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Accident Compensation Cases

Primary Producers Co-Operative Society Ltd v Accident Rehabilitation and Compensation Insurance Corporation (DC, 14/09/99)

Judgment Text

RESERVED JUDGMENT OF JUDGE M J BEATTIE 
Judge M J Beattie
The issue in this appeal is whether the claimant suffered solvent neurotoxicity, being a gradual process injury, arising out of and in the course of his employment with the appellant. 
The circumstances of this case to the point of this appeal are that the respondent has accepted that the claimant is entitled to cover pursuant to section 7 of the Act in respect of the gradual process injury of solvent neurotoxicity suffered by the claimant in the course of his employment with the appellant. The appellant contends that the claimant's condition, whatever it may be, has not been caused or contributed to by the environment of the workplace in which the claimant was employed by the appellant. 
The claimant commenced employment with the appellant in 1977 and continued in that employment until April 1994. For the last 11 years of that period he was employed as a labourer in the Steel Room. The Steel Room was the place where skids and gambrels were cleaned. It is a room that was unusual in its shape being 9.5 metres wide at its widest point and 2.5 metres wide at its narrowest and being 21 metres in length. Its height was 2.55 metres. Overall the area of the room was 298.35 sq. metres. In that room was located the chemicals and baths and tanks which were used for the cleaning process. 
The major chemicals used were sodium hydroxide, potassium hydroxide, phosphoric acid and the water displacement wax which had a content of 88 per cent of white spirits. Ordinary water was also used in the process. 
The skids and gambrels were moved from one tank to another by means of an overhead hoist. The alkaline tanks and the acid tanks were heated. The wax tank was not heated but received hot skids placed in it and thereby it was said caused it to give off fumes. 
The ventilation system was of the extraction type in the ceiling which had been upgraded in 1991. The evidence given at the review hearing was that the ventilation problem in this room had been the subject of several OSH inquiries, the contention being that this ventilation system neither worked properly nor was adequate. The only natural ventilation was through a door to a corridor which for most times was required to be kept shut as it led through to the cooling floor. The claimant's description of the steel room was that it was hot, humid, steamy and fumy. 
For the first 7 years of working in the steel room the claimant did so on a year round basis but for the last 4 years, prior to ceasing work in April 1994, he had only worked there for 8 months of the year during the season, being from November to July. 
On 4 April 1994 the claimant lodged a claim for cover, reciting recurrent headaches, eye and nose irritation and other symptoms due to exposure to chemicals at work. 
The claimant completed a gradual process questionnaire indicating that his condition had developed over 11 years. He stated that he had been experiencing headaches, nausea, fatigue, sore neck, eye and nose irritation and joint and chest pains. That he attributed his symptoms to poor ventilation, the absence of breathing masks and the heat in his working environment. 
In June 1994 Dr Jayasinghe, Physician at Balclutha Hospital, provided a report to the respondent detailing that the claimant had a history of headaches over the past three years which had been getting progressively worse. He also recorded episodes of dizziness and light-headedness. Dr Jayasinghe indicated that he would have to carry out particular tests in order to establish a diagnoses and that he would report further when those investigations have been completed. 
At the same time the claimant had been referred to Dr Glass, Occupational Medicine Specialist, by his GP, Dr Cook. 
In October 1994 Dr Jayasinghe again reported to the respondent indicating that as a result of the tests which he had carried out, it had led him to the conclusion that it was highly unlikely that there was a neurological or endocrine basis for the claimant's symptoms. 
Dr Glass reported to the respondent on 5 October 1994 and it must be noted that the physical dimensions of the steel room, as given to Dr Glass by the claimant, was smaller by about 1/3 than the actual dimensions of the room as measured. 
In his summary Dr Glass states as follows: 
“1.
Acute 
(a)
‘Irritant in nature’ from the acid and alkali involving nasal and eye irritation and chest tightness. 
(b)
‘Solvent based’ that is his light headedness, and to some extent a reinforcing of the irritant effects of the alkali and acid fumes (solvents are also irritants). 
2.
Chronic 
With time other symptoms developed, in particular lethargy, tiredness and mood changes. These are commonly seen with long term solvent exposure — in this case due to the white spirit which is a volatile. It would have evaporated to a great extent in the hot conditions and would have built up in concentration due to the lack of ventilation. 
The provision of masks is insufficient to deal with this sort of problems, proper ventilation, local and general is required as well as replacing the solvent based mix. I understand this has now been done. 
With his time off work — 6 months Stephen's health has returned to normal, further support for a work based condition. It is imperative he does not return to the same working conditions as before. 
On enquiry there was no evidence of any other illness or factors which could have led to this condition. 
Opinion 
It is my opinion that Stephen suffered an illness involving his respiratory system and his central nervous system as a result of exposure to a mixed fume of acid/alkali and solvent in a working environment which was inadequately ventilated, very hot, so increasing the fume concentration and exacerbating the effects of the fumes. ”
Following the reports of Dr Glass and Dr Jayasinghe the claim was referred to the respondent's Assistant Corporate Medical Advisor, Dr Bremner, and it was his advice that cover should be accepted for the claimant's claim as a work injury. 
In November 1994 the appellant advised that Dr Glass' report contained errors and that it did not accept his report and that it did not accept responsibility for the claimant's condition. 
The claimant did not commence work again in November 1994 at the start of the season and it was the appellant's contention that the claimant was suffering from psychological problems unrelated with his employment and that this was the cause of his condition. 
The appellant also noted that it had carried out a further up-grade of the ventilation system in the steel room and that a new form of wax was being used. It was stated that the OSH inspector was satisfied with the changes. 
On the strength of that advice the respondent sought to inquire further into the claimant's medical condition and in the first instance referred him to a psychiatrist at Dunedin Hospital, Dr Taghavi. Dr Taghavi advised the respondent that the claimant was probably suffering from affective syndrome and that it was more probably related to neurotoxicity. 
In April 1995 a Ms Ivory, Clinical Psychologist, provided a 9 page neuropsychological report. She advised that tests had indicated that the claimant had experienced a marked deterioration in general intellectual functioning and she gave as her opinion as follows: 
“Given the consistency between the clinical interview and test data obtained during this assessment, the close relationship between the onset of the cognitive impairments and the temporal relationship between these and exposure to a particular worksite, my opinion is that occupational solvent neurotoxicity is playing a significant role in Mr Thomson's cognitive deficits. 
It is my opinion that Mr Thomson's deficits are more than would be expected from inadequate attentional resources, secondary to depressed mood, thereby suggesting that Mr Thomson demonstrates marked changes in both affect and cognition subsequent to chronic toxic exposure. ”
Dr Taghavi also commented on the findings of that neuropsychological report and he advised: 
“Considering his exposure to the chemical, and his clinical features, the onset of his symptoms, his treatment response, and the result of neuropsychological testing, it seems to me that exposure did have a major role. I would not be able to comment on what percentage directly, although I think it would be high. His drinking problem with full remission would unlikely be related to his present picture. His positive history of affective illness might play some role, even though the process of his depression and his treatment response is not supporting that notion. ”
Throughout this time and subsequent, the claimant was receiving weekly compensation and other entitlements. In August 1995 the claimant's GP advised the respondent that the appellant was suffering from depression and had been admitted to hospital to receive treatment. She further noted that he was still getting a lot of headaches which she considered related directly to the original chemical poisoning. 
For whatever reason the question of final acceptance of the claim appears not to have been communicated to the appellant and the respondent has acknowledged that it had not made a formal decision in that regard. By letter of 1 April 1996 the respondent advised the appellant that it had accepted the claimant's claim for cover as a gradual process work injury pursuant to section 7 of the Act. The basis given for acceptance was that several specialists reports confirmed that the claimant's exposure to acid and alkaline fumes used in the steel room significantly contributed to his neurotoxicity condition. Following receipt of that advice the appellant lodged an application for review. 
For the purposes of that review the appellant sought the opinion of Dr John Alchin, Specialist Occupational Physician. Dr Alchin's report was based on the various reports that had been earlier obtained on the claimant's condition. In reviewing those reports Dr Alchin noted that Dr Taghavi and Ms Ivory were both cautious in their opinions and did not exclude the possibility that non-occupational factors may be the cause, but even if occupational exposure was the major cause there was evidence of non-occupational factors (anxiety and hypochondriasis) worsening the symptoms. 
Dr Alchin stated that because of its very nature solvent neurotoxicity is a diagnosis which is impossible to be made with certainty because symptoms are non-specific, prevalent in the general population (even those with no solvent exposure), and because there is no specific diagnostic test available. He went on to state: 
“On the basis of the information provided in Dr Glass' and Mr Stewart's reports, I would be inclined to the view that this initial symptom (headaches) was not work related. That is because the time sequence of this symptom is not consistent with Mr Thomson's occupational exposures. This opinion of mine is based on the belief that headaches from solvent exposure are generally accepted to be part of the acute toxicity rather than chronic toxicity. In saying this I am mindful of the dissenting view … but this is a dissenting view rather than the common view. Therefore, if I had been presented with reports up to and including that of Dr Glass (i.e. excluding the psychiatric and psychological reports from Dunedin Hospital in March 1995) I would have probably agreed with Mr Stewart, and disagreed with Dr Glass, that the headaches were not caused by Mr Thomson's occupational exposure. However, apart from headaches, there were other symptoms (light-headedness and mucosal irritation) which were consistent with acute workplace exposures to solvent vapour and acid and alkali fumes, as outlined in Dr Glass' report, and like him I agree that these symptoms could plausibly be attributed to these acute workplace exposures. 
However, Mr Thomson subsequently was admitted to Dunedin Hospital with symptoms of major depression which proved resistant to normal therapy. Neuropsychological testing there showed abnormalities consistent with those described for chronic solvent neurotoxicity. This and the other symptoms discussed on page 5 of Dr Glass' report (lethargy, mood changes) certainly raises the possibility of chronic solvent neurotoxicity as the diagnosis: I note that this is a different diagnosis from the clinical problem considered a year earlier by Mr Stewart and Dr Jayasinghe. It is important to note again … that this is a diagnosis which is impossible to make with certainty. Nevertheless, there are guidelines published to help attain some consistency with this diagnosis. The guidelines in New Zealand published by Occupational Safety and Health of the Labour Department several years ago are based on Scandinavian guidelines. There are four criteria in the guidelines to be satisfied for a diagnosis of chronic solvent neurotoxicity to be made. 
1.
Exposure to a significant level of organic solvent at work for at least 10 years. 
2.
Consistent symptoms 
3.
Exclusion of other known medical causes of the symptoms. 
4.
Confirmatory evidence e.g. consistent neuropsychological test results. 
Considering these four criteria in Mr Thomson's case: 
1.
Mr Thomson worked for 11 years, although the last four of this was for eight months a year. Based on Dr Glass's report there could well have been significant air concentrations of solvent vapour. However I note that Dr Glass, like myself, has not personally inspected the Steel Room at Finegand, and that no measurements of solvent vapour have been performed. In addition, Dr Glass comments that the solvent in the wax has been replaced, so workplace measurements in this case would no longer reflect the conditions that prevailed when Mr Thomson worked there. So I find it difficult to be certain of whether there were high air levels of solvent vapour over Mr Thomson's 11 years in the Steel Room, although like Dr Glass, from the description of Mr Thomson, I believe that it is quite possible that there were. 
2.
Mr Thomson's symptoms are consistent with those described for chronic solvent neurotoxicity, although again it is important to note that these symptoms are non-specific, and occur commonly in the general population even with no solvent exposure; eg, anxiety and hypochondriasis are common. In addition, Rosenstock and Cullen (op. cit. page 506) note that major depression has a five percent lifetime prevalence, ie Mr Thomson has a one in twenty chance of having major depression even if he never worked with solvents. 
3.
I believe that the evidence indicates that, apart from the possibility of major depression unrelated to solvent exposure, there are no other known medial causes of Mr Thomson's psychological symptoms. 
4.
The neuropsychological testing lends support to the diagnosis of chronic solvent neurotoxicity, although once again this is non-specific rather than diagnostic of itself. 
Considering all this, like Dr Taghavi and Ms Ivory I am of the opinion that it is plausible that Mr Thomson has chronic solvent neurotoxicity. Like them the major condition which I cannot exclude is major depression unrelated to his occupation (see criterion 3 above: major depression, unrelated to work, cannot be excluded). In addition, we have no certainty that there was a high level of solvent vapour in the air, although from Dr Glass' report this is likely (see criterion 1 above). 
In summary, I am not certain of the diagnosis, and whether Mr Thomson's condition is due to solvent exposure at work or not; there is some element of doubt about whether (a) and (b) of Section 7 are fulfilled or not. At this stage, on the information presented to me, I would tend more towards the view (based largely on the report by Ms Ivory) that it is certainly possible that work exposure to solvent vapours has been a significant cause of Mr Thomson's condition; but even while stating that I feel uneasy because I am well aware that I could be wrong, and that he may have depression unrelated to his occupation. I apologise that I have not been of more assistance in this case; but as stressed in this report, and as indicated in the reports by Dr Taghavi and Ms Ivory, it is impossible to exclude with certainty non-occupational causes. This is for two reasons: firstly, there are no specific tests for diagnosing chronic solvent neurotoxicity, even with comprehensive data on work-place exposure levels, because symptoms and tests are non-specific rather than diagnostic, and because symptoms are prevalent in the general population with no solvent exposure, and overlap significantly with common psychological and psychiatric conditions; secondly, because in this specific case we have no data on workplace solvent in air concentrations that Mr Thomson was exposed to. ”
A review hearing took place on 31 October 1997 at which was produced a letter from OSH dated 3 December 1990 evidencing a complaint from the claimant and clearly indicating his concern at that time of his exposure to chemicals and the need for protective equipment to be used. 
Before delivering his decision the Review Officer sought further particulars from the claimant's GP, Dr Cook, as to the length of time that the claimant had been complaining of headaches and other symptoms as it had been identified by the appellant that the claimant's symptoms purportedly first appeared during a non-work period, that is prior to the season commencing. On 11 November 1997 Dr Cook advised as follows: 
“Looking back in Mr Thomson's notes between 1990 and 1993 Mr Thomson consulted the practice about his asthma on several occasions, and certainly on at least one occasion in December 1992 for headaches, although these appeared to be associated with some upper respiratory tract infection. … His first of the ongoing complaints of headaches seemed to be in September, October 1993 when he presented with what I thought was sinusitis. Basically it was difficult to improve his headaches in spite of treatment of sinus related conditions and then for possible musculoskeletal causes of headaches. It was really only in April 1994 when we began to look at the fact that Steven's symptoms were not improving and consider his working environment that we started to think about chemical poisoning as a possibility. In retrospect we found a number of symptoms which were typical of chemical poisoning and that had been going on for some time, and I think that the diagnosis of chemical poisoning is made only when we excluded other things. 
In comment on Mrs Thomson's reference to the other ‘vague symptoms’ it may be possible that Steven did come to me with other vague symptoms that I have not recorded in the notes. I am certainly aware of Steven having had a number of consultations related to a variety of different symptoms of which headaches were probably the most important. Again with a patient presenting reasonably frequently there may not always be a note of every single symptom. ”
In addition, the claimant's advocate referred him to Dr Ding, Consultant Psychiatrist, for a report. For the purposes of his report Dr Ding had copies of all relevant clinical and psychiatric reports and Dr Ding also examined the claimant personally. It was Dr Ding's conclusion that in the absence of other organic factors explaining the claimant's cognitive impairment, the most likely cause for it was chemical toxicity and he concluded that the claimant's ongoing psychological problems were due to physical impairment of his brain function rather than personality factors. 
In his decision dated 23 December 1997 the Review Officer confirmed the respondent's decision to grant cover and that the claimant had met the criteria required of section 7 of the Act. The Review Officer found on the evidence that the claimant had displayed symptoms of headaches for several years prior to September 1993 and that this had been referred to in Dr Jayasinghe's report, as well as that of his GP, Dr Cook. 
The appellant thereupon lodged an appeal to this Court against that decision and for the purposes of this appeal further Occupational Medicine Specialists' reports were sought by the appellant and the respondent from Dr Turner and Dr Dryson respectively. In addition, there is a further consulted Neuropsychologist report from Dr Gromwall. 
In his report of 5 June 1998 to the respondent, Dr Dryson stated as follows: 
“Chronic solvent neurotoxicity is a diagnosis which is based on the balance of probabilities and as Dr Alchin points is made by meeting four criteria established by the New Zealand Department of Labour in 1993. These are: 
1.
typical symptoms 
2.
sufficient exposure to solvents 
3.
presence of an objective measure such as neuropsychological tests 
4.
other conditions being excluded 
It is clear from reading the file that many of his symptoms (but not all) are consistent with chronic solvent neurotoxicity, the neuropsychological tests are also consistent with solvent neurotoxicity and other conditions have been excluded apart from depression. 
It must be reiterated that deficiencies on neuropsychological testing are not diagnostic for solvent neurotoxicity but that similar deficiencies can occur for other reasons such as alcohol abuse, drug abuse, head injury, and cerebro vascular disease. Depression may also cause the same symptoms but this is complicated by the fact that depression is often a feature of chronic solvent neurotoxicity per se or may be a consequence of chronic solvent neurotoxicity because of the reaction to being unwell. 
So far therefore I am satisfied that Mr Thomson does have typical symptoms, does have changes on neuropsychological assessment which are consistent with solvent neurotoxicity, and has had other neurological disorders excluded by means of CT scan and physician assessment. There remains therefore the issue of the exposure to solvents. 
It is with some concern that I read that the only reference to the actual exposure to solvents is contained in Professor Glass' report of 5 October 1994 (unfortunately truncated at page four in the file you sent me). This is in turn based entirely on the testimony of Mr Thompson at the time. This is hardly objective evidence. There is no mention anywhere of any independent investigation of this workplace. I believe that this is the crux on the claim because if he has not been exposed to significant amounts of solvent he can hardly have solvent neurotoxicity. ”
Dr Dryson suggested that clarification of the claimant's exposure to solvents be sought and to this end the respondent referred the matter to L Hodgkinson, Occupational Health Scientist, who advised as follows: 
“Given that one of the chemicals used contained 88% white spirits, there would have been the opportunity for reasonable exposure to solvent vapour. From what is said about the operation in Bill Glass's report and considering that the vapour pressure of the white spirit is relatively low I would think that the chances of the exposures being in excess of the Workplace Exposure Standard would not have been particularly high. This of course does not preclude the possibility that the worker was in some way effected by his work in the steel room. Exposure to alkali and acid ‘fumes’ would not be expected from the operation. ”
That report was referred to Dr Dryson who commented on 9 July as follows: 
“The OSH solvent panel has seen cases with exposure below the WES, but would expect the exposure to have been prolonged. I consider 11 years exposure to be prolonged. 
The various affidavits point to substandard conditions in the steel room. 
I am able to accept therefore that exposure has been significant and taken in conjunction with the points raised in my report of 5 June 1998 would consider that Mr Thomson has chronic solvent neurotoxicity. His ongoing symptoms are due to his original exposure. ”
On 31 August 1998 Professor Des Gorman, Head of Occupational Medicine at the University of Auckland - Faculty of Medicine, advised that it was difficult to determine the likelihood of the claimant having suffered any neurocognitive injury at work. The reason for this difficulty being that there were no objective workplace exposure measurements. He agreed with the observation of Dr Dryson in that regard. Dr Gorman indicated that there was a need to measure exposure levels. 
Finally Dr Turner, Occupational Medicine Specialist, provided a written brief of evidence outlining his opinion. That brief was tendered by the appellant and was accepted in the form of a brief by the respondent. Dr Turner did not give evidence in person but his brief of evidence was accepted as evidence in the appeal. 
Dr Turner also noted the lack of objective of measurement of chemicals or fumes to which the claimant may have been exposed. Dr Turner has reviewed all the various reports that had been made in relation to this claim and he identifies three groups. The first group in effect being Dr Glass who identifies true occupational disease as existing. A second group consisting of Dr Alchin, Dr Jayasinghe, Ms Ivory, Dr Taghavi and Dr Cook, whom he sees as forming a group who are unable to be sure that a true occupational disease exists. He then identifies a third group who do not see an occupational cause for his condition, that group including Mr Stewart, ENT Surgeon, and Dr K Bremner, Occupational Physician. 
Dr Turner advised that it was impossible to confirm that the claimant suffers from an occupational disease and he did not consider that the standard of proof on the balance of probabilities had been satisfied. The reasons he gave for this view were as follows: 
i)
The occupational history does not support an occupational cause for his symptoms. 
ii)
Dr Glass' assessment does not confirm a diagnosis of either occupational solvent neurotoxicity, occupational asthma or occupational rhinitis/sinusitis due to inadequacies of assessment. 
iii)
The initiation of onset of Mr Thomson's symptoms arose at a time when he was away from work in the off season 
iv)
Mr Thomson's symptoms did not resolve despite cessation of exposure 
v)
Mr Thomson's symptoms profile does not accord with that which is considered to be typical of long term solvent neurotoxicity. 
vi)
The evidence on file does not disprove or exclude that Mr Thomson's ongoing symptom profile (headaches, lethargy, mood disturbance, muscle and joint aches and pains, light headedness) have arisen as a function of his major depressive illness hypochondriasis and affective syndrome. 
vii)
The balance of probabilities points towards this man having a form of somatisation disorder as the cause of his chronic symptoms. This occurs when a stressed and vulnerable personal has a normal response to a stressor but finds that symptoms failed to abate in the expected time frame. 
In the final analysis Dr Turner advised that the claimant probably suffered from acute solvent exposure at work but that the symptoms of this are by definition transient and resolved with a cessation of exposure. He considered that the progression to a chronic condition of solvent neurotoxicity was not a condition that could have arisen from his work environment. He therefore, found that section 7(1)(a) criteria was fulfilled insofar as acute toxic condition was concerned but not for chronic solvent neurotoxicity. 
The claimant's claim for cover has been brought under section 7 of the Act which provides as follows: 
“7.
Personal injury caused by gradual process, disease, or infection arising out of and in the course of employment --- 
(1)
Personal injury shall be regarded as being caused by gradual process, disease, or infection arising out of and in the course of employment only if --- 
(a)
In respect of a period that ended on or after the 1st day of April 1974, the employment task performed by the affected person, or the environment in which it was performed, had a particular property or characteristic which caused or contributed to that personal injury by gradual process, disease, or infection; and 
(b)
The property or characteristic is not found to any material extent in the non-employment activities or environment of that person; and 
(c)
The risk of suffering that personal injury is significantly greater for persons performing that employment task in that environment than for persons who do not perform that task in that environment. ”
Ms Chesterman, counsel for the appellant, submitted that there was insufficient evidence which could establish the causation necessary to make a positive finding under section 7(1)(a). She submitted that in effect all the experts relied for their prime source of evidence on the opinion of Dr Glass and that his report must be regarded as being suspect as some of the information he relied on, namely the dimensions of the steel room, were quite wrong. 
Counsel submitted that all the experts in the occupational medicine field had doubts as to a causal link and that the claimant's condition could equally have arisen from causes unconnected with the employment environment. 
Ms Rice, counsel for the respondent, submitted that there was sufficient evidence of the claimant's work environment having the necessary properties or characteristics which caused the claimant's solvent neurotoxicity. She submitted that the fact that Dr Glass' information about the size of the room was incorrect did not affect his opinion as to the properties or characteristics within the room which were the cause. She further submitted that there was clear evidence that the appellant had been suffering from the effects of exposure for some years prior to bringing his claim and the OSH report in 1990 demonstrates this. 
Counsel submitted that the weight of opinion from the specialists in occupational medicine supported the proposition that the claimant's workplace contained concentrations of solvent vapour which contributed to his condition. She submitted that there was no evidence that those same properties or characteristics were found outside the workplace and even if it be found that other factors may have contributed to his condition outside the workplace, that was not the test in s 7(1)(b). 
Mr Miller, counsel for the claimant, supported the submissions made by counsel for the respondent. He further submitted that the Accident Compensation regime was a no fault scheme and that implicit in that concept was that a high standard of proof ought not to be required and further that a claimant ought to be given the benefit of the doubt. 
Decision 
This was a claim for cover for solvent neurotoxicity suffered by the claimant and found by the respondent at first instance and by the Review Officer at review to have been caused or contributed to by the fumes and toxic substances emitting into the atmosphere in the steel room where the claimant was usually engaged for the whole of his working day. 
For such a claim it might be thought that one or two, possibly three opinions from suitable experts would be all that would be required to establish or disclaim entitlement to cover under section 7 of the Act in the particular factual circumstances of this case. Such however, has not been the case in this claim where this Court has had produced to it for reference no less than 21 opinions and reports from specialists of various disciplines. There have been six psychological reports and ten occupational medicine specialist reports. A number quite unprecedented in my experience in dealing with appeals in this jurisdiction. 
This Court on appeal is required to consider that evidence and determine whether it has been established on the balance of probabilities that the respondent's decision, confirmed by the Review Officer, was wrong. 
This is not a case where a claimant's entitlement is either in or it is out based on some single crucial but identifiable fact or state of affairs. 
In this case the various occupational medicine specialists have identified that by its nature solvent neurotoxicity is a diagnosis which is impossible to be made with certainty because the symptoms are non-specific and because there is no specific diagnostic test available. It was for this reason that Dr Alchin said “that any opinion expressed with dogmatism is therefore unscientific and should be treated with suspicion by Courts even though a definite answer would be attractive for such non-scientific people required to make a definite decision, they need to understand that certainty in this subject is not possible in our current state of knowledge”

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