisoning.  In May 1995 he was interviewed by the Liverpool Post claiming permanent injury as a result of organophosphate exposure.  A claim which he said was supported by his union.
174.	For all those reasons I struck out Tyrer’s claim as having no realistic prospect of success.
Wilkes’s Claim.
175.	Wilkes’ who is now aged 43, took over the management of the family farm when he was about 20 years old.  He kept sheep which entailed periodic dipping.  In about 1986 or thereabouts he began trading as a sheep scanner under the name of Wilscan Services.
176.	Sheep scanning involves ultra sound pregnancy diagnosis in sheep to determine the number of foetuses.  A probe is applied to the sheep’s belly.  Wilkes would sit on the ground with his face touching its flank.  Over the years Wilkes scanned very many thousands of sheep.
177.	Clearly he was exposed to organophosphates both during sheep dipping and through contact with fleeces containing the residues of organophosphate dips during scanning.  On one occasion he fell into a sheep dip tank although with no apparent ill-effects.
178.	Wilkes’s medical history is summarised in a letter from his G.P. Dr Winter, dated the 12 January 2000, (File 21 p.85-87).  From the 12th December 1997 there has been marked decline in Wilkes’s state of health.  Dr Winter concludes his letter by saying:-
"He has undergone a large number of normal investigations.  No other cause has been found for his symptoms of intermittent dysuria, and urinary frequency but they coincide with the occurrence of his other neurological symptoms.
I have no concrete proof that Mr Wilkes suffers from chronic low dose organophosphate poisoning but from my experience a clear historian such as Mr Wilkes is usually correct and should be listened to very carefully indeed."
179.	Wilkes’ main problem seems to have been urinary infection and frequency.  Neither the neurologist, Dr Nightingale, nor the urologist, Mr Beacock, specifically attribute Wilkes’s ill-health to organophosphate exposure (See File 21 p.77-83).  However Dr Nightingale does say:-
"It may well be that some people are particularly susceptible to the side effects of chronic low dose exposure to organophosphates.  He certainly feels that it is responsible for some of his symptoms.
I would not have thought that further investigation is likely to help.  In the absence of any overt neurological signs, nerve conduction studies would not show any evidence of chronic neuropathy; MRI scanning and lumbar puncture are normal in organophosphate intoxication. Nor, I am afraid, is there any specific treatment for low grade organophosphate intoxication.  If this is the problem, the symptoms are likely to gradually improve as time goes by"
180.	Dr Barrowclough, the neurologist, in his letter of the 4th February 2000, (File 21 p.75-76) does support Wilkes’s claim on causation saying:-
"On examination there was no focal neurological abnormality.
I feel that the initial development of symptoms in January 1998 including widespread muscle weakness, tremor and limb incoordination may well have been due to organophosphate exposure.  However, the recurrence of symptoms now on exposure to non organophosphate products particularly aftershave and perfume does not suggest on-going organophosphate poisoning"
181.	Further limited support for Wilkes’s claim is to be found in the report of Sarah Mackenzie Ross (File 21 p.41-61) who concludes:-
"It is my opinion, on the balance of probabilities, that Mr Wilkes’ cognitive deficits are more likely to relate to organophosphate poisoning, than mood disorder."
182.	I have considerable sympathy with Mr Wilkes.  He did not issue his claim form until the 12th January 2001 serving it on the 9th May 2001.  The Part 24 applications to dismiss the group action had already been served in August 2000.  However Wilkes joined the group action with its benefits and burdens.  The burdens include his individual liability for his share of the costs ab initio of the Group Action.  The benefits include the research and investigation into the adverse effects of prolonged but low level exposure to organophosphates including the results, mixed and minimal although they are for the claimants, of the Pilot Study costing upwards of £800,000.
183.	I do not consider that the overall evidence would justify striking out Wilkes claim on an individual basis.