Anderson v Accident Rehabilitation and Compensation Insurance Corporation

Decision NO 230/97 IN THE DISTRICT COURT DCA 69/95 HELD AT AUCKLAND BETWEEN JEFFREY STEVEN ANDERSON Appellant AND ACCIDENT REHABILITATION AND COMPENSATION INSURANCE CORPORATION Respondent Date of Hearing: 20 June 1996 Date of Judgment: 13 November 1997 Counsel: SJ Ewen for Appellant AE Howman for Respondent RESERVED JUDGMENT OF JUDGE JH LOVELL-SMITH Solicitors: Cairns Slane Barristers & Solicitors, DX CP24005, Auckland for Appellant Bell Gully Buddle Weir, DX SX11164, Wellington for Respondent [PA\LOVELLJ\DECISION\ANDERSON.DOC sb] 2. Course of the Hearing This matter was adjourned sine die on 20 June 1996. The purpose of the adjournment was to enable additional material provided by Counsel for the Appellant to be placed before Professor Glass, an occupational medicine specialist, for his expert opinion. A joint letter of instruction from the parties was sent to Professor Glass on 23 July 1996 requesting his comments. Professor Glass provided a report and covering letter dated 5 November 1996. His report did not refer to the additional material for which comment had been sought. It transpired that this additional material never reached Professor Glass. Accordingly a further joint letter of instruction and the additional material was sent to Professor Glass in February 1997. Professor Glass' subsequent report and covering letter were received by the Corporation in May. Both are dated 5 November 1996 but were prepared in or about February 1997. Both counsel for the appellant and respondent then made further written submissions. I am obliged to Counsel for their careful and comprehensive submissions. Background The appellant was a self employed contractor and claimed compensation due to incapacity through his work as an agricultural contractor spraying herbicides. The 3 . appellant gave evidence at the review hearing. The appellant said that he commenced spraying on or about 20 October 1991 which was the first job he had undertaken of this nature. He had been contracted to a farmer who supplied the chemical "Grazon" for the eradication of gorse. The farmer asked him to use an unmarked container described by the farmer as marker dye to confirm that the gorse had been sprayed. The appellant mixed the "marker dye" with the Grazon which was contained in a chemical tank on his tractor. The appellant proceeded to spray the gorse. There was no sign of dye on the plants so he put more of the substance from the unmarked container into the tank and resumed spraying. The appellant was wearing a singlet and overalls with no face mask or respirator and probably wore a sun hat. The day was fine and calm. He applied some 900 litres of chemical and during this operation the chemical drifted and made contact with his exposed face, hands and arms. Halfway through the day his overalls were removed down to his waist and he completed the work over a period of some seven to eight hours. He used the substance the farmer had told him was marker dye only on the first day as it did not appear to be working. The whole job took a week. Over the next two or three days however, the muscles in his legs, arms and whole body felt as if he had strained them. He described the symptoms as similar to those experienced after a hard game at rugby league. He finished the work and did not tell the farmer as he was not so disabled as to be unfit for work nor did he complain of any problems. 4. The appellant's condition worsened however, and he saw his general practitioner in November 1991. By that time he had sores around his eyes and his general practitioner had to lance them. In February or March 1992, the appellant asked the farmer what was contained in the unmarked can. Because the appellant did not obtain a straight answer from the farmer he returned later to take a sample that was subsequently identified as paraquat by a relative of the appellant who was a registered chemical applicator. He also took a sample to Lee Patersen, a homeopath who identified the substance as paraquat. The appellant also obtained a description of paraquat from the manufacturers which conformed with a sample he had taken. The appellant was originally examined by his General Practitioner, Dr Devcich. Dr Devcich had first seen the appellant in October 1991 and concluded that he had developed multi site arthritis. The corporation wrote to the appellant on 24 February 1994 advising him that his claim had been declined because he had supplied insufficient medical evidence to establish his exposure to paraquat and to confirm that such exposure was the cause of his symptoms. The appellant applied for a review of the corporations decision. Dr Devcich wrote to the corporation on 4 May 1994 and reported that the appellant's symptoms included swollen joints on the right and left hands, end of 5 . wrists and swollen and restrictive movement of pronation and supination, dry skin on both hands, blistering of thumbs and fingertips, hardening of the right thigh muscle and calcification of that muscle and tenderness and pain about the left knee. Dr Tye provided the corporation with a report dated 20 May 1994. He reported that the appellant was suffering from some restriction in the movement of his fingers and that he suffered from other joint problems. He recommended an expert examination. Lee Petersen, the homeopath, wrote the corporation on 10 June 1994 confirming that the chemical to which the appellant had been exposed was paraquat. The corporation referred the appellant to Dr Dryson who provided a report of 6 September 1994. He had previously examined the appellant and included a copy of his previous report dated 22 April 1994. Following the review hearing, the review officer referred all the information he had to Dr Dryson, an Occupational Medicine Specialist. Dr Dryson confirmed he had seen the applicant on 29 March 1994. In his report of 6 September 1994 Dr Dryson stated: The difficulty with these claims is that the symptoms do not correlate with the known and published symptoms relating to acute poisoning by these agents, and the long-last nature of the symptoms are also not consistent with an acute poisoning. Published data on chronic (that is, long term) poison by pesticides are usually confined to measurable outcomes like cancer, and adverse reproductive outcomes. It is not the case therefore that Mr Anderson has been poisoned in the classical toxicological sense. 6. It is claimed by some people that pesticides and other chemicals can adversely affect people's immune systems, and so produce multi-system symptoms. There is currently however no plausible explanation as to how the immune system is affected, since tests of immune function in people with these reputed conditions have shown no consistent pattern. Similar multi-system disorders, such as chronic fatigue syndrome, as known to occur in people with no chemical exposure. In that case, a viral infection has been implicated as a possible cause. So even if an immune dysfunction can be shown, it cannot be said with certainty that the chemicals caused it. In the midst of all this uncertainty therefore, and with no tests available which would help to establish causation, I have to say that it has not, and cannot, be established that Mr Anderson has suffered personal injury by accident, or by gradual process as a result of his exposure to chemicals." The review officer declined the applicant's application for review in a decision dated 21 October 1994. The review officer formed the view that the specialist opinion by Dr Dryson did not provide a basis to accept that the appellant's symptoms and incapacity are attributable to chemical exposure. The appellant's appeal against the review officer's decision was to be heard on 14 February 1995, but the matter was adjourned to enable further medical evidence to be obtained. Further Evidence The appellant obtained two further medical reports. The first report was obtained from Dr R. R. Grigor, a visiting rheumatologist dated 13 March 1995. He examined the appellant in early 1995. The appellant had complained of a three year history of muscular skeletal symptoms which appeared to comprise his forearm, wrist and 7. fingers. The appellant also complained of blueness of his toes. Dr Grigor concluded that the appellant was probably suffering from dermatomyositis. A report dated 1 March 1996 was provided by Professor Bill Glass. He reviewed the appellant's history and the previous medical opinions and he considered the types of chemicals to which the appellant had been exposed and the circumstances in which the appellant claimed exposure had taken place. Professor Glass described the health effects suffered by the appellant during and after spraying: Physically the demands associated with spraying were far less than those with shearing and he did not suffer any musculo-skeletal aches or pains as a result. On most days after a days spraying Jeff felt "crook", he was headachy, nauseous and off his food. He also had what he described as "muscle tightness" most noticeable ankles, hips and shoulders Although he felt better next morning as far as his general symptoms were concerned, there was usually a stiffness in his muscles which took an hour or two to disappear. He also noticed a burning and blistering of the skin of his hand and in particular the skin over the tip of his right forefinger, his trigger finger. With time, other features developed. He found he couldn't drink beer anymore, as it "knocked him out". Fatigue and tiredness became a feature of his health state - he would go to bed at 8 o'clock. His mood became very irritable, impatient and intolerant. He also had episodes of eye irritation and reddening. His wife complained about his breath which was foul after a days spraying. As a result of all this, by April 1992 he was so ill that he stopped spraying but continued other tractor work - even though he was still extremely fatigued. Finally in December 1992 he stopped work altogether and tried shearing but had no strength. By early to mid 1993 there was some noticeable improvement in his health with, initially, a reduction in nausea, headaches and diarrhoea, as well his swollen hand joints began to improve. By the end of 1993 his mood was improving as were his energy levels, and his foul breath. AT INTERVIEW FEBRUARY 1996 Jeff is now a different person, he exercises each day and in December 1995 he had a try at shearing. His general and specific symptoms have improved, his home life is good. 8. Professor Glass also considered Dr Grigor's diagnosis of dermatomyositis and discussed this diagnosis with Dr Grigor. Both doctors were more inclined to a diagnosis of connective tissue disorder. Professor Glass went on to say: "My argument is, however, that given all the evidence it is clear that the diagnosis of a herbicide induced illness can be sustained on the basis of the circumstances of Jeffrey's exposure to herbicides, the nature of his symptoms and the temporal relationship of those symptoms to his exposure, and in particular his recovery once he stopped spraying The question of the dermatomyositis or a connective tissue disorder could also well be a consequence of such exposure but it cannot be proven. Considering all the evidence it is my opinion that Jeffrey Anderson suffered the symptoms of over-exposure to herbicides in the course of his work and that this resulted in a defined acute and chronic illness. It is also clear that coincidentally symptoms of muscle stiffness, muscle calcification and skin changes have led to a range of diagnoses, the most likely of which is dermatomyositis or possibly a connective tissue disorder and there is some evidence from the literature that solvents are causative but in this case cannot be proven. Jeffrey thus suffered two clearly defined conditions. One of which is linked to his herbicide exposure, the other may possibly have been." The Corporation's Position Having considered the new medical evidence from Dr Grigor and Professor Glass the Corporation wrote to the appellant's solicitor on 4 June 1996 indicating that it was willing to consider a settlement of the appellant's claim that he had suffered a chemical induced illness which had accounted for many of the symptoms of which he complained including muscle stiffness, eye irritation, intolerance to alcohol, mood changes, irritability and unexplained fatigue and tiredness. The Corporation maintained that the appellant had made a gradual recovery from these symptoms following the cessation of chemical spraying and indicated that it was not prepared 9. to accept that the connective skin disorder, of which the appellant complained had been shown to be causally connected to his exposure to herbicides. The appellant's solicitor wrote to the Corporation's counsel on 12 June 1996 seeking clarification of the aspects of the claim accepted by the Corporation but said that the appellant was to proceed to a hearing on the question of whether the appellant's connective tissue disorder was causally connected to his exposure to chemical sprays which is the issue in this appeal. Professor Glass' Further Report The Corporation further acknowledges that Professor Glass' latest report concludes that he now supports a proposition the appellant's connective tissue disorder is on the balance of probabilities causally connected to exposure to herbicides. The Corporation submits however the evidence of Professor Glass as contained in his latest report should be given little or no weight by the court for several reasons. The first ground is that Professor Glass has incorrectly adopted the role of an advocate rather than a neutral expert in his report. The Corporation refers to Professor Glass' covering letter in which he stated: "I am sorry for the delay, I have been out of the country but in addition it has taken quite some time to put an argument together." 10. I do not accept the interpretation placed on this letter by the Corporation. His report was in response to a specific question, namely: "Is Mr Anderson's connective disorder, on the balance of probabilities, causally connected to his exposure to herbicides?" The Corporation .referred to Mr Blackwood's decision in Marriot (402/92). In referring to a specialist medical report made by Professor Glass, Mr Blackwood said: "If a medical specialist submits a report which appears to contain elements of advocacy, then the appeal authority may have to review that report with some reservation." Mr Blackwood however in that case did go on to rely on Professor Glass' report. The second ground relied on by the Corporation is that Professor Glass' later report directly contradicts his earlier and more thorough report of 1 March 1996 in which he concluded that the appellant's connective tissue disorder could not be proven to be related to herbicide exposure. In his later report however, Professor Glass concludes that the appellant's herbicide exposure was causally connected to his connective tissue disorder on the balance of probabilities although he does not refer to his earlier contrary finding and relies on Harrison's Principles of Internal Medicine, Volume 12, 1994 not referred to in his earlier report. The Harrison text was not one of those references provided for comment by both parties. 11 In my view, Professor Glass is entitled to rely on the Harrison text. He is an occupational medical specialist providing an expert opinion. Professor Glass was asked to provide a further report in response to a specific question. He was not obliged to refer to his earlier report. Professor Glass considers the two possible diagnoses of the connective tissue disorder i.e. dermatomyositis and sclerodermar. I set out below his report largely in its entirety: DERMATOMYOSITIS Dermatomyositis, or Inflammatory Muscle Disease, is one of the connective tissue disease family as noted by evidence of autoimmune associations Dr Grigor recorded a number of classical features associated with the disease on examination of Mr Anderson. They included: 1 . violaceous rash over the dorsum of the fingers heliotrope discoloration of his eyelids WN calcification over the right lateral thigh severe Raynauds on the lower extremities in particular. Dr Grigor speculates that Mr Anderson may evolve into something more akin to limited sclerodermar in time. What evidence is there for an environmental cause for Dermatomyositis? Firstly, let us look at the occurrence. Adult onset dermatomyositis has a mean age at diagnosis of 40 (Jeffrey was 32) and occurs more frequently in women, 2:1. It is a rare disease (2-10 cases in a million). Causative factors could include an interplay between host genetic factors, viral infection and autoimmune mechanisms. There is one paper I have read on solvent induced myopathy which references a number of other papers indicating that" occupational exposure to solvents remains a possible explanation for myopathic changes in muscles as indicated by a raised serum creatinine kinase (CK)." This evidence is in its early days. Sclerodermar (Systemic Sclerosis) Again, this is a rare disease (4-12 cases per million). The onset of the disease is highest in the 4th and 5th decade and is 3-4 times more common in women than men. 12. When looking at causation, environmental factors are possible and include silica dust, vinyl chloride, exposy resins, trichloroethylene and other solvents. There are no strong genetic links. I also attach a comment by Dr Michael Beasley, Toxicologist, University of Otago, when commenting on a case of sclerodermar in a radiographer, as well as a report on a Case Referent study in Italy. Jeffrey Anderson developed his connective tissue disorder at age 32, an age below the mean for either dermatomyositis or sclerodermar. Jeffrey is male and thus is less likely to get either of these connective tissue disorders. Both diseases occur rarely. Thus his illness is outside the usual pattern. Further Comment Based on Reference Material as under. 1. Extract on Connective Tissue Disorders: polymyositis, dermatomyositis, and sclerodermar. Oxford Textbook of Medicine 2. Sclerodermatous Syndrome after Occupational Exposure to Herbicides - Response to Systemic Steroids. Dunnill and Black, Clin. & Exp. Derm. 1994. 19 : 518-520. 3. Sclerodermatous Syndrome with unusual features following prolonged occupational exposure to organic solvents. Bottomley et al. Br. J. of Derm. 1993, 128 : 203-208. 4. Chloracne, Palmoplantar keratoderma and localised sclerodermar in a weed sprayer. Poskitt et al. Clin. & Exp. Derm. 1994, 19 : 264-267. 5. Community Exposure to Paraquat Drift. Arnes et al. Arch. En. Hith. 1993, 48 : 47-54. DEALING WITH THESE REFERENCES IN ORDER 1. The Oxford Textbook of Medicine. a Details causes, pathology and presentation of polymyositis and dermatomyositis and in this section notes that "a rare presentation is acute sclerodermar-like thickening of the skin making the diagnosis more difficult." When making a diagnosis sclerodermar is listed as a condition to differentiate from. As far as causation is concerned, viral, genetic and immunological mechanisms are listed. b. Details causes, pathology and presentation of sclerodermar. Causes include: immunological (minimal), familial as well as environmental factors. 13. MY COMMENTS These excerpts indicate that both conditions are connective tissue disorders, that clinical patterns vary and that there is a possible overlap when polymyositis presents rarely with sclerodermar-like characteristics. 2. Paper by Dunnill and Black. It is of interest to note that patients with occupational sclerodermar have many features of ideopathic systemic sclerosis and that syndromes associated with particular chemicals are usually atypical in their presentation and pattern of organ involvement. In Harrison's Principles of Internal Medicine Vol. 12 1994, International Edition, reference is also made to the fact that sclerodermar can also occur in a localised form limited to the skin subcutaneous tissue and muscle. The article further points out that systemic sclerosis also occurs in association with features of other connective tissue disorders, the so-called syndrome. Clearly Dr Grigor sees Mr Anderson's condition as a likely overlap situation when he speculates that Mr Andersons' dermatomyositis may evolve into something more akin to limited sclerodermar. Thus the Harrisons' review, the article by Dunnill and Black and Dr Grigor's opinion all indicate a diagnosis which is not water tight and which can overlap between dermatomyositis and limited sclerodermar. Given this viewpoint, which I believe is a reasonable one in Mr Anderson's case, the question as to causation becomes a little clearer. 3. The case reported in this paper by Bottomley et al again indicates that occupational exposed sclerodermar-like conditions are not classical in their presentation which again supports the likelihood that Mr Anderson's condition is work related. 4. This paper by Poskitt et al is fundamentally a case of chloracne but with some overlap into the connective tissue group of disorders. 5. This paper on paraquat adds little to this case. COMMENTARY The reference material assists Mr Anderson's claim in that it indicates that connective tissue response to a variety of solvents, herbicides and other chemicals is not classical in its symptomatology or appearance. This supports the viewpoint of the rheumatologist, Dr Grigor, who sees an overlap between Mr Anderson's dermatomyositis and the development of sclerodermar. Given the other features such as age of occurrence, gender distribution and temporal relationship with work exposure, I would support the proposition that Mr Andersons' connective tissue disorder is, on the balance of probabilities, causally connected to his exposure to herbicides." The standard of proof is the balance of probabilities. 14. Credibility is not an issue. It is not disputed that the appellant was exposed to herbicides. The onset of the appellant's symptoms were contemporaneous and the record is not disputed. It is accepted that there were no pre existing conditions. The conditions themselves are rare. Dr Grigor and Professor Glass are agreed that there is an overlap between these connective tissue disorders. The research material considered by Professor Glass supports a claim that connective tissue disorders can be caused by chemical exposure. In my view the totality of the evidence establishes the causative link between the exposure and the illness. Conclusion On the balance of probabilities the appellant has established that he suffered a personal injury as a result of chemical exposure, not only from the onset of the herbicide induced condition as accepted by the Corporation but through the onset of a connective tissue disorder. The appeal is allowed. The appellant is entitled to costs. If these cannot be agreed then the parties have leave to make further submissions. (JH Lovell-Smith) District Court Judge