Accident Rehabilitation and Compensation Insurance Corporation v Hancock

IN THE DISTRICT COURT HELD AT WELLINGTON Decision No. 38 /99 UNDER The Accident Rehabilitation and Compensation Insurance Act 1992 AND IN THE MATTER of an appeal pursuant to section 91 of the Act BETWEEN ACCIDENT REHABILITATION AND COMPENSATION INSURANCE CORPORATION a body corporate duly constituted under the provisions of the said Act Appellant (Appeal No. DCA 40/97) AND RAYMOND HANCOCK of Blenheim Respondent HEARING at Nelson on the 8th day of December 1998 APPEARANCE/COUNSEL A H Johnson for appellant Respondent in person RESERVED JUDGMENT OF JUDGE A W MIDDLETON The issue in this appeal is whether the appellant should be granted leave to appeal out of time against the decision of the review officer issued on 21 July 1995 in which he held that the primary decision of the appellant was wrong and that the respondent was entitled to cover under s.7 of the Act for his exposure to lead poisoning. The facts which gave rise to the application are that the respondent lodged a claim for cover in 1993 in which he stated that he suffered lead poisoning in 1975 when working as a marine engineer with Cavalier Yachts. 2 On 29 November 1993 the respondent lodged a Gradual Process, Disease or Infection General Practitioner Questionnaire form completed by his general practitioner, Dr Anne Brown. She noted that his symptoms were renal damage and hypertension as a result of having suffered lead poisoning. Attached to that report was the discharge report completed by Dr D Durham, a physician at Wairau Hospital who reported that a number of tests were conducted on the respondent including EDTA tests from which Dr Durham diagnosed that the respondent suffered chronic renal impairment and hypertension secondary to occupational lead poisoning. In his claimant questionnaire the respondent stated that he had developed the condition in 1975 over three weeks when exposed to melting lead fumes in a confined space without protective apparatus. The appellant then obtained a report from Dr W E D Turner, a specialist occupational physician which is dated 15 February 1994 in which his opinion was: "Clearly this man was exposed to lead consistently for a period of 3 weeks in his occupation as a marine engineer and as a result has developed a body burden. Dr Durham has presented his opinion in a letter dated 14/06/93 which I enclose for your information in which he states that 'it seems likely that he has chronic renal impairment and hypertension secondary to occupational lead poisoning'. It would appear from this that the burden of lead he was exposed to for the 3 week period has complexed with his bone and has also affected his kidneys with possible effects upon his brain and blood pressure. The sodium EDTA test confirms complexing of lead to bone and his renal biopsy displays a double pathology namely glomerular sclerosis secondary to hypertension and a tubular pathology namely interstitial nephritis commonly seen when lead is concentrated in the kidney. Perusal of the literature reveals that chronic lead exposure with high body burden over the life time of an individual can lead to chronic nephropathy which will in itself lead to hypertension. Similarly there are numerous published studies on the affects of acute and chronic lead exposure on the central nervous system leading to fatigue, weakness, nervousness, hyperirritability, sleeplessness, anxiety as well as neuropsychological change evidenced by long term memory loss, verbal and visospatial abstraction and reduction in psychomotor speed. Whilst it must be accepted that Mr Hancock's initial symptoms can be put down to acute lead fume exposure the ongoing long term symptom complex in its entirety is more difficult to define in terms of causality. Considering his hypertension one must also take account of his weight [107.9 kg] on 17/06/93 as well as his past history of smoking and lack of exercise. Whilst one can not be one hundred percent sure I would tend to support Dr Durham that there has been some influence on renal function from exposure to lead as well as accepting that his hypertension has also played a part. I believe these two factors have acted in concert rather than one particular factor dominating to produce the renal pathology. Thus, it must be concluded that Mr Hancock has, at least in part, an occupational lead poisoning affecting renal function. I am less convinced in respect of the effects of lead on the central nervous system particularly in the light of the fact that there are some elements of depression evident in his present emotional make up. Indeed, at my 3 consultation on 05/11/93 I recommended to his general practitioner that he be prescribed a course of anti-depressant medication on a trial basis.' The appellant then sought the advice of Dr Keir Howard, a consultant in occupational medicine, who provided a report on 4 May 1994 in which he raised doubts regarding the cause of the respondent's hypertension and renal dysfunction. He considered that lead exposure may be associated with renal damage but stated that this was not common and was only encountered after long periods of chronic exposure. Dr Howard said that he was not convinced that lead was the primary cause in the respondent's illness. As a result of that report the appellant notified the respondent that his claim for cover was declined. The respondent applied for a review of that decision and prior to the review hearing submitted a report from Professor Bill Glass, an occupational medicine specialist. As that report gives a detailed history, I propose to refer to it in full. The report was received by the appellant on 14 February 1995 and states: "Mr Hancock's Work With Lead - 1975-1976 Cavalier Yachts During his employment with Cavalier Yachts in Auckland Mr Hancock had a three week job cleaning out the lead from steel moulds which had distorted during the lead pour. In order to do this he used an MMA arc welding machine. He worked at this job five hours a day for five days a week for three consecutive weeks. The working space was not large: 10 m x 5 m x 3 m high. There was no general nor local ventilation, no masks were provided. Mr Hancock was unaware of any hazard to health. He told me 'you could not see across the room for the fumes'. Corroboration of the working situation is provided by a note from Alvin Crosby, a fellow worker at the time. 'Dear Ray I am writing to confirm that I was employed as an Electrician by Cavalier Yachts Ltd, of 81 Ellice Road, Glenfield, Auckland from 1975-1977. My duties were carried out in association with yourself and the late Mr Ron Ludolph. On numerous occasions I witnessed health damaging situations which concerned me at the time. These were mainly the lack of proper factory ventilation and inadequate fume extraction, especially with welding fumes from lead contaminated steel keel moulds, styrene fumes from the fibreglass shop and excessive airborne glass fibre from grinding. Although I generally avoided these situations my health suffered for years afterwards from this working environment. This was the main reason I quit my job as my eyes were badly scoured, not to mention my lungs. Also my blood lead level was high, since then I have taken steps over the years to reduce it to a safe level.' Apart from this specific exposure to lead at Cavalier Yachts, Mr Hancock did general marine engineering, repairing motors and grinding headstays. Keels were hung in this general work area and were disc sanded from time to time. This resulted in a degree of general lead dust contamination of the work place. 4 In summary then from the history Mr Hancock gave me he worked in a lead dust contaminated work environment for a two year period during which time he carried out a particularly hazardous lead burning/welding job for a three week period. The Effects of Lead on Mr Hancock's Health 1. The Acute Exposure Episode in 1975 In the second week of this task Mr Hancock developed chest tightness, difficulty in breathing and severe throat irritation. He had some chest soreness and felt generally unwell with nausea and abdominal pain. He told me he thought his 'stomach ulcer' had flared up. From his story and his comments of the company doctor's view, there was a blood test done, but not apparently for lead, no spirometry and he was told to go back to work . In retrospect it would appear that this illness represented the acute irritant effects of welding fumes, together with acute lead poisoning with nausea and stomach pains. 2. Chronic Exposure 1975/1976 From the history already given, he continued to work in a lead dust contaminated environment. He would have therefore absorbed low doses of lead for the next year or more but with no further evidence of clinical symptoms. 3. Mr Hancock's Subsequent Health Dr Turner notes that Mr Hancock developed general symptoms towards the latter part of 1977 with: poor sleep patterns . . increasing tiredness tingling in his hands and feet irritability . . . poor concentration port (sic) short term memory These symptoms continued and developed during the period up to 1987. My interview with Mr Hancock indicated some worsening of these symptoms, particularly 1979-1987. Interpretation of these symptoms have led to some conflict of views between Dr Turner and Dr Howard who was asked to review the file for the ACC. 5 Mr Hancock worked long hours from 1977-1979, six to seven days a week, 12 hours a day, at machine engineering work. Such work intensity could in itself account for poor sleep patterns, increasing tiredness and irritability. However, there is another feature to this story and this relates to Mr Hancock's alcohol intake. This history is of importance when considering lead poisoning as alcohol in sufficient amounts can lead to a release of accumulated bone lead back into the blood stream and excretion through the kidney. I would at this point like to comment on the toxicokinetics of lead (ie the behaviour of lead in the body) as I believe it is most relevant in this case. Blood is the major transport medium for lead after uptake into the body from the lungs and/or the alimentary system. The blood transports the lead to the body tissues where it accumulates and after a time is released, re-enters the blood circulation and is excreted via the kidneys. Accumulated lead is mainly sequestered in the bone, the cortical bone and the trabecular bone. It is believed that there is a three compartment model whereby the lead turnover (half life) is about one month for the soft tissues, about one year for trabecular bone and decades for cortical bone. Thus, after exposure to lead, as in the case of Mr Hancock, the absorbed lead is distributed according to the above pattern with the bulk of the absorbed lead settling in the two bone compartments. Mobilisation of absorbed lead can occur as a result of alcohol intake, flue like illness and chelation tests. It is likely that the soft tissues and the trabecular bone are the main sources of such 'mobilised lead' and also that it is lead from these two body compartments which cause lead toxicity. Now let us return to Mr Hancock's alcohol intake. When I took his history he indicated to me that his symptoms as listed tended to become more marked between 1979-1987. His alcohol intake pattern was as follows: 1975-1976 Very modest 1977-1979 Much the same - he was working too long hours to drink much 1979-1981 Three to four bottles a day 1982-1987 Regular drinking at above level continued It is thus reasonable to relate his increasing symptom severity to the effect of his heavy drinking on his accumulated body burden of lead (in particular trabecular bone lead). 6 As a consequence there would have been a continuing excretion of lead from his blood through his kidneys with the possibility of consequent damage to the kidneys. Dr Turner makes the point that Mr Hancock was a heavy man and had a past history of smoking and these factors also need to be taken into consideration as far as his blood pressure is concerned. Dr Durham's Evidence Dr Durham saw Mr Hancock on 28 June 1994 at Wairau Hospital. At this time it was noted that Mr Hancock had: ischaemic ECG changes exertional dyspnoea drinking 2 litres of beer a day quite overweight - 107.9 kilograms blood pressure - 256/148 ex-smoker - 5 years Dr Durham notes that he has: 'accelerated hypertension with renal impairment and possible chronic lead poisoning' whole blood lead 0.5 micromols (N=0.28-08) red blood cell lead 1.05 seconds (N=0.5-1.9) urinary led (24 hours) 0.1 micromols (N=0-0.72) Subsequently, Dr Durham carried out a diagnostic chelation test with a rise in urinary led to 1.3 micromols. This was confirmed with a subsequent test. A discussion with the late Professor Neale of Wellington resulted in Dr Durham carrying out a kidney biopsy. I have no copy of this but in Dr Durham's letter to Dr Ann Brown it is stated that: This doesn't show any specific other glomerular nephrology sclerosis which may be due to his hypertension or related to his interstitial nephritis which is also seen with lead.' Dr Durham goes on to say: 'At least this means we don't have to treat any other condition just to carefully control his BP and look at treating his overload.' This Dr Durham proceeded to do with ongoing chelation therapy. In a letter to Dr Ann Brown, 17 November 1993, Dr Durham notes: Ray's last EDTA excretion showed normal led level so we may have cleared his bones of excess lead.' 7 My Comments The evidence is clear that in 1993 Mr Hancock had excess lead in his body (chelation test positive). It is clear too that this resulted from his exposure some 18 years previously as recorded. It is my view that his symptoms (1979-1987) as noted by Dr Turner and confirmed at my interview could largely have been explained by alcohol mobilisation of accumulated trabecular lead. What then of his hypertension? This issue is not completely black and white as to causation. However, I believe lead exposure cannot be discounted as one of the factors in the development of Mr Hancock's blood pressure and I would thus concur with Dr Turner. My Opinion I believe Mr Hancock suffered serious ill health effects particularly over the period 1979- 1987 as a consequence of the mobilisation of his body burden of lead which occurred during his work at Cavalier Yachts. I am also of the view that this lead absorption and subsequent excretion over the years was an important factor in the development of his hypertension." When it received Professor Glass's report the appellant again sought the views of Dr Howard who said that he accepted Professor Glass's interpretation of the data as being plausible but was unconvinced that the urine lead levels which he considered excessively high were sufficient to induce renal damage. The review hearing took place on 6 July 1995 when the respondent and his counsel were present but the appellant was not represented. The review officer concluded that on the basis of s.7(1)(a) the nature of the appellant's employment task had a particular property or characteristic which caused or contributed to his disease, particularly having regard to the opinion of Professor Glass. He also found that the respondent satisfied the other provisions of s.7 and that he was entitled to cover because of his exposure to lead. Thereafter the respondent applied for various entitlements under the Act including loss of wages. The appellant requested Dr Brown to provide a certificate that the respondent was unfit for work and in doing so Dr Brown noted that the original date of disability due to lead poisoning was 14 June 1993 being the date upon which the respondent was admitted to Wairau Hospital. In a subsequent query to Dr Brown on 18 March 1996 the appellant requested her advice as to whether she had seen the respondent on a regular basis since 14 June 1993 and whether she could certify him as being unfit for work since that date. On 18 April 1996 Dr Brown replied that the respondent had stopped work due to headaches and his admission to Wairau but 8 that he had since developed angina for which hypertension was one of the risk factors. Dr Brown said that hypertension was one causative factor for a multifactoral disease. The result of these reports was that the appellant was concerned as to what was the respondent's predominant condition and referred the respondent to Dr A McDonald, a consultant nephrologist, for his opinion concerning the relationship between hypertension and lead nephropathy. After examining the respondent Dr McDonald reported on 11 August 1996 that on balance there was circumstantial evidence to incriminate lead as a causative factor in the respondent's hypertension and renal impairment. As a result of further doubt the appellant requested the opinion from Dr J Alchin who stated on 23 September 1996 that it was unlikely that the respondent's alleged exposure in 1975 was a significant contributor to his renal failure. Dr Alchin noted that he had referred the matter to the Nephrology Department at Christchurch Hospital for an opinion as a result of which Dr R Bailey, a nephrologist at the hospital, considered that there was little evidence to incriminate lead nephropathy and recommended that a report be obtained from Professor B T Emmerson of Brisbane, a worldwide authority on that particular issue. Professor Emmerson provided the appellant with his report which is dated 23 November 1996 and states: "I have perused the complete file on this patient on several occasions, the first time before obtaining further specific details of his EDTA test in 1993 and the second time after this was available. Most of the reports have assumed that the EDTA test was abnormal and, on this basis, have judged lead to be responsible for his hypertension and nephrosclerosis. Studies of the lead excreted in the urine after the administration of EDTA are generally accepted as reflecting the amount of chelatable lead stored in the body and thereby reflect the amount of lead which has been absorbed, particularly that which is in soft tissues and which is in equilibrium with bone lead. Renal insufficiency of any degree with increase the movement of lead stored in bone into the soft tissues and will thereby increase the amount of lead excreted into the urine after EDTA. In this patient, there had been an 18 year interval between the exposure in 1975 and the administration of EDTA. He also had some renal impairment at that time. In this case, data are available on two occasions when the patient received EDTA. On the first occasion, the increase in lead excretion was 1.2 umols (subtracting what would have been excreted without the EDTA from what was excreted) and on the second occasion the increase was 3.1 umols. On the second occasion there was a slight carry over the increase to the second day which is to be expected from the degree of his renal insufficiency. Even if some allowance was made for this on the first occasion, I would conclude that the amount of lead excreted after EDTA was within the normal range on both occasions. This is in contrast to the report from the 'Christchurch laboratory' which quoted normal as being less than 0.72 umols per 24 hours. My studies have indicated that the normal range certainly goes up to an increase of 3 umols, and 3.1 is not significantly different from this. 9 In justifying this interpretation, I would refer you to an article I wrote in 1963 (Australasian Annals of Medicine, Vol 12. Pp 310-324) (enclosed) which I believe sets out the response to an EDTA infusion in patients with (i) normal renal function, (ii) chronic lead nephropathy, (ifi) chronic renal disease not due to lead, and (iv) a number of patients with a history of industrial lead absorption. (In this particular study, the results are given in milligrams and one needs to use a conversion of 3 umols of lead as being equivalent to 0.6 milligrams or 600 micrograms). The increase in lead excretion after EDTA in the normal and control groups can range up to 3 umols or 0.6 milligrams. In particular, may I refer you to the short paragraph on page 317 relating to patients with previous industrial exposure. Subsequent to this article, I undertook EDTA testing for a further 20 years or so and nothing that I saw in that time indicated to me a viable alternative to the upper limit of normal of about 3 umols or 0.6 milligrams. Thus, the increase in Mr Hancock was at the upper limit of normal and this was not consistent with his having had a greater past lead absorption than would be seen in most healthy people in the community. Studies undertaken in the USA and elsewhere with EDTA tests have again confirmed an upper limit of normal values of approximately this amount. Thus I question the basic assumption on which all these reports were made, namely that there was excessive excretion of lead after the EDTA infusion. As such, lead no longer becomes an important potential causative substance. In general, patients with significant past industrial lead absorption excrete many time this amount of lead after EDTA. I would also concur with the generally expressed view of your renal consultants that lead damage to the kidney from industrial exposure results principally from very prologued and relatively high level exposure to lead, not that from an acute exposure over a short period. The presence of some renal insufficiency at the time when the EDTA infusion was given, also increases my confidence that the EDTA-induced lead excretion would be increased rather than normal if there had been an underlying lead etiology for the renal disease or excessive lead absorption in the past. There are a few additional features against the presence of lead nephropathy, none of which is absolute, but which taken together make it unlikely. Firstly the kidney size was normal and kidney size is usually symmetrically reduced in chronic lead nephropathy. In addition, hyperuricemia is usually present in chronic lead nephropathy and also the degree of proteinuria is usually mild and not as high as is recorded in this patient. The renal biopsy does not really help one way or another. Thus, my conclusion is that there is no evidence that excessive past lead absorption has caused this man's renal insufficiency and hypertension. In general, I would be supportive of the views put forward by Dr Keir Howard and of the nephrologists who have given you reports. I'd be happy to elaborate further on any of these aspects if they are not clear." When that report was received the appellant concluded that it had sufficient information to proceed with an appeal and consequently the application for leave to appeal was filed on 19 February 1997. 10 The issue before me is whether the appellant is entitled to succeed on its application for leave to appeal the review officer's decision. The issue falls to be determined on the principles enunciated by Mr Justice Casey in Mcdougall v ACC (1983) 4 NZAR in which he set out the criteria which should be applied in determining whether to grant leave to appeal out of time against a review decision under the Accident Compensation Act 1982. He considered that the fundamental question was whether it was just to grant the extension and the factors which should be considered in making a decision. "1. The length of the delay beyond the time allowed. 2. The reasons for the delay. 3. The strengths or merits of the applicant's case. 4. The prejudice to the respondent if the extension is granted." Length of Delay The length of the delay is almost 18 months which by itself is inordinate, but may not necessarily be fatal if the merits warrant relief. Reasons for Delay The appellant has submitted that at the time of the review officer's decision the medical evidence was contradictory or even ambiguous, particularly having regard to the opposing views of Dr Howard and those of Dr Turner and Professor Glass. It is submitted that until it heard from Dr Brown in April 1996 as to the respondent's then condition that the appellant considered further evidence needed to be obtained. It was not until it received Professor Emmerson's report that the appellant felt that it had sufficient evidence to support the application for leave to appeal. The respondent considers that there was a concerted effort on the part of the appellant to find evidence which supported its opinion and thus avoid the cost of the respondent's compensation. Merits of Appeal The principal issue in applications of this nature is usually whether the merits of the appeal warrant the grant of the application. In support of the application the appellant has submitted: "1. It is submitted that the medical evidence now available demonstrates that there is no causal link between the respondent's exposure to lead and his symptoms. 2. In this case there have been an unusually large number of specialist opinions obtained. The appellant relies primarily on the medical opinion of Professor Emmerson who concluded that there is no evidence that excessive past lead absorption had caused the respondent's renal insufficiency and hypertension. 11 3. It is respectfully submitted that Professor Emmerson's opinion ought to be given substantial weight. In determining whether the respondent's exposure to lead caused his symptoms it is necessary to ascertain whether the respondent has excessive lead in his body. The 1993 EDTA test were conducted for this purpose. The central issue then concerns the proper interpretation to be given to the 1993 EDTA test results. Professor Emmerson is of the opinion, having analysed the 1993 EDTA test results, that the respondent's lead levels were normal. 4. Professor Emmerson has conducted EDTA testing for at least 20 years. He has written articles as far back as 1963 on the subject. As Dr Bailey stated in his correspondence dated 2 October 1996, Professor Emmerson introduced the EDTA mobilisation test and its interpretation and is a world authority on this area. Dr Durham who conducted the 1993 EDTA test results also acknowledged in his correspondence of 16 December 1996 that Professor Emmerson is a world authority. Given Professor Emmerson's experience in this area it is respectfully submitted that his opinion ought to be accepted. 5 . Insofar as the other specialists are concerned they appear to be evenly divided over the issue of causation. Dr Durham, Dr Turner, Dr Mcdonald and Professor Glass supported a link between the respondent's symptoms and his exposure to lead. It is respectfully submitted that, given that their opinions are largely based on the false assumption that the 1993 EDTA test results showed that the appellant had excessive lead in his body, their opinions ought to be given little if no weight. 6. In respect to the opinions of Dr Howard, Dr Alchin and Dr Bailey each considered it unlikely that the respondent's symptoms were caused by his exposure to lead in 1975. These specialists did not believe that there was evidence of high levels of lead in the respondent's body. Dr Alchin and Dr Howard considered it most unlikely that the respondent's brief history of lead exposure would have caused his present symptoms. Dr Alchin pointed out that such symptoms ordinarily arose from lead exposure only after heavy and prolonged exposure lasting 10 years or more." The respondent appeared on his own behalf because he was unable to afford representation, but he did so in support of very extensive submissions prepared by his counsel to which were attached various extracts from medical and scientific journals relating to the issues before the Court (which documents are now on the file) and to which reference is made in the extensive submissions. The respondent submitted that the only specialists who examined him were Dr Brown, Dr Durham, Dr Turner, Professor Glass and Dr Mcdonald. In contrast to that, the appellant seeks to rely on comments made by other specialists to whom I have already referred but who have not examined the respondent. The respondent submitted that regard should be had to Dr Mcdonald's statement that: "In summary there is a short documented lead exposure, an absence of gout, there is a positive EDTA test for an elevated urinary lead and a biopsy that would be compatible 12 with lead nephropathy. On balance I think that there is circumstantial evidence to incriminate lead as a causative factor in this man's hypertension and renal impairment." It is submitted that that finding is in contrast to the finding of Dr Alchin who did not think that it was likely that lead was a major contributor. However, the opinion of Dr Bailey, the nephrologist who did not examine Mr Hancock was "it was possible his initial exposure may have given him acute lead poisoning" and he concluded "my own view is that there is little evidence to incriminate lead nephropathy, but I suggest the best thing you could do would be to contact Professor Emmerson." It was as the result of that opinion that the appellant obtained Professor Emmerson's report. Thereafter, in his submissions the respondent has detailed the submissions which he considers demonstrate that the Court should not follow Professor Emmerson's opinion. The respondent submits that the first EDTA test level was 1.2 umols, the second 3.1 umols which Professor Emmerson considered to be within normal range. The respondent submitted that Professor Emmerson's opinion was based on his study from 1963 whereas the Christchurch Laboratory considered the normal to be less than .72 umols. The respondent then refers the Court to Professor Emmerson's article in "Kidney International" at page 2 in an article on chronic lead nephropathy which states: "Moreover the US cases failed to show an increase in urinary lead after the administration of EDTA, a finding which led Chisholm to conclude that lead absorption in the Queensland cases must have been of a much more prolonged variety, whereas that in the US cases would have been more acute." In that report Professor Emmerson went on to say: "studies undertaken in the USA and elsewhere with EDTA tests have again confirmed an upper limit of normal values of approximately this amount." In an article in the "Environmental Health Perspectives Volume 78 in 1988", Richard P Wedeen of the VA Medical Centre, East Orange, New Jersey, in relation to lead hypertension and lead nephrology noted: "Also the generally accepted upper limit of normal for the EDTA lead mobilisation test of (3.1 umols lead chelate/day) is undoubtedly too high." The respondent then submitted: "Professor Glass's report and the ILO Encyclopedia of Safety and Health page 1202 both consider that alcohol and flue mobilise lead back into the system from storage in the bones. Professor Glass 'mobilisation of absorbed lead can occur as a result of alcohol intake, flue like illness and chelation tests'. 13 ILO 'drinking bouts and sports activities during weekends may precipitate an attack due to mobilisation of lead from accumulations'. Professor Emmerson makes no mention in his report of anything other than EDTA mobilising lead.' The respondent then referred to an article in the "Canadian Centre for Occupational Health and Safety Issue", August 1998 which states: "It can take more than 20 years for half of the inorganic lead in the bones to be removed from the body." The respondent submitted that this was in line with Professor Glass's report that: 'I believe Mr Hancock suffered serious ill health effects particularly over the period 1979-1987 as a consequence of the mobilisation of his body burden of lead which occurred during his work at Cavalier Yachts. I am also of the view that this lead absorption and subsequent excretion over the years was an important factor in the development of his hypertension." The respondent submitted that on that basis Professor Emmerson's report could not be regarded as conclusive. As Dr Durham had already noted that there was a "variation in the literature" and the fact that Professor Emmerson had not personally examined the respondent. The respondent then referred to the fact that Professor Glass had made special mention of the storage of lead and the mobilisation leading to more damage in his report of 1995 when he particularly stated: "Accumulated lead is mainly sequestered in the bone, the cortical bone and the trabecular bone. ' Mobilisation of absorbed lead can occur as a result of alcohol intake, flue like illness and chelation tests'." The respondent submits that this opinion is supported by the "Canadian Centre of Occupational Health and Safety Issue" August 1988 at page 5 in which it notes: "Some lead is not excreted, but is stored in the bones and accumulated in the body. It can take more than 20 years for half of the inorganic lead in the bones to be removed from the body. Lead which is released from the bones can cause health effects, even if there is no current exposure to lead. In some cases lead can be rapidly released from the bones because of fractures, infections or other stresses on the body." Numerous other references are made from various extracts from encyclopedias and health authorities all along similar lines. Reference is made in the articles by Professor Glass to the presence of gout which was noted in Dr Durham's report when he stated: "Diagnosis - Unstable angina, hypertension, chronic renal failure, gout, chronic lead poisoning." 14 That issue is further expanded by Dr McDonald in his report of 1996 when he said that: "There is a curious relationship between gout, hypertension and renal impairment. Mr Hancock has never had proven gout and interestingly his uric acid level was normal in 1993 although I see it elevated recently to a level of 0.56 mmol/1. Mr Hancock continues to suffer from gout or gouty arthritis and regularly requires medication for it." The respondent takes issue with Professor Emerson's failure to make no mention at all of whether the respondent had gout or not, particularly having regard to his article in Kidney International 1973 Volume 4, page 4 at note 19 where he noted: " Emmerson recorded that 50 percent of his cases with chronic lead nephropathy had, at one time or another, suffered from acute gout arthritis." As to the issue of whether the respondent's present problems, including hypertension may have been the result of lead absorption, the respondent again referred to Richard P Wedeen's article on "Bone Lead, Hypertension, and Lead Nephropathy" issued in 1998 in which he stated: "A relationship between lead, high blood pressure, and disease of the kidneys. There is now considerable evidence that excessive lead absorption causes slowly progressive renal disease and that lead predisposes individuals to hypertension even in the absence of detectable renal failure. In adult lead workers, transient hypertension is common during the acute phase. Continuous lead absorption at levels insufficient to produce the hallmarks of acute intoxication, increases the body burden of lead and can induce hypertension, interstitial nephritis, and behavioural abnormalities after a few years." That is in contrast to Professor Emmerson's report regarding hypertension which was: "There is no evidence that excessive past lead absorption has caused this man's renal insufficiency and hypertension." Again, the respondent takes issue with Professor Emmerson's own article in the "American Journal of Industrial Medicine 1994, Occupational Exposure to Lead, Kidney Function Tests and Blood Pressure" at page 641 where the Professor stated: "Previous studies on cardiovascular mortality under conditions of moderate exposure to lead have suggested that kidney damage was the etiological factor involved in the association between lead and hypertension. (Emmerson, 1973; Batuman et al, 1983) Uncertainty persists about whether chronic exposure to lead causes hypertension and hypertension induces renal damage, or whether lead accumulation in the kidneys induces subclinical renal dysfunction, which in turn leads to hypertension or, yet again, 15 whether these effects are not related to one another (Sharp et al, 1988). The absence of correlation between enzymeria and blood pressure and the kidney are independent and that they do not reflect the extent of renal involvement, at least during the initial stages of lead action." The respondent referred to an article by Joel Schwartz in Environmental Health Perspectives Volume 91, pages 71-75 issued in 1991. Under the heading "Lead, Blood Pressure, and Cardiovascular Disease in Men and Women" Mr Schwartz stated: "Using electrocardiogram data from NHANES II, this study confirms the expected association of lead with left ventricular hypertrophy. Such an association with permanent cardiovascular changes adds weight to the blood pressure findings. The NHANES II included electrocardiograms as well as blood pressure measurements, and the association of lead with both outcomes was examined. Prospective studies of cariodvascular disease, such as the Framinghjam study (21), clearly demonstrate that the risk of cardiovascular disease varies continuously with blood pressure. No plausible reason exists to assume that increases in blood pressure due to lead exposure would not have the same impact. Left ventricular hypertrophy is also a prevalence, rather than incidence measure. This increases the power to detect a direct cardiovascular impact of lead. The findings of a significant association between blood lead levels and left ventricular hypertrophy in both men and women leaves little doubt that lead exposure is not merely raising blood pressure but producing the expected cardiovascular impacts." The respondent submits that again Professor Emmerson makes no mention of left ventricular hypertrophy based on his 1963 research. I do not propose to quote from all the literature which is now on the file. I have identified some of the submissions which the respondent has made in support of his contention that while Professor Emmerson says that he supports the views of Dr Howard even his own research and that of others in the field over a number of years appears to contradict some of his statements. Prejudice to the Respondent While the appellant submits that there is little or no prejudice caused to the respondent by the delay as he had been advised in May 1996 that the appellant was reconsidering the extent of its responsibility to the respondent in the light of Dr Brown's diagnosis. I consider that there has been a considerable prejudice to the respondent in that he has been put to the task of defending the position and particularly assembling the medical evidence to answer the report of Professor Emmerson. To that extent he has been involved in considerable expense by way of legal fees in a vast amount of research into the medical aspects of the claim. The issue under s.71(a) is whether working conditions at the time caused or contributed to his disease (emphasis mine). While the evidence may not go so far as 16 to satisfy the contention that it caused it is certainly clear to me on the balance of probability that his exposure to the lead while working at Cavalier Yachts did certainly contribute to the respondent's present medical condition. As I have already said, I have concluded that on the merits the appellant would not be successful if its application for leave to appeal was granted. I consider that on the totality of the evidence the exposure to lead fumes in 1975 certainly contributed to the respondent's present condition. In making that decision, I have come to the conclusion that while Professor Emmerson was provided with all the material on the file he may not have been made aware of the wording of s.7(1)(a). He may not have been alerted to the fact that under that section it is only necessary to establish that the exposure made a contribution to the condition. The application for leave to appeal out of time is declined. The appellant has been put to considerable expense by way of legal fees and his counsel has provided the Court with extensive submissions and excerpts from various scientific journals which have been of great assistance in reaching this decision. There will therefore be costs to the respondent of $5,000. While the respondent requested a grant of compensation that is not within my jurisdiction. DATED at WELLINGTON this 23" day of February 1999 bwoundaldin A W Middleton District Court Judge Dca4097.doc(rd) IN THE DISTRICT COURT HELD AT WELLINGTON Decision No. 38 /99 UNDER The Accident Rehabilitation and Compensation Insurance Act 1992 AND IN THE MATTER of an appeal pursuant to section 91 of the Act BETWEEN ACCIDENT REHABILITATION AND COMPENSATION INSURANCE CORPORATION a body corporate duly constituted under the provisions of the said Act Appellant (Appeal No. DCA 40/97) AND RAYMOND HANCOCK of Blenheim Respondent HEARING at Nelson on the 8th day of December 1998 APPEARANCE/COUNSEL A H Johnson for appellant Respondent in person CORRIGENDUM TO RESERVED JUDGMENT 38/99 The penultimate paragraph on page 16 commences "The appellant". That is incorrect and should be corrected to commence "The respondent". DATED at WELLINGTON this day of March, 1999 Devinadub A W Middleton District Court Judge Dca-4097.doc(rd)