England and Wales High Court (Queen's Bench Division) Decisions

"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."

"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"

"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"

"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"

"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."

"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."

"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?"

"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."

"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

"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"

"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."

"Mr Bruce’s clinical history and symptoms are typical of chronic OP poisoning. This needs substantiating with tests"

"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."

"The only positive finding was a positive coxsackie B IgM, this is consistent either with a recent entroviral infection or persistent entroviral infection"

"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"

"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."

"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"

"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."

"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."

"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"

"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."

"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 "

"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”

"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"

"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."

"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."

"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."

"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."

"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."

"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. "

"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."

"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."

"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."

"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."

"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."

"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"

"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."

"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."

"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)"

"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."

"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."

"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."

"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."

"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"

"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"

"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"

"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"

"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.”

"Mr Snell has symptoms of depression and chronic fatigue which could well be caused by chronic organophosphate exposure "

"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."

"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"

"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"

"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."

"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."

"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."

"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."

"I think the highest I can put it is that it is a case in which there should be further investigation”"

"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."

"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."

"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)."

"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."

"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."

"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."

"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."

"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."

"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"

"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."

"I doubt that there is an organic neurological disorder here and I doubt that his present disability can be related to OP poisoning"

"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."

"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"

"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"

"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."