Ministry of Defence v Wood

This is an appeal from the order of HH Judge Taylor sitting as a Deputy High Court Judge in Middlesbrough on 5 May 2010. The claimant, Shaun Wood claimed damages for a neurological condition akin to Parkinson’s disease which he alleged had been caused by his exposure to organic solvents during the course of his service in the RAF. During the hearing, which was limited to issues of liability and causation, the Ministry of Defence (MOD) made an admission of breach of duty but continued to dispute that its breach had caused the claimant any damage. Issues of limitation had been resolved in the claimant’s favour at an earlier hearing.

Mr Wood was born in 1958 and served in the RAF from 1975 until 1995. Immediately after his initial training, he became a painter and finisher and remained in that trade throughout his service. It was common ground that, in the course of his work of stripping, painting and finishing aircraft, he used a variety of organic solvents and was exposed to them both by inhalation of fumes and by skin contact which could result in absorption into the body. During his service, the claimant had been moved to various different RAF bases but the methods of work were not, in general, very different. However, the claimant alleged that, towards the end of his service at Bruggen in Germany, which ran from 1987 to 1991, his working conditions were particularly bad. They were also bad when he was moved to RAF Leeming in 1991. The claimant became unfit for work on account of his increasingly disabling symptoms and was discharged from the RAF in 1995.

The claim against the MOD was limited to exposure which had occurred after 1987 and the MOD’s admission of breach of duty was limited to that period. It was common ground that, whatever the working conditions, the MOD was entitled to rely on Crown immunity from suit before that date. Thus the breach of duty covered exposure during the period between 1987 and 1995.

It was common ground that the solvents used by the claimant - and in particular dicholoromethane and trichloroethylene which he used very regularly - are neurotoxic substances: that is that they are capable of causing damage to the nervous system. The claimant alleged that he had suffered permanent organic damage to his nervous system resulting in a condition akin to Parkinson’s disease. The MOD contended that, although solvents could cause temporary effects on the nervous system - and could even cause death if the dose were large enough - there was no satisfactory scientific evidence that they could cause permanent damage short of death. Moreover, the MOD contended that the claimant had not suffered any permanent neurological damage and that his symptoms were entirely or almost entirely due to psychological factors. The main questions for the judge were therefore (i) whether the claimant was suffering from an organic condition as opposed to symptoms due to psychological factors; (ii) if so, whether that condition had been caused or contributed to by negligent exposure to organic solvents at work. The second question necessarily involved consideration of whether the solvents the claimant had been exposed to were capable of causing permanent organic damage of the kind which the claimant contended he had suffered.

The judge answered both questions in the claimant’s favour. The MOD now appeals that decision with permission granted by Toulson LJ.

Before describing the history of the development of the claimant’s condition and the diagnostic problems which arose, it may be helpful if I describe the medical conditions under discussion.

Parkinson’s disease (PD) is a progressive neurological disease of insidious onset which usually develops in the second half of life. It is due to degenerative change in the ganglia at the base of the cerebrum, leading most commonly to a deficiency in a neurotransmitter called dopamine. The damage is often described as extra-pyramidal. The condition is usually described as idiopathic because the cause or causes of the degeneration are not known. However, genetic factors appear to play a large part. The condition manifests itself by increasing rigidity of the muscles. This can result in a tremor of the hand or hands, often exaggerated by excitement and ceasing during sleep. Often there is bradykinesia (slowness of movement). In the face, there can be loss of expression and the voice may be affected by the loss of play in the lips, tongue and larynx. Later the limbs become rigid and the patient can develop a tottering or shuffling gait. There is no cure but drugs such as levodopa can reduce symptoms.

Multi-system atrophy (MSA) is also a neurological degenerative disease of unknown aetiology. It is very rare, much more so than PD. The early features are usually of parkinsonian type (eg tremor and rigidity) and the condition is often mistakenly diagnosed as PD in the early stages. However, as time goes by, autonomic features appear, such as bowel and bladder dysfunction allowing the diagnosis of MSA to be made. A full house of signs and symptoms usually takes many years to develop. An abnormal anal sphincter EMG is said to be diagnostic in most if not all cases but a positive diagnosis which can differentiate the condition from PD can only be confirmed at autopsy. Treatment is usually the same as for PD, namely levodopa-containing agents. These often give a good result in the early stages but the duration and quality of benefit are often disappointing. Sufferers usually have a quite short expectation of life, on average 8.6 years from diagnosis.

Much of the discussion between the medical experts turned upon whether the claimant had PD or MSA or whether he had a non-specific degenerative neurological condition which did not fit the diagnostic criteria of either PD or MSA. In the end, that was his contention, although at the outset he had pleaded that his condition was MSA and PD. The defendant contended that his condition was almost entirely non-organic – in other words it was due to psychological factors.

In addition to disputing that the claimant’s condition was organic, the MOD was anxious, for reasons which will appear later, to establish that the first manifestation of the claimant’s neurological disturbance (tremor) had begun during the late 1980s. The claimant’s case was that it had not developed until about the end of 1992 or early 1993. I will deal with this issue now.

The claimant first consulted his squadron medical officer on account of his tremor in April 1993. The contemporaneous record of that consultation suggests that it had first been noticed about 4 months earlier. The judge noted that in previous years, the claimant had consulted the RAF doctors on a number of occasions about a variety of matters and there had been no reference to a tremor. True it was that, in later records, beginning in 1995, there were references to the onset of a tremor at earlier dates, sometimes 1987 and sometimes 1989. However, the judge found that the tremor had not manifested itself until about December 1992. In view of the contemporaneous records of 1993 and the claimant’s evidence (accepted by the judge) that in 1992 he had run a marathon in just over 3.25 hours but in the following year he had found his running ability impaired, in my judgment the judge’s finding as to the onset of symptoms cannot be challenged.

At an early stage of his judgment, the judge considered the claimant’s medical records in some detail. The purpose of this was to set the scene for the rival contentions of the medical experts called at the trial.

Early assessment of the claimant by RAF medical staff in April 1993, when a tremor was observed, resulted in a tentative diagnosis of PD. In August 1993, Group Captain Merry, consultant adviser in neurology, recorded an involuntary rhythmic resting tremor of the right arm, with minimal bradykinesia and rigidity of the limb. There were no other signs of cerebella ataxia. Gait was normal with a normal swing of the right arm. Facial expression was normal. Again the tentative diagnosis was PD. Medication was commenced but apparently not levodopa. On review in September 1993, it was recorded that the previously reported symptoms of tiredness and aching had improved since medication had begun but otherwise the picture was much the same. In November 1993, when reviewed by Squadron Leader Gregory, who was later to become a professor of neurology, the note reveals the presence of further neurological signs, including paucity of facial movement, some axial limb rigidity and abnormality of the right arm swing. There was tremor and bradykinesia in the hand. The claimant reported urinary frequency which was the first autonomic sign mentioned. He was referred to the National Hospital for Neurology at Queen Square, London for further investigation of this problem. Presumably because MSA was suspected, one of the tests carried out there (in 1995) was an anal sphincter EMG. The result was normal, suggesting that the claimant did not have MSA.

Squadron Leader Gregory saw the claimant on several further occasions before he was discharged from the RAF in 1995. At some stage, the claimant began treatment with levodopa and initially obtained a good response to it. At the time of the claimant’s discharge from the RAF, Squadron Leader Gregory wrote to the claimant’s GP indicating that the diagnosis was of a condition of a Parkinsonian type with some atypical features.

Following discharge from the RAF, the claimant was living in Northallerton and his care was taken over by consultant neurologists in the Teesside area. By October 1996, his treating consultant recorded that there had been no significant deterioration in the ‘Parkinson’s condition’. In the ensuing years there were referrals to various other consultants for advice and treatment of particular symptoms but no change to the overall diagnosis and no suggestion that the claimant’s condition was anything other than organic.

In 1999, the claimant came under care of Dr Peter Heald, consultant neurologist, who noted that the symptoms were not completely typical of idiopathic PD. He noted instability of blood pressure and various other symptoms and signs which included tremor, stiff legs, tiredness, poor energy levels, depression and swallowing difficulties. There were also complaints of bladder instability and dryness of the mouth associated with lack of sweating. These latter symptoms were indicative of disturbance of the autonomic nervous system and were suggestive of MSA. A diagnosis of MSA was eventually made in 2001. The condition was described as MSA with prominent Parkinsonian features for which the accepted shorthand is MSA-P.

In the early 2000s, the claimant took part in a study at the Freeman Hospital, Newcastle upon Tyne and was examined and reviewed by many doctors. He also continued under review in Teesside where there was a change of consultant in 2006. Throughout this time the diagnosis was still MSA or MSA-P. The notes record the development of further autonomic features, including dizziness and blackouts. The claimant’s bladder dysfunction became so severe that he had to self-catheterise.

It is to be observed that not once during all this time was there any suggestion that the claimant’s condition was not organic. It was not suggested that the symptoms of which he complained were inconsistent with objective neurological signs detected on examination. The only suggestion that psychological factors might be playing any part came in a report from a psychologist who saw him in 1999 and who suggested that anxiety might account for the variability in the assessments of his cognitive function.

The claim for damages was issued in May 2007. The particulars of claim dated 1 December 2007 alleged exposure to solvents in the period 1987 to 1995 which had caused the claimant to suffer from MSA and PD. A medical report of Professor Anthony Seaton, Professor of Environmental and Occupational Medicine at the University of Aberdeen, dated 21 November 2007 was served with the pleading. Professor Seaton is not a neurologist. His medical specialty was in the field of lung disease but he has developed an interest in many occupational conditions and has published several studies relating to the effect of organic solvents on the nervous system. Thus, his primary function in this litigation was to give an opinion on causation rather than diagnosis. He took a history of the claimant’s employment and the development of his condition. He carried out a clinical examination. He considered the general practitioner records from 1995 onwards and saw some personnel records disclosed by the RAF. He noted the diagnosis of MSA. He then discussed issues of causation to which I will return in due course and concluded with his opinion that the claimant had “developed multiple system atrophy, a type of parkinsonian syndrome with additional neurological features, as a direct response to chronic intoxication by organic solvents”. The professor also stated that, in his experience of other cases of solvent-induced brain damage, “the neurological pattern is not a classical one of any well-recognised disease but rather shows evidence of several different parts of the nervous system being damaged”. Shortly afterwards, in January 2008, Professor Seaton examined the RAF medical records which were by then available but these did not cause him to change his views.

The defence, dated 29 January 2008, said to have been served without the benefit of a medical report, made a general admission that the claimant had ‘sustained’ MSA and PD but nothing further. In fact the MOD had obtained a medical report dated 27 January 2008 from Dr Colin Mumford, Consultant Neurologist at the Western General Hospital in Edinburgh. He gave an opinion based on examination of the medical records (RAF, GP and hospital) and perusal of Professor Seaton’s report. He had not at that stage examined the claimant. After reviewing the records, he declared that he was in no doubt that the diagnosis of MSA was the correct one. The claimant had been appropriately investigated. Dr Mumford considered that the diagnosis was secure regardless of the fact that he could not find the results of a sphincter EMG test which he believed, (mistakenly as it turned out) had been carried out in 2007. Dr Mumford then said that the condition was not related to solvent exposure but was idiopathic. Thus he disagreed with Professor Seaton on causation, a topic to which I will return.

In April 2008, the claimant obtained a medical report from Dr Peter K. Newman, Consultant Neurologist at the South Tees NHS Trust. Dr Newman examined the claimant and considered the available medical records. He concluded that the diagnosis of MSA was correct. He pointed out that the differential diagnosis with PD was difficult and could not be ascertained with certainty until autopsy. He also noted that the claimant’s case was unusual in that he had not deteriorated as quickly as was usual in cases of MSA; he was still independent and had no life threatening complications.

Also in April 2008, the MOD obtained a report from a second medical expert, Professor Nicholas Wood, Professor of Clinical Neurology at the Institute of Neurology, Queen Square, London. He received all the medical records and copies of Professor Seaton’s report and Dr Mumford’s report of January 2008. His conclusion was that clinically it appeared that the claimant had MSA-P but this could not be confirmed until autopsy. On the available information he thought that the diagnosis was probably correct. He expressed one caveat; the claimant was very young to have developed MSA. He turned to discuss causation and opined that it was possible that solvent exposure could have contributed to the neurodegenerative disease, but there was no proof. He gave an opinion on prognosis and fitness for light work.

In July 2008, the MOD arranged for both their medical experts to examine the claimant clinically. Dr Mumford examined the claimant in mid-July and provided a second report dated 26 July in which he confirmed his opinion that the diagnosis of MSA with predominant Parkinsonian features was correct. He reported the presence of various neurological signs which were consistent with that diagnosis. He gave an opinion on prognosis; the gradual deterioration would continue. He repeated his opinion that the condition was idiopathic and unrelated to exposure to solvents.

Professor Wood saw the claimant on 30 July 2008 and reported on 1 August. The clinical examination took place about an hour after the claimant had taken his medication. The possible significance of that is that the medication would be providing maximum effect at that time. Professor Wood was surprised at how well the claimant was, given his long medical history since 1993. His gait was narrow-based but not shuffling. His facial expression was more mobile than in many patients with PD. The tremor was mild when he was being distracted in conversation but increased during physical examination. It never completely disappeared. Eye movements were normal. There was some facial asymmetry but no definite weakness. There was no change in tone in any limb. Power was preserved ‘with encouragement’, although there might have been some weakness in the right foot on dorsiflexion. Reflexes were normal. Sensory examination was abnormal but the professor thought that the claimant’s responses to these tests were indicative of a non-organic sensory disturbance. He found no evidence of postural hypotension. On the basis of these findings, the professor expressed his doubt about the correctness of the diagnosis of MSA-P. He accepted that there were mild features of Parkinsonism. His concern about the diagnosis was fortified by his earlier observation that the claimant was very young to have developed MSA. Also, the slow rate of progression was most unusual. He asked to see the results of the sphincter test which had taken place in 1995 and of various MRI scans. He also recommended that there should be a Dopamine Transfer (DAT) scan.

In September 2008, Professor Wood wrote to the MOD’s solicitors to discuss his state of puzzlement about the claimant’s case. He called for further investigations. By November 2008, there had been a further sphincter EMG which was found to be normal, as had the previous test in 1995. Professor Wood opined that that meant that there was no denervation of the sphincter. The claimant had also had autonomic function tests, the results of which, although not entirely normal, were not, in Professor Wood’s view, compatible with a diagnosis of MSA. The professor had also seen some neuro-imaging and an MRI scan from January 2008. These showed no evidence of atrophy of or damage to the basal ganglia. The professor’s conclusion was that he could not say what the claimant’s condition was. If he did have neurological dysfunction, (which had not been absolutely confirmed) the question remained as to whether exposure to solvents had played a role. The professor thought there was no evidence of such an association.

On 1 April 2009, Professor Wood and Dr Mumford met to discuss the case. In a joint report (which is dated 19 May but which, for reasons which will shortly be obvious, must have been prepared before then) they expressed their agreement that there was considerable doubt about the diagnosis. Dr Mumford’s first diagnostic opinion (MSA-P) was acknowledged but, since that time, further information had become available. A recent cranial MRI scan was normal, as was the sphincter EMG. The autonomic function tests were only mildly abnormal. These results undermined the diagnosis of MSA. The doctors acknowledged that the diagnosis of MSA had been made or approved by a number of respected neurologists. They noted particularly the claimant’s participation in the Freeman Hospital study; the consultant in charge of that was of particular eminence. They wondered whether the claimant might have been seen only by more junior doctors. They recommended a DAT scan. This would not distinguish between MSA and PD but would be useful because, if it were completely normal, it would make it ‘relatively unlikely’ that there was any significant extra-pyramidal or neurodegenerative disease present. They would then recommend a neuropsychiatric assessment. If the DAT scan were abnormal, the conclusion would be that the claimant had an unusual Parkinsonian syndrome. As to causation, the two neurologists expressed their joint view that the claimant’s clinical syndrome was causally unrelated to solvent exposure.

The DAT scan, performed a short time later, was normal. Professor Wood and Dr Mumford considered it together in a joint report dated 16 April 2009. (That is why I say that the joint report dated 19 May must have been written earlier). They both concluded that the claimant did not have either PD or MSA. There was, they said, no evidence of a degenerative parkinsonian syndrome.

In May 2009, Professor Seaton and Dr Mumford produced a joint report outlining their areas of agreement and disagreement. This is a puzzling document as it was signed by Dr Mumford on 8 May 2009, about three weeks after he had apparently agreed the content of his joint report with Professor Wood on 16 April in which he had concluded, in the light of the DAT scan, that the claimant had neither PD, MSA nor any Parkinsonian syndrome. In his joint report with Professor Seaton, he agreed that the claimant had a neurological condition but, in the light of recent investigations, he had ‘reservations’ about the diagnosis of MSA. He said that the claimant’s neurological condition was “possibly neurodegenerative, but possibly also with some components that take origin on a psychological basis”. Professor Seaton remained of the view that the claimant had an unusual neurological syndrome caused by heavy solvent exposure.

In June 2009, there was a discussion between Professor Wood and Dr Newman. The report of this is another puzzling document because Professor Wood does not express the firm conclusion that he had earlier expressed in the light of the further investigations and DAT scan. Indeed, there is no reference to that test. Professor Wood said that, following his earlier examination, he had suggested that the case for the claimant suffering from either MSA or PD was ‘unproven’ and had recommended DAT scanning. Dr Newman acknowledged that there were features of the claimant’s condition that were not typical of MSA; in particular, its progress had been very slow. However, Dr Newman was satisfied that definite clinical signs had been detected by many neurologists over the years, including himself and Dr Mumford, and his conclusion remained that the claimant had an unusual Parkinsonian condition.

Dr Newman commented on the DAT scan in a letter dated 9 April 2010. He said that this did not exclude organic disease of the extra-pyramidal system. There were some patients (he suggested about 10%) with PD who had a normal DAT scan. By the time he came to give evidence, he had located a research paper which suggested that about 17% of MSA sufferers had normal DAT scans.

On 8 April 2010, the MOD served a further pleading denying that the claimant had MSA or PD or any other Parkinsonian syndrome. It was contended that these conditions had been excluded by various investigations, in particular the recent DAT scan which was normal. There was no evidence of any neurological abnormality. In the alternative, causation was denied.

No other medical evidence was obtained by either side or, if it was, it was not disclosed. In particular, the MOD did not obtain or disclose any neuropsychiatric report such as had been suggested would be helpful in the event that the DAT scan was normal.

For the sake of completeness at this stage, I mention that the claimant had, in January 2010, obtained a scientific report from Dr John Cherrie PhD, BSc, FFOH of the Institute of Occupational Medicine, Edinburgh. This assessed the solvent exposure to which the claimant had been exposed and concluded that it had often been many times greater than the permitted exposure levels. This report was plainly relevant to the issues of breach of duty but was also potentially important in relation to causation. The MOD did not obtain a report to challenge Dr Cherrie’s opinion. Nor did it obtain any further medical report specifically dealing with causation. It appears that shortly before trial the MOD sought permission to do so but this was refused and the refusal was not appealed.

Dr Newman went first. He accepted that the claimant was not a typical case of MSA and the presentation was most unusual. He conceded that some of the features exhibited by the claimant were psychogenic or partly so. The tremor was exacerbated by anxiety or pressure and the claims of sensory abnormality were non-organic. Otherwise, the signs which had been detected by several neurologists over the years were indicative of an organic condition. He explained that the reason that the tests of autonomic function performed in 2008 showed so little abnormality was that the claimant had been taking a drug designed to stabilise his blood pressure and, although he had been taken off the drug for three days immediately prior to the test, the drug would still have been exerting an influence. He also considered that the reason why the claimant’s clinical signs were less marked when he saw Professor Wood than when he had seen the other doctors was because he had taken his levadopa medication only an hour earlier and it would have been providing the greatest benefit at that time. He referred to the study which showed that 17% of all MSA sufferers had normal DAT results. The judge regarded him as an impressive witness, careful, measured and well-balanced in his opinions.

Professor Wood went next. He explained his reasons for saying that this was not a case of MSA. The age of onset was too young and the rate of deterioration had been too slow. He explained why he thought that the condition was largely psychogenic. The signs he had observed were very slight and the claimant’s reactions to sensory testing were not organically feasible; that suggested that psychogenic factors were in play. The bladder dysfunction could be neurological but could also be psychogenic. The tremor was variable and not entirely Parkinsonian. The autonomic function test results were not typical of MSA. Taking into account the MRI scans, the negative sphincter EMGs and the normal DAT scan, Professor Wood concluded that the condition was mainly psychogenic in origin. He did not suggest that the claimant was malingering or consciously exaggerating his difficulties, but he thought that they were psychogenically driven. In cross-examination, he accepted that other neurologists, who were skilled clinicians, had found far more convincing clinical signs than he had found. He did not accept that the signs he observed were reduced because the claimant had recently taken his medication. Even though the others had found convincing clinical signs he maintained his position that this was mainly a functional condition although he accepted that it had probably started as an organic one. In re-examination he clarified that he did not think that the original organic component was MSA. The judge asked a number of questions about the claimant’s favourable response to levadopa, which might be thought to indicate that the drugs were having an effect on an organic condition but Professor Wood responded with the view that the drug might be having a placebo effect.

Dr Mumford was the last of the three medical experts to deal with the issue of diagnosis. It will be recalled that Dr Mumford had performed a volte face on this issue, after his discussion with Professor Wood and the availability of a second sphincter EMG, the autonomic function tests and the DAT scan. He had changed his view from being “quite satisfied” that this was a case of MSA to being convinced that overwhelming majority of the claimant’s problems had a deep-seated psychological basis. He too excluded fabrication or conscious exaggeration. His explanation for the tremor observed by all the clinicians was that it was a benign essential tremor, in other words a natural phenomenon. He did not accept Professor Seaton’s view that the claimant had an atypical Parkinsonian type of condition. He repeated his views about causation.

In cross-examination, he acknowledged that he had been satisfied with the diagnosis of MSA simply after perusing the medical records and before he carried out his own clinical examination. He then said that his first doubts arose at the time of that examination and that he regretted that he had ‘down played’ these in his second report. He had to agree that the second report contained no reference to any doubts at all; on the contrary, he had repeated his confidence in diagnosis. In evidence, he asserted that he had changed his mind only because of the gradually increasing availability of the results of objective tests.

On the issue of causation, Dr Mumford said that he could not remember why he had expressed a view when he had not been asked to do so but could see no reason why he should not; it was an issue in the case about which he knew something although he was not a toxicologist or an occupational health physician. He was then asked about another case in which he had reported, that of a man named Clarke who had also been exposed to solvents while working as a painter in the RAF and who had developed Parkinson’s disease. In a medical legal report for that case, Dr Mumford had said that certain neurological syndromes were recognised to be the result of exposure to chemicals and it was his understanding that chemicals of this nature (viz the kind of solvents used by Mr Clarke) could from time to time give rise to a clinical syndrome which was clinically indistinguishable from PD. That statement was starkly different from the view he was expressing in the present case. When that was pointed out, his response was to say that the Clarke report had been written a long time ago. A little later in the same report, he had said that he felt unable to express an opinion as to whether Mr Clarke’s condition had in fact been caused by exposure to chemicals at work because such an opinion would be outside the area of his expertise. In a later report in the same case, he had declined to comment on the opinion of Professor Seaton (to the effect that Mr Clarke’s condition was to be attributed to solvent exposure) on the ground that he was not qualified to do so.

In his judgment, the judge set out the history of the development of the claimant’s condition and the various examinations he had undergone in rather more detail than I have provided. He described the expert medical reports and evidence. He was of the view that Dr Newman was an impressive expert witness, careful and well-balanced. His view of Dr Mumford however, was most unfavourable. He said in terms that the witness’s approach was disingenuous, his credibility worthless and that he gave “no credence to his evidence whatsoever”. The judge’s reasons for taking this extreme view were, first, the way in which Dr Mumford had performed a volte face on the issue of diagnosis (the circumstances of which I have described above) and second his approach to causation. In particular, the judge was incensed that, in the case of Clarke, Dr Mumford should have said that there was some evidence of a connection between chemical exposure (in fact to the same solvents as the claimant used) and a neurological syndrome akin to Parkinson’s disease and yet had denied any such connection in the present case. Also, in the Clarke case Dr Mumford had said that it was beyond his expertise to give an opinion on causation in the individual case whereas in the present case he had done so without even being asked to. The judge also added that he had found Dr Mumford to be arrogant. He described him as the worst professional witness he had come across in many years.

It was submitted before this court that the judge’s adverse reaction to Dr Mumford was intemperate and quite out of proportion. The extremity of his language demonstrated that his attitude to the witness was irrational. Dr Mumford had changed his mind on diagnosis only because of the new evidence. That was a perfectly rational thing for him to do. The judge should have accepted that. Instead, the judge went ‘over the top’ about Dr Mumford and he allowed this to affect his view of the MOD’s case on diagnosis.

Because of this criticism I have read the whole transcript of Dr Mumford’s evidence. As a result, I have come to the conclusion that the judge was entitled to form this strongly adverse view of the witness. The written word does not always reveal a witness’s attitude but in this case the transcript does reveal that Dr Mumford was disingenuous. It is not impressive that Dr Mumford should claim that he had had reservations about his original diagnosis and regretted that he had ‘down played’ them when in fact he had made no mention of them at all. The judge was in my view entitled to be sceptical of the value of the changed opinion given the full circumstances in which it came about. He was also, in my view, entitled to regard Dr Mumford’s general credibility as gravely damaged as the result of the exchange about causation. The assessment of a witness’s approach and demeanour is peculiarly a matter for the trial judge; nothing in the transcript undermines the judge’s view that Dr Mumford was arrogant. In short, I think the judge was entitled to reject Dr Mumford’s evidence and to disregard it. As I shall shortly demonstrate, the judge did not reject the whole of the MOD’s case on diagnosis simply because he rejected Dr Mumford; he gave careful consideration to the evidence of Professor Wood. So it cannot be said that the judge’s strong disapproval of Dr Mumford governed his approach to the whole issue.

The judge then turned to Professor Wood and said immediately that he was ‘very experienced, highly qualified and highly articulate’. He had recognised from the start the problems associated with the diagnosis of MSA which had been given and accepted by the treating clinicians. The judge accepted Professor Wood’s opinion that this could not be said to be a case of MSA. However, as the judge was anxious to point out, the real question for him was not whether the claimant had MSA but whether he had a predominantly organic condition or a predominantly psychogenic one. Even Professor Wood, who had found only modest neurological signs, conceded that there was some organic basis to the condition. The modest nature of the neurological signs found by Professor Wood was an important factor in his opinion that the condition was largely psychogenic. The judge accepted Dr Newman’s opinion that the reason why Professor Wood had found such modest signs on his clinical examination was the effect of the levodopa medication which the claimant had taken shortly before the examination. He was satisfied that the neurological signs were usually quite well defined, as observed by many other clinicians, including Dr Newman and even Dr Mumford.

In the end, the judge was satisfied that the condition was organic, possibly with some psychogenic factors. He was not prepared to categorise the condition as PD or MSA or MSA-P. He so concluded first because of the long and gradually developing picture which had been observed over the years by many well-respected treating neurologists, none of whom had thought that the condition was anything other than organic. All those neurologists had found clinical neurological signs. All or most of them had also found some signs of autonomic dysfunction. He thought that they could not all be wrong. Also, he accepted the evidence of Dr Newman.

On this appeal it is said that the judge was not entitled to reach that conclusion, either because such a conclusion was irrational or because he had not given sufficiently cogent reasons for rejecting the opinion of Professor Wood.

I would reject that submission. First, possibly save in respect of one small matter, I do not accept that the judge’s conclusion was irrational. It was soundly based in the medical history and the expert opinion of a witness, Dr Newman, whom he was entitled to accept. The small issue over which I think his holdings might be open to criticism is his conclusion that there is only a possibility of some functional overlay. I think that the evidence pointed fairly clearly to the presence of some functional factors, in particular in relation to the abnormality of sensory perception. That was accepted by Dr Newman and I can see no basis for rejecting Dr Newman on that point. If this point had been raised in the appeal I would have held that the judge’s conclusion should be modified so as to replace the word ‘possibly’ with ‘probably’, in connection with the presence of some psychogenic factors. However, this point was not taken; probably it was thought to be too small to matter.

As to the alleged inadequacy of the reasoning, I would accept that the analysis ought perhaps to have been more detailed, and in particular might well have dealt more explicitly with the judge’s reasons for rejecting the view of Professor Wood. However, I do not think it can be said that the reasoning was such as to leave the parties in doubt as to why the judge had held as he did. The judge had already outlined the differences of view between Dr Newman and Professor Wood. Dr Newman did not regard the normality of the sphincter EMG and DAT scans as being as important as did Professor Wood. He produced a research paper to demonstrate his point that these tests were not conclusive. Also, Dr Newman thought that there was an explanation for the paucity of autonomic signs found in 2008 which Professor Wood regarded as a telling feature. But Dr Newman had given reasons for his view and in my judgment not only was the judge entitled to accept that view but no one could have been left in any real doubt as to his reasoning. I would dismiss the appeal on this issue.

Before coming to the expert and scientific evidence on which this issue depends, it is necessary to refer to the evidence of exposure put before the judge. Apart from the claimant’s evidence, the judge received statements from other RAF painters, (including Messrs Clarke and Baker who had also developed PD or Parkinsonian conditions) and who had worked in similar conditions to the claimant. None of this was challenged. It was the basis on which Dr Cherrie had reported. Dr Cherrie also gave oral evidence. The MOD did not call any evidence in opposition and the judge accepted Dr Cherrie as a wholly reliable expert witness. It is not suggested that he was wrong to do so.

The thrust of Dr Cherrie’s evidence was that the claimant’s exposure to trichlorethylene and dichloromethane (used for long periods during stripping operations) was often at a concentration many times the Occupational Exposure Limit (OEL). During one operation at Bruggen, the exposure was estimated to be at or about the level which gave rise to immediate danger to life or health. Exposure during the run up to the Gulf War was very high when the claimant was working on the preparation of Tornados. He was working long hours and was using adhesives to apply anti-missile patches. Also the mixture of chemicals used in paint spraying gave rise to exposure well above the recommended level. The protective measures taken by the RAF were quite inadequate.

The significance of these results will become apparent when I come to consider such scientific studies as have been conducted into the health effects of solvents.

As the judge observed, the only evidence of substance on this causation issue came from Professor Seaton. The MOD had not instructed either Dr Mumford or Professor Wood to give an opinion on causation although they had both volunteered their views that there was no scientific evidence to support a link. As for Dr Mumford, I have already referred to the judge’s reaction on learning that, in a report for the case of Clarke given some years earlier, the doctor had said that there was some evidence of a link. The judge regarded his evidence in the present case as valueless. As for Professor Wood, I have already noted that he had conceded that a causal link was possible; but it was unproven. Also the judge had earlier noted a contribution to the Oxford text of Neurology where he had stated that:

“A number of toxic agents can produce progressive cerebellar dysfunction, including pharmaceutical products, solvents and heavy metals.”

Later in that article, Professor Wood had said:

“recreational or accidental exposure to a number of solvents, including carbon tetrachloride and toluene causes cerebellar ataxia along with other neurological problems, including psychosis, cognitive impairment and pyramidal signs in the case of toluene. The neurological deficit is potentially reversible, but may persist after prolonged exposure in solvent abusers.”

The judge observed that Professor Wood was conceding that solvents do have a known toxic effect and also remarked that he did not think that the Professor would ever have come across a case where there had been such a concentration of solvent exposure as there had been in this case.

The judge turned to consider Professor Seaton’s evidence. As I have said, the judge accepted Professor Seaton’s opinion that solvent exposure was capable of causing permanent neurological damage and had in fact done so in this case. The MOD challenges the judge’s entitlement to accept Professor Seaton’s opinion; it contends that this opinion is not soundly based in scientific work and that Professor Seaton is an evangelist in the cause of establishing a causal link between solvent exposure and neurological harm. As an evangelist, he has lost his objectivity and sees a connection where none can logically be found. Because of these contentions, it is necessary for me to quote the relevant passages from the professor’s reports and evidence and to examine the authority lying behind his views.

On page 11 of his first report (dated 21 November 2007) Professor Seaton stated his general proposition as follows:

“Organic solvents are known neurotoxic agents with both acute effects in terms of causing drunkenness, nausea and unconsciousness and chronic effects associated with neuropsychological impairment. In the Nordic countries, this syndrome is known as Painters’ Disease or Chronic Solvent Neurotoxicity.”

I note that Professor Seaton did not quote any authority for this general proposition. However, only one aspect of the proposition is controversial, namely whether there can be chronic effects as well as temporary ones.

The professor then described his own clinical experience of patients who had been exposed to high concentrations of organic solvents (three while working in a naval dockyard) and had developed serious chronic neurological conditions with a variety of symptoms which did not fit the usual pattern of any recognised neurological disease. The spectrum of disease observed resembled that described in solvent abusers. In September 1992, he and others published a report of five such cases in the Quarterly Journal of Medicine New Series, 84 case reports no 305 at page 707. This paper was intended to draw attention to the possibility of a connection between solvent exposure and multi-focal damage to the central nervous system. The authors specifically recognised that their reports were anecdotal but drew attention to other papers which had in the past reported neurological abnormalities in painters and workers exposed to solvents and aviation fuel. The authors suggested that the incidence of three cases out of a workforce of 200 in the same naval dockyard seemed likely to be more than coincidence but it is now accepted that the workforce figure was inaccurate and the suggestion therefore not acceptable.

Because his interest was sparked by his knowledge of the above cases, Professor Seaton had obtained funding for research into the workforce of the naval dockyard and the possible connection between solvent exposure and neurological damage. As a result, he and others published a series of papers. In the first, “Health effects of solvent exposure among dockyard painters: mortality and neuropsychological symptoms” (Occup Environ Med1 1999; 56:383) the neuropsychological symptoms suffered by 260 painters exposed to solvents were compared with those suffered by 539 non-exposed controls. It was found that there was a significant excess of symptoms among the painters. Moreover, there was an association between symptoms and years of exposure. The discussion at the end of the paper accepted that the methodology was not perfect; for example, solvent exposure was assessed simply by reference to years of work. Also, selection methods may have introduced bias in an unknown direction. However, the results had been replicated in a similar study in China (Occup Environ Med 1999; 56 388).

In 2000, Professor Seaton and others published the results of further work on a cohort of 78 painters who had worked in the naval dockyard and 42 community controls. The painter subjects were selected because of their responses to the symptom questionnaire used in the earlier study. All participants were subjected to detailed psychometric testing and neurological examination. The solvent exposure of all was carefully assessed. A paper giving some preliminary findings was published in QJ Med 2000: 93, 655. This described five case studies of painters with high solvent exposure; examination had shown neurological disease with particularly striking features in the form of colour vision deficit, coarse tremor, impaired vibration sensation in the legs and cognitive impairment. The authors suggested that there was a strong suspicion that work as a painter was in part responsible for these abnormalities.

Professor Seaton also referred to two further papers which, as I understand it, related to further results of this programme of research. He stated in his report that, as the result of this research, he had become convinced there was “a link between chronic exposure, usually at very high concentrations, to organic solvents and a range of neuropsychological impairments of a chronic nature, some severe but resulting from damage to multiple different parts of the nervous system”.

The professor then described further research in which he had been involved, in particular a multi-centre case control study of patients with Parkinson’s disease, known as the Geoparkinson study. This had examined nearly 2000 individuals with Parkinson’s disease and a similar number without that condition and had examined their exposure to a range of chemicals and the presence of various genetic factors. The results, published at Occup Environ Med 2007; 64: 666 showed an association between Parkinson’s disease and exposure to pesticides. However it did not show any association between the disease and solvent exposure save in the additional presence of certain genetic factors. Professor Seaton pointed out that this was a community-based study and did not include any individuals with the high exposures found in the naval dockyard studies. Examination of table 2 of that study confirms that that was so. Accordingly Professor Seaton expressed the view that this study did not undermine his view that prolonged exposure to high concentrations of organic solvents can cause Parkinson’s disease and similar syndromes.

The professor then acknowledged that the medical literature does not prove an association between organic solvent exposure and Parkinson’s disease. However, he said that doctors did not always require scientific proof before they could come to a conclusion on the causation of a disease. Often an initial suspicion of an association arose because of the existence of a small group or cluster of patients with the same condition who had been exposed to the same environmental factor. Such evidence might be more convincing if the condition occurred at a younger age than was usual. He gave two examples of such ‘clusters’. One was the naval dockyard cluster described in his papers and the other was a group of three men, of which this claimant was one, all of whom had worked as painters in the RAF and all of whom had been diagnosed at a young age as having a Parkinsonian syndrome. He considered that the presence of three such cases in the RAF workforce was unlikely to be a chance occurrence. He thought that it would be unlikely that there would ever be an epidemiological study which would demonstrate a clear association between solvent exposure and chronic neurological damage because most solvent exposure was of low concentration, insufficient even to cause symptoms of intoxication let alone permanent damage. Solvent induced brain damage would be a rare event because the necessary intensity of exposure would rarely occur. In his opinion the lack of an epidemiological study capable of demonstrating an association did not mean that one could not infer an association. He remained of the view that his own work and other work done in other countries suggested that an association was likely. He added that there would usually need to be a genetic predisposition to the kind of condition which the patient had developed before the environmental factor (in this case the solvent exposure) had an effect.

In oral evidence, Professor Seaton referred to an additional paper published in 2008 entitled “Trichloroethylene: Parkinsonism and Complex 1 Mitochondrial Neurotoxicity” Ann Neurol 2008;63:184. This paper reported the examination of 30 individuals who had worked at a factory in Kentucky at which trichloroethylene (TCE) was used. It was found that the three workers who had been positioned closest to the TCE source had Parkinson’s disease and that other workers who had been stationed further away (but still with chronic exposure) displayed many features of Parkinsonism. The research also entailed the post mortem examination of rats which had been exposed to TCE. It was found that the rats had suffered damage to the midbrain with loss of dopamine neurons. Professor Seaton was of the opinion that this work supported his conclusion that there was an association between prolonged heavy solvent exposure and Parkinsonian syndromes. He did not claim to know exactly how the damage occurred; that was not understood. He suggested a possible mechanism but did not claim that this was the true explanation.

In cross-examination, it was suggested to Professor Seaton that without scientific proof of a causal link, his opinion was undermined. The professor repeated his acceptance that there was no scientific proof, established by epidemiological studies, that solvent exposure could cause permanent neurological damage. But he maintained that that did not mean that a doctor (or the court) could not properly conclude that there probably was such a link. He was, as it seems to me, drawing a distinction between the standard of proof which scientists look for when drawing conclusions from an epidemiological study and the standard of proof required in a claim for damages. Whereas an epidemiologist will not declare that there is an association unless the study shows that it is 95% certain that the apparent association cannot be the result of chance, the judge in a civil claim need only be satisfied that it is more likely than not that the condition in question has been caused by the alleged exposure. The thrust of the Professor’s argument was that, even where there is no supportive epidemiology, there are other means by which causation or a causal link could be established. He referred to the Bradford Hill criteria of causation with what amounted to an assumption that the judge knew what he was talking about. Neither counsel nor the judge asked the witness to explain what these criteria are. I propose to explain them because it is clear from the witness’s evidence that he was relying on them.

Sir Austin Bradford Hill was an eminent statistician and epidemiologist who, among other things, pioneered work on randomised clinical trials. Working with Sir Richard Doll, he was the first to demonstrate the link between cigarette smoking and lung cancer. Of importance for present purposes was his presentation in 1965 of a paper entitled “The Environment and Disease: Association or Causation?” published in the Proceedings of the Royal Society of Medicine, 58 (1965) 295-300. He there outlined nine criteria which would help to establish the existence of a causal link between exposure to an environmental factor and condition or disease. These criteria are still recognised as a sound basis on which reach to conclusions and it is not surprising that counsel for the MoD did not seek to challenge Professor Seaton’s reliance on them. It is not necessary for me to set out all the criteria; to do so and to explain their significance would unduly lengthen this judgment. However, it is implicit from the paper that Sir Austin recognised that it is not always necessary to have scientific proof by epidemiological study before one can reach a sensible conclusion that a particular agent has caused a certain effect. Other forms of evidence are of probative value.

The professor asserted that small case studies such as he had been concerned with were of some value in proving a causal link. It was not necessary to have a large scale epidemiological study. Sometimes, it would be virtually impossible to arrange such a study. There had not been any study which was likely to prove an association between solvent exposure and a Parkinsonian syndrome. The solvent exposures in the Geoparkinson study were quite low and one would not expect any effect to be demonstrated.

At one stage, it was put to the professor that he had not conducted a meta-analysis of all the epidemiological work on the subject; he agreed that he had not because he was of the view that the material he had put forward demonstrated that it was probable that this claimant’s condition had been caused by solvent exposure. But he was willing to discuss any epidemiological work which counsel wished to ask him about. The point was not pursued by counsel, who then turned to attack the professor’s clinical judgment. Much of this seemed to amount to a criticism of the witness’s refusal to say that the claimant had either PD or MSA and his insistence that what the claimant had was brain injury resulting in damage to various parts of the peripheral nervous system.

Then followed an attack on the professor’s reliance on the cluster of three Royal Air Force painters which he had cited as one of his reasons for his conclusion on causation. It was first suggested that this was not a true cluster because two of the cases appeared to be of PD and the claimant did not have PD. The professor would have none of that. He had already explained that the diagnostic label was unimportant; what mattered was that there were three men with similarly high exposures to similar solvents who had similar (although not identical) neurological effects. He accepted that it was possible that these three cases, arising within a population of about 500 painters, might simply be the result of chance. But he thought that was unlikely.

Although other matters were touched upon, it seems to me that that was the substance of the cross-examination so far as causation was concerned. It appears to me that no significant inroad was made into the professor’s opinion. In the absence of any evidence to contradict this opinion, it seems unsurprising that the judge should have accepted it, as he did, at paragraph 104 of his judgment where he said:

“As I say, my approach to this must be the balance of probabilities, more likely than not. I do not need scientific proof. Not every case that comes before the Court can have scientific proof. I am allowed it seems to me to have regard to the chronic nature of the exposure to the substances concerned, to the dangers that they pose and the period over which it went on, the fact that there was no protection to mitigate the exposure in any way, shape or form. I give some regard to the fact that three very young men seem to suffer similar type of symptoms from similar exposure over a short period of time. I pay regard to the analogous situations of the glue sniffers, who can suffer irreversible brain damage as a result of sniffing solvents, of the long and well-known toxic effects that they have, even if there is not a widely published view about a scientific link. On balance, I am satisfied that causation is made out in this case.”

In this appeal, Mr Johnson for the MOD made a number of criticisms of the judge’s reasoning on the causation issue and the way in which he had considered the evidence. He had made a number of errors. In the passage just quoted, the judge had made a mistake. He had said that there had been no protection against solvent exposure in any way, shape or form. That was plainly wrong. There had been some attempts at protection but it was accepted that these were inadequate.

Further, it was pointed out that, in his consideration of the various scientific papers, the judge had made a number of errors. For example, when quoting from Professor Seaton’s 1992 paper in which five case studies were described, the judge referred to the passage in which it was claimed that, in the naval dockyard, there had been three cases of serious neurological disease out of a workforce of 200, but did not note that this workforce figure was erroneous. Another error which the judge made related to his understanding of the 2007 American paper on the effects of trichloroethylene exposure in a factory in Kentucky. After quoting (accurately) from the headnote, the judge demonstrated that he had not understood the import of that paper as he said:

“This was a case where people were using that substance in machine tool making. The dosage occupational exposure limit is not demonstrated in any detail. It does not appear that the amount was anywhere likely to be the same as there was in this case but there did appear to be in 3 out of 30 cases some Parkinsonian symptoms.”

It must be accepted that the judge had not understood that paper. In fact, there were 3 cases out of 30 with PD and other cases within the exposed group with Parkinsonian symptoms. In effect, the judge had understated the probative value of this study to the claimant’s case.

A further complaint was that the judge had not dealt properly with the Geoparkinson study. I would accept that he did not. After noting that the study had found an association between PD and pesticides but no such association between PD and solvents, the judge remarked (irrelevantly as it seems to me) that tables 2 and 3 of that paper made it look as if one were better off exposed to more solvents rather than less and thought that that perhaps showed what use could be attached to scientific papers – not much. I would accept that that was not a proper description of the Geoparkinson paper. It did not do justice either to the defendant’s argument or to Professor Seaton’s explanation of it.

Mr Johnson made a particular point about the judge’s attitude to Professor Seaton. In paragraph 103, the judge quoted from Professor Seaton’s report three reasons he had given for concluding that the claimant’s condition had been caused by solvents. The first, expressly accepted by the judge, was that organic solvents are known neurotoxicants and the claimant had been exposed to very high concentrations. The second reason related to the existence of the ‘cluster’ of three RAF painters (out of a comparable workforce of just over 300) who had developed Parkinsonian syndromes at a young age. The third was as follows:

“My clinical and epidemiological experience has convinced me that brain damage of this type occurs in individuals exposed to such concentrations which are far higher than the highest ones recorded amongst the 4,000 participants in the Geoparkinson study ”

The judge then commented:

“While I accept the exposure was far higher, but to a certain extent the third point does tend to be near to his alleged Evangelism than it does to a real identification here.”

Mr Johnson’s point was that, far from accepting Professor Seaton’s reasons, the judge was criticising the professor for being evangelistic, the very criticism which the MOD had levelled against him.

What do these errors and inadequacies amount to? It seems to me that, taken singly, none of them could be said significantly to undermine the judge’s conclusion. For example, the mistake in paragraph 104 about the complete absence of protective measures has no effect on the reasoning. The sense of the sentence would have been just the same if the judge had said that the protective measures taken were quite inadequate. As another example, I do not think that the fact that the judge thought that Professor Seaton was expressing himself a little too enthusiastically could be said to amount to a rejection of his opinion overall.

Taken together, I have to say that these errors were unfortunate. I think they demonstrate that this judge had not given himself sufficient time to prepare his judgment. This was a difficult and complex case. The hearing lasted for nearly 5 days. The judge then took only a long weekend (the weekend included a Bank Holiday Monday) to prepare the notes from which he gave what was in effect an ex tempore judgment. I note that these errors came only at the end of this long judgment of 48 pages; there were none in the early stages. I suspect that by the end, the judge may well have been flagging. In my view, the judge’s decision to give his judgment so quickly was heroic but unwise. He would have done better justice to himself if he had allowed more time for thought and preparation. I do not criticise him as I have no doubt that he was under pressure to complete this case and to get on with other work. But the question is whether these shortcomings have so undermined the judgment that it cannot be allowed to stand.

In my judgment, even taken collectively, they do not give rise to any real suspicion that the judge had not understood and accepted the main arguments advanced by Professor Seaton. I have already said that, in the light of the lack of any evidence to contradict him, it is not surprising that the judge should have accepted the professor’s view. In my judgment, the evidence on causation put before the judge permitted only one conclusion on causation.

First, there was clear evidence of a very high level of exposure, in particular over the period between 1989 and 1992 or 1993. This was sometimes at a level several times greater than the permitted exposure levels for the two solvents mainly involved.

Second, there was some scientific evidence of an association between heavy solvent exposure and neurological damage. The case studies relating to the naval dockyard were admittedly anecdotal in nature and the methodology of the first attempt at an epidemiological study was open to some criticism. Nonetheless, the results, which showed a clear association between exposure and symptoms, were replicated in a study in China. This work was published in reputable scientific journals and no real attack was made on it, save to say that it did not provide scientific proof of an association. The Kentucky study, the probative value of which the judge understated, was helpful to the claimant in two ways. It suggested an association between trichloroethylene and Parkinsonian symptoms and showed that those with the highest exposure (the three nearest the source) were the most seriously affected. This study was quite independent of the work done by Professor Seaton and his team. The study also showed that rats exposed to the same solvent suffered brain damage, thereby suggesting that such damage as is alleged is biologically plausible.

The only study which was relied on by the defendants to show that those relied on by the claimant could not be right was the Geoparkinson study. It seems to me manifestly obvious that that study does not disprove the claimant’s case at all. True it does not support it but it does not damage it either because the levels of solvent exposure under examination were nothing like the levels to which the RAF painters, the naval dockyard workers or the Kentucky factory workers were exposed. The exposure levels were roughly at or below the accepted safe exposure level. As Mr Hogarth QC submitted in the course of argument, this study only shows that the current accepted exposure level is satisfactory. It says nothing about the safety of exposure levels well in excess of that.

Taken together, those studies are in my view sufficient to demonstrate that there is probably a link between heavy and prolonged solvent exposure and neurological damage. By that I mean that they are sufficient to satisfy a judge on the balance of probabilities. I accept that they do not provide ‘scientific proof’. I leave aside whether they are sufficient to ‘convince’ someone. It may be that Professor Seaton expressed himself too strongly and with too much enthusiasm when he said that he was convinced. But it matters not.

Third, in my view, the judge was entitled to take into account the two further factors which he mentioned: the existence of the cluster of three RAF cases and the analogy between solvent exposure and glue sniffing. In fact glue sniffers often sniff solvents rather than glue and even the glues are not so very different chemically from solvents. Dr Newman accepted the analogy. Neither of these factors seems to me to be of great significance but they can and do add a little weight to the argument. I would mention in passing that, although the Kentucky group was not regarded as a cluster, in fact it was and quite a telling one at that.

The judge did not say and I would not say either that it is now established in the scientific sense that there is a causal connection between heavy solvent exposure and neurological damage. However, I consider that, on the evidence called by the claimant, unrebutted by the defendant, in legal terms a probable connection has been made out in this case.

If the connection is accepted, it is but a short step to conclude that this claimant’s condition was caused by solvent exposure. I have already said that high levels of exposure were established by the evidence of Dr Cherrie and accepted by the judge. The timing of the onset of the signs and symptoms was wholly consistent with the exposure blamed. Dr Newman had been asked how long he thought would elapse between exposure and the manifestation of symptoms; he said between two and four years. There was no challenge to that. It was the claimant’s evidence that, although he had been exposed to solvents throughout his service with the RAF, the exposure had become much more concentrated from 1989 onwards. The judge found that the first symptoms manifested themselves in about December 1992. Thus a coherent picture was presented of heavy exposure and manifestation of symptoms at about the time when, if they were to appear at all, they might be expected.

That last point leads me to the final ground of appeal raised by the appellant in written argument (although hardly mentioned in oral argument) namely that the judge had failed to deal with the question of whether the damage had been caused by exposure during the period for which the MOD was not covered by Crown immunity. It is true that the judge did not deal with this but that is hardly surprising. As I have just said, although there had been some exposure before 1987, the whole thrust of the claimant’s case was that he was really complaining about the exposure from 1989 onwards and in particular that which occurred during the preparations for the Gulf War. Thus there never really was any need for the judge to deal with pre-1987 exposure. For the sake of completeness, I would say that even if pre-1987 exposure had made some contribution to the claimant’s injury, the contribution of the post-1987 exposure was plainly material and would found liability for the whole injury.

For those reasons, I would dismiss this appeal and direct that the case be listed for a trial on quantum if damages cannot be agreed.

I agree.

I also agree.