Grouwstra v Accident Rehabilitation and Compensation Insurance Corporation

IN THE DISTRICT COURT Decision No. 7/96 HELD AT TAURANGA IN THE MATTER of The Accident Rehabilitation and Compensation Insurance Act 1992 AND IN THE MATTER of an Appeal pursuant to Section 91 of the Act $7 / 92 / 31 12 . BETWEEN SHERYL ENID GROUWSTRA Appellant (Appeal No. DCA 155/94) AND ACCIDENT REHABILITATION AND COMPENSATION INSURANCE CORPORATION a body corporate duly constituted under the provisions of the said Act Respondent HEARD on the 4th day of August 1995 APPEARANCES Mr Ryan for appellant Mr A Barnett for respondent DECISION OF JUDGE D A ONGLEY At the end of the hearing counsel asked for an opportunity to make further submission on the oral medical evidence heard on this appeal. Those submissions were received after a delay in obtaining the transcript. The issue in this appeal was a medical question as to whether the appellant suffered incapacity by reason of organophosphate poisoning. In July 1987 Mrs Grouwstra began work in a greenhouse business growing orchids for the export market. Her work involved moving plants from shed to - 2 - shed and removing dead leaves and weeds. For a short period a poison named Temik was used for pest control and the workers were issued with protective gloves, but otherwise they were not provided with gloves or protective clothing or equipment. The appellant did not spray plants but she would shift the plants before and after spraying. The appellant said that she had always been a relatively healthy person apart from gall bladder trouble that she experienced from about 1983. She had gall bladder surgery in 1987 and she said that she recovered normally. In November 1987 she began to feel tired and listless and suffered from diarrhoea, and sleeplessness. She continued to work until February 1988 when a number of employees undertook blood tests and as a result of negative indications of her blood test she ceased working. Another employee collapsed and it is thought that she was diagnosed with spray poisoning but there is no comprehensive or comparative information available about that other case. The appellant made a claim which was accepted by the Corporation. The Corporation terminated the appellant's compensation in 1992 when it was no longer satisfied that she was incapacitated. The appellant says that at that time she was still unwell. She said that she had diarrhoea, nausea, headaches, erratic heartbeat, loss of memory and vision and extreme weariness. She had steadily improved but she said that by September 1992 she could still not lead a normal life and she had good days and bad days. She said that any exertion like an outing would take days to recover from. In 1988 the appellant's general practitioner, Dr T F Smart confirmed a diagnosis of organophosphorous poisoning. He considered that her symptoms were typical of organophosphorous poisoning and the probability was confirmed by her reduction in pseudocholinesterase levels. He was so certain of his diagnosis that he thought there could be "absolutely no doubt". Dr Smart referred the appellant to Dr A M Graham, consultant physician of Tauranga who gave his opinion in a letter of 26 September 1988. He said: "Symptoms are consistent with a chronic organophosphorous poisoning syndrome and this would be supported by the persistently low levels of cholinesterase, through as you know at least 10% of the population have this as a genetically low level (as you say her parents have this problem). I have recently seen another lady with the same problem and cannot help but feel that there is a significant influence of these patients one on the other." Dr Graham saw the appellant again in December 1988 and he said that she reported considerable improvement generally in her well-being. He said: "Laboratory investigations were largely unremarkable except that her thyroid function is borderline high and this warrants rechecking. She also has a slightly low gamma globulin G though in isolation it is of doubtful significance. She continues to have a low pseudocholinesterase level though - 3 - as mentioned in the previous correspondence, because there is no pre- organophosphorous exposure this may be an inherited abnormality. However if subsequent pseudocholinesterase levels are within the normal range this would argue for organophosphorous poisoning. All other laboratory investigations are unremarkable. I should like to review her once more in 3 months time." In April 1989 Dr Smart informed the Corporation that the appellant was no better: "Sheryl continues to remain symptomatically unwell, although her cholinesterase levels have stabilised. She had not been able to return to any work as she remains constantly unwell with tremulousness, recurrent bronchospasm and problems of salivation. She also suffered from a general lethargy which is significantly debilitating. She has received specialist attention on a number of occasions in this regard and, unfortunately, as you know, there is no treatment that can be undertaken except time and removal from the exposure. There have not been any underlying contributory conditions." The significance of pseudocholinesterase levels had been regarded by Dr Smart as an indication confirming his clinical diagnosis of organophosphorous poisoning. But in later reports, and in the evidence heard on the appeal, its significance was diminished by the fact that the appellant was likely to have had a genetically low level, although there was no known pre-morbidity level to draw a conclusion. In May 1992 the Corporation embarked on an assessment of permanent disability. It arranged for the appellant to see Dr Graham again and he reported on 14 May 1992: ".. she reports continued improvement but persistence of many of her previously reported symptoms, particularly diarrhoea, palpitation, memory problems, breathlessness on exertion, and some mood swings, as well as low libido. She reports not being capable of working for a living at this stage and has had not further contact with organophosphate compounds. Her social circumstances are unchanged. She continues to smoke 10 cigarettes/day, drinks almost no alcohol, has no children by choice and is living with her husband who has regular employment. I again examined her and found no objective abnormal findings, particularly no neurological abnormality. Comprehensive laboratory tests have again been performed. Serum pseudocholinesterase, as mentioned before, was low. Creatinine, liver function tests, calcium phosphate, sodium, potassium, full blood count, ESR, thyroid function tests, serum cortisol, CRP, anti-nuclear factor, iron studies, MSU, B12 and folate were all normal. IgA and M were again normal. Serum IgG remains modestly depressed at 6.4 gm/l (n = 7.7 - 16.9) Chronic neurobehavioural syndromes have been described in individuals who have had excessive levels of organophosphate exposure. - 4 - Symptoms of these syndromes include drowsiness, mental confusion, anxiety, emotional lability, depression, fatigue and irritability. In addition axonal degeneration of peripheral nerve has been reported, which improves over months to years, often with some residual impairment. There is no definite history in this case however of severe acute toxicity syndrome. Extensive testing has not defined another explanation for her symptoms. She has minor abnormalities on laboratory testing (low C3 level, low IgG level and borderline hyperthyroidism on one occasion). As mentioned she also has mild obstructive airways disease. These abnormalities are too incongruous however with the severity of her symptoms to explain completely her symptoms. The symptoms could fit with a chronic organophosphate toxicity state though again this is the lack of a typical acute toxicity episode. There is also no objective neurological abnormality present on examination to suggest a chronic neuropathy. Therefore I am not comfortable in categorically stating that this woman has organophosphate poisoning. I would think that her symptoms could be well explained by a primary depressive disorder, and it may be valid for her to see a psychiatrist for formal assessment. I would be pleased to discuss this report further with you if you would like me to. The information that people with inherited pseudocholinesterase deficiency may be predisposed to the toxic effects of organophosphate is also not clear cut I believe." The Corporation then asked for a psychiatric report from Dr Cliffe. He reported on 6 August 1992: "In my opinion there is little doubt that this woman has been suffering from a Major Depressive Episode, albeit with slightly atypical features. The nub of the matter however is whether or not it could be reasonably attributable to alleged poisoning by insecticidel chemicals. Unfortunately one does not know with certainty as to which substances she was exposed, nor the concentration thereof, and again the duration and frequency of exposure. Assuming for the moment that these substances were organophosphates and carbamates, I can offer the following opinion: Firstly, intoxication by carbamate insecticides is most unlikely as a cause of her symptoms. these substances produce a picture of cholinergic excess similar to, but considerably less severe than, that produced by organophosphate poisoning. In particular the carbamates enter the central nervous system in insignificant amounts and any intoxication directly due to such substances resolved in the vast majority of cases in less than 24 hours. The picture with organophosphate poisoning is less clear cut; however there appears to be no evidence that Ms Grouwstra suffered from acute, severe intoxication because this would certainly have so disabled her as to require medical resuscitation. The chronic picture certainly can be associated with a variety of physical and mental symptoms some of which she has complained. The difficulty lies in the -5- fact that although persistent neurobehavioural symptoms can develop after organophosphate poisoning, diagnosis is limited by the nonspecificity of the symptoms, and the relatively poor sensitivity of the neurophysiologic and neurophsychologic tests currently used. Persistent neurological and behavioural abnormalities attributable to organophosphate exposure include (as Dr Graham stated in his report) drowsiness, fatigue, emotional lability including depression and anxiety, irritability and mental confusion. However, it is generally accepted that most of the persistent symptoms that develop after acute organophosphate exposure resolve within 12 months. The exception seems to be mixed sensorimotor peripheral neuropathy but this occurs in association with particular organophosphate substances which Ms Grouwstra would most unlikely have encountered, and moreover she does not have symptoms which would be consistent with such a diagnosis. In summary, not only do I share Dr Graham's reluctance to attribute this woman's symptoms to organophosphate poisoning, but I will further opine that I think it very unlikely that her illness has been caused directly by exposure to toxic chemicals. I think it more likely that she became very anxious about such substances, and not being in possession of technical knowledge about such chemicals she possibly drew the wrong conclusions about toxicity. Moreover from her description of her reactions I feel that there was also an element of antipathy towards her employers (who in turn may not have handled the situation in the wisest fashion), which led her to angry embitterment, and probably compounded her distress. The persistence of her symptoms simply does not fit the picture that one would expect from organophosphate poisoning but does very well fit into the diagnostic framework of a depressive illness. Unfortunately I think it most unlikely that she would be prepared to acknowledge this, as she seems to have a fixed attitude towards any explanation other than that which she prefers, namely one of insecticidel poisoning. Treatment therefore is likely to be problematical." It is necessary to set out Dr Cliffe's opinion at length because it provided the basis for the Corporation's decision to cease compensation, and because it provided a diagnosis that explained the persistence of symptoms. On 16 September 1992 Dr Smart wrote: 'As a consequence of her significant ill-health and chronic toxic state, she continued to become progressively depressed. I do not doubt that the assertion that she is depressed is correct, as this is obviously the case, but like other chronic illnesses, reactive depression is a normal consequence of sequelae of chronic, debilitating ill-health. She at this time continues to be in this state, and is aware that the depressive state is a consequence of the toxic exposure, rather than a predisposing factor. She continues to remain significantly unwell, with low cholinesterase levels and clinical symptoms of carbamate toxicity." - 6 - Dr Smart placed reliance on the appellant's low cholinesterase levels as an indicator of continuing organophosphorous poisoning. He introduced the question whether her depression was reactive and was itself a consequence of chronic organophosphorous poisoning rather than an independent explanation of symptoms that did not qualify for compensation. In his evidence on the hearing of the appeal Dr Graham discounted the significance of the appellant's cholinesterase levels. It was known that the appellant had a genetically low cholinesterase level but there was no evidence of her levels before exposure. The appellant provided a table of cholinesterase test results over a period from March 1988 to October 1994. From about mid 1992 her levels increased, but Dr Graham said in his evidence, and Dr Walls agreed, that the levels remained generally low and the increase recorded in 1992 was within a range that could have been attributable to a difference in assay or hormonal change. The Corporation sought a further report from Dr Cliffe. He provided a report on 14 October 1992. He clarified a point about which Dr Smart had been mistaken, that is to say that carbamates do not biodegrade within the body to organophosphorous compounds. That issue tended to eliminate the possible connection between the chronic symptoms and a soil granule carbamate compound called "Temik" to which the appellant had been exposed. Dr Cliffe said that carbamate pesticides are also cholinesterase inhibitors but their effect is short-lived. He said that for a diagnosis of carbamate poisoning there must be an acute and severe clinical picture producing immediate and severe collapse. There was however a history of exposure to organophosphate pesticides. He concluded: "... there is insufficient evidence to link [exposure to organophosphates] with her claim of prolonged ill health. In particular, I reiterate that in order for a chronic intoxication picture to develop there must have been an initial acute and severe exposure: it is insufficient to attribute such symptomatology to chronic low dose exposure, even in an individual with inherited pseudocholinesterase deficiency. Moreover, Mrs Grouwstra worked for only seven months in the greenhouses, has had no exposure to organophosphate compounds for about four years, and yet has disabling persistent symptoms. I remain of the opinion that her primary problem has been one of a depressive disorder." The Corporation then formed a view that the appellant had never suffered personal injury by accident by organophosphorous poisoning. It relied on Dr Cliffe's opinion that there would have had to be an acute episode. That opinion was confirmed by Dr Graham. Dr Graham supplied a further report of 2 February 1994 at the request of the Corporation. It confirmed his earlier views. A review of the Corporation's decision was conducted on 2 December 1992. The appellant gave evidence of her history including her first symptoms, which were serious and which were contemporaneous with her work in the greenhouse. She produced evidence of the change in her capability and her personality and after the -7- hearing she furnished further material to the review officer. That material included a good deal of technical information which the review officer was not able to assess. He considered whether the opinion of an occupational disease specialist might be useful and referred the question to the Corporation's medical adviser who replied as follows: "I believe strongly that the only useful contribution that could be made by an occupational disease specialist would be an opinion as to whether the claimant suffered possible toxicity from agricultural chemicals. This has been accepted. With due respect to such specialists I would point out that the point at issue appears to be whether or not the claimant's ongoing problems stem from that cause and that such a determination is far outside the expertise of such specialists. This required a widely experienced general practitioner who has had experience in assessments of this nature. There are only a handful of such people in this country. If the suggestion is taken up I would suggest Dr D J Gudex of Hamilton or perhaps Professor Ibbotson of Auckland should be asked to review this case." The suggestion of obtaining an opinion from those doctors was not taken up. The review officer asked Dr Graham to comment on the question of causation by exposure to toxic chemicals or otherwise. Dr Graham said: 'I have no knowledge of her pre-accident personality, thought she stated to me that she was a well person prior to her exposure. She also has a persisting low level of pseudocholinesterase and there has been little variation in the results of the assays for plasma pseudocholinesterase levels recorded on her over a number of years now. This is despite there being no ongoing exposure to either organophosphates or Carbamates. It must therefore be assumed that she has inherited deficiency of the enzyme. There is some evidence in the literature that this predisposes such people to increased acute toxicity to organophosphorous and Carbamate compounds, though I can find no evidence to support the likelihood of such people developing chronic toxicity to organophosphorous and Carbamate compounds, nor could I find evidence in the literature on the subject of chronic Carbamate toxicity from short term exposure, and I cannot say therefore whether such a condition exists or not (though it would seem unlikely). A premorbid level of pseudocholinesterase is unknown for Mrs Grouwstra. I am unable however here to make a diagnosis that would explain her persisting symptoms, except that as previously mentioned in my letter of May 1992 there are some mild laboratory abnormalities that have been found (slightly lower levels of immunoglobulin G and some reduction of the C3 component of compliment). Nonetheless I do not believe that a chronic chemical toxicity state is a diagnosis of exclusion. However, I would also accept that the area of chemical toxicity has associated with it considerable controversy." - 8 . The review officer eventually delivered a decision in which he concluded that the weight of the medical evidence was that the appellant's problems are not as a result of poisoning arising from her work and so he confirmed the Corporation's decision. The Corporation's medical adviser's note that it had been accepted that the appellant had suffered toxicity from agricultural chemicals is not quite correct. Two primary issues of incapacity arise under s 37. The first is whether the appellant suffered from chronic organophosphorous poisoning. The second is whether as a result of carbamate or organophosphorous poisoning she suffers from disease or depression by reason of which she is unable to engage in her former employment. The question of secondary depression was not given much attention although it was identified by Dr Smart. If the appellant suffers from a reactive kind of depression by reason of organophosphate poisoning then the question whether she is consequently unable to engage in her former employment may rest on a different basis from incapacity through chronic poisoning symptoms. The question would be whether her fatigue and other symptoms render her unable to perform the work, rather than whether her susceptibility to injury puts her at risk when exposed to pesticides. Although no attention may have been given to the distinction, it appears to have been accepted that the appellant suffers serious symptoms including unusual tiredness after only moderate exertion, so there seems little doubt that she would be unable to resume her former kind of employment even if she was safe from the possible toxic effects of pesticides. In answer to a question in the course of argument Mr Barnett said that the Corporation took the view that the appellant had not in fact suffered toxicity from pesticides. The Corporation's view is that she did not suffer from toxicity either in an acute or chronic form. Of course if that view was wrong the question of reactive depression associated with organophosphorous poisoning would have to be addressed as a disability that qualified under s 37. That is to say that if there is sufficient medical evidence of depression, then the question whether it is a consequence of even a limited period of toxic chemical symptoms has to be addressed. The Corporation contested whether the appellant had suffered from any significant toxic effects sufficient to bring about her present disability either as a chronic disability or as a resulting depressive illness. After the decision on review, which was delivered in June 1994, the appellant's solicitors took up the question of whether there had been sufficient medical and scientific evidence before the review officer. There was a short exchange of correspondence about a question whether the appellant had failed to keep specialist appointments, but that is now of no consequence. Dr Smart referred the appellant to Dr C Walls, a specialist in occupational medicine. Dr Walls reported on 30 January 1995. After referring to the appellant's symptoms and history he said: "Mrs Grouwstra has what amounts to a 'chronic fatigue syndrome' (CFS). As you know this is rather a controversial diagnosis and refers to chronic fatigue - 9 - developing after a viral infection. Considerable speculation exists as to whether this is a psychological or a medical diagnosis though I think most people are favouring the latter (having excluded the former) There is considerable overlap between the symptoms reported for CFS, fibromyalgia and another vogue diagnosis 'multiple chemical sensitivity' which is even less well supported than the former diagnosis. I don't think it unreasonable to use the term 'chronic fatigue' in Mrs Grouwstra's case and consider whether she had sufficient exposure to any toxic substances that have been proven to cause these sorts of symptoms." Dr Walls referred to the literature relating to organophosphorous poisoning, in particular Casserat & Doull, The Basic Science of Poisons 4th Ed. He said, when giving evidence on the hearing of the appeal, that symptoms of toxic origin could follow from heavy exposure causing collapse, or from a series of moderate exposures followed by one that produced symptoms. If the appellant suffered from an inherited pseudocholinesterase deficiency she would probably have been more susceptible and may have shown a more severe reaction. He said that he had discussed the "spectrum of symptoms" with other specialists and obtained some confirmation that they were consistent with specific insults to the human system. He said the appellant did not exhibit typical neurologic or neuropsychiatric symptoms associated with toxic effects. The classic chronic symptoms were not present. He said the appellant's present symptoms were associated with anxiety or stress and are representative of irritable bowel syndrome, they are symptoms of a person chronically unwell. He considered that the original cause was likely to have been exposure to a combination of chemicals. The effect of organophosphorous poisoning is to block the ability of cells to absorb oxygen. The poisoned cells should be replaced in three months and the continuing problems are consequential neuropsychological and neuropsychiatric effects. He said that the appellant did not appear particularly depressed but she fitted the profile of chronic fatigue syndrome. In Dr Walls' view the symptoms had to be traced to a cause and the only cause was to be found in the workplace. He considered that depression had not been established Although Dr Smart had prescribed antidepressants and the appellant had not responded, the dose was too low to have excluded depression as a reason for her current symptoms. Dr Graham also gave evidence. He thought that the pseudocholinesterase reduction had steered the doctors towards a diagnosis of organophosphorous poisoning. Recovery from organophosphorous poisoning could usually be expected in one to three months from exposure. His initial belief that the appellant's low pseudocholinesterase levels might have been inherited were borne out. He referred to Dr Cliffe's diagnosis of depression. He said that there was doubt whether chronic organophosphorous poisoning existed as a real entity. He could not discount the possibility that the appellant had experienced organophosphorous poisoning but as a matter of experience and judgment of probabilities he did not consider that she had. - 10 - From an uneducated perspective there are compelling aspects of evidence that the appellant was exposed to pesticides without protection, that her health was affected in a way she had never experienced before, that other employees exposed to chemicals were also affected in some way, and that she has never recovered her own good health. They all tend to point to a conclusion that the appellant suffered an illness caused by exposure to toxic chemicals and she is still incapacitated by reason of that exposure. She is convinced of that conclusion, she has resorted to literature to inform herself and she and she is supported by Dr Smart and Dr Walls in some of her conclusions. But the issue on appeal has to be weighed according to the probabilities depending on the medical evidence including the oral evidence and the written reports. The Court cannot decide intuitively or without regard to the weight of professional medical opinion. Dr Cliffe's diagnosis, that the appellant's primary problem has been one of a depressive disorder, is not much disputed by the other doctors who have examined the appellant. It was thought probable by Dr Graham in 1992. Dr Smart agrees that she is depressed but attributes it to metabolic illness. Dr Walls thought that she was not depressed but diagnosed chronic fatigue syndrome and wished to see the diagnosis of depression tested by suitable doses of anti-depressants. On the available evidence the predominant medical opinion is that the appellant suffers from depression. No diagnosis can be made to exclude reactive depression as a result of organophosphorous poisoning unless that supposed event can itself be eliminated. The case for the appellant was not advanced on the footing that she suffers from depression by reason of organophosphorous poisoning, but on the basis that she suffers from chronic fatigue syndrome or chronic organophosphorous poisoning. A diagnosis of depression on its own is too general to be linked to a workplace disease or injury. The claim was accepted in 1988 on the footing that organophosphorous poisoning was the probable cause of the appellant's illness. It is now clear that Dr Smart's reasons were doubtful because the symptoms were not in fact typical and the pseudocholinesterase level was not a clear indicator. Mr Barnett for the respondent submitted that Dr Smart's opinion should not be preferred over different specialist opinion, and he submitted also that Dr Smart took an over committed position with which none of the specialists concur. Dr Smart's opinion was not shared by Dr Graham who at that stage was unable to give a diagnosis. Dr Graham did say that the symptoms were consistent with organophosphorous poisoning but at the same time he expressed doubt. He was influenced by the low pseudocholinesterase levels which he later discounted when they did not return to normal levels, thus indicating an inherited abnormality. He eventually rejected chronic organophosphorous poisoning by virtue of incongruity of symptoms and the lack of any history of severe acute organophosphorous poisoning. Dr Cliffe reached the same conclusion, influenced by lack of acute symptoms. He considered that the appellant's symptoms were typical of depression and thought that the depression might be associated with her concerns about organophosphorous poisoning. - 11 - The only opinion supportive of the appellant's case is that of Dr Walls who gave evidence at the hearing of the appeal. He also dismissed the possibility of chronic organophosphorous poisoning because the appellant's symptoms are not consistent with that condition. But nevertheless, he said that after reviewing the toxicological evidence he felt that if there had been a problem to trigger the appellant's symptoms it was most likely an organophosphate, or a combination of several organophosphates, and was probably aided by her genetically lowered serum cholinesterase. He recommended a low dose of a suitable antidepressant to see whether there was some improvement. The dose was not high enough to treat a depressive illness and did not exclude that possibility. He described chronic fatigue syndrome as a diagnosis that needs to be knocked out. He said even he was in two minds about a diagnosis of chronic fatigue syndrome and that he would be assisted by a trial of a suitable antidepressant at a sufficient dosage to determine whether there was a clinic depression. On reviewing the whole of the medical evidence it has to be considered unlikely that the appellant ever had a severe acute episode of organophosphorous poisoning and the clear weight of medical opinion is that she does not now suffer from chronic organophosphorous poisoning. The only viable question on the appeal is whether the appellant suffers chronic fatigue syndrome resulting from organophosphorous poisoning. That itself involves three principal questions, first whether the appellant suffered organophosphorous poisoning (not necessarily a severe acute episode), whether she suffers chronic fatigue syndrome (not clinical depression) and finally whether the chronic fatigue syndrome was caused by organophosphorous poisoning. Dr Walls view is the only specialist opinion favouring the appellant, supported by Dr Smart. Dr Walls practises in a field of occupational medicine and freely acknowledges that he, or another specialist, may have a bias towards diagnosis of causes within his specialist field. Nevertheless he is satisfied that the 1987 exposure was of a kind that could have led to organophosphorous poisoning without an acute episode and that the present symptoms, in his view representative of chronic fatigue syndrome, can be ascribed to the same cause. Medical opinion is divided on the question of chronic fatigue syndrome resulting from organophosphorous poisoning. Dr Graham adheres to a conservative view until more research is available. Consideration has to be given to the fact that Dr Graham is an experienced consultant physician who described his orientation in medicine as towards the specialty of general medicine involving all sub- specialties with expertise in dealing with multi-system disease. Dr Cliffe's opinion is more definite if anything, offering a cause which is not a direct consequence of toxicity, but of anxiety associated with the dangers of exposure. Mr Barnett referred to decisions of the Appeal Authority in Teixeria 28/91 and Crawford 328/89 for the proposition that in consideration of causation the mere fact that the claimant is free of symptoms prior to an accident and has symptoms after the accident does not necessarily establish cause and effect. He referred also - 12 - to decisions concerning the degree of persuasion that a tribunal must have before deciding a question on the balance of probabilities. In this case there are possible causes that are not connected with injury in the course of employment and there is serious doubt whether any such injury occurred. The decision is one that has to be reached with regard to divided medical opinion. On the available evidence, and taking account of the additional evidence available on the hearing of the appeal, I am not able to find that the review officer was wrong in his conclusion. For those reasons the appeal is dismissed. DATED at WELLINGTON this 6 - day of MARCH 19% D A Ongley District Court Judge