Matthews v Accident Rehabilitation and Compensation Insurance Corporation

IN THE DISTRICT COURT Decision No. 62 /97 WELLINGTON REGISTRY 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 BETWEEN CATHERINE MATTHEWS Appellant (Appeal No. DCA 121/96) AND ACCIDENT REHABILITATION AND COMPENSATION INSURANCE CORPORATION a body corporate duly constituted under the provisions of the said Act Respondent HEARD on the 28th day of November 1996 J A Wilton for appellant G S Hancock for respondent J B Stevenson for Taranaki Newspapers Ltd DECISION OF JUDGE D A ONGLEY This is an appeal against a decision on review given on 29th March 1996 declining cover for a gradual process injury. The appellant claims to suffer multiple chemical sensitivity arising out of and in the course of her employment with Taranaki Newspapers Limited (TNL) at New Plymouth during two periods of time, first for a short period of about four months from April 1994, and secondly for a longer period from October 1994. There is no dispute about the history of the appellant's employment but it is inherent in the nature of the dispute on appeal that the appellant's reported history, of onset of symptoms linked directly to the periods of her employment, are not fully accepted by the respondent and the employer. - 2. The history as set out by Dr Tim Sprott, occupational physician, in a letter of 13 July 1995: "Catherine has been involved in graphic design since the age of 20. For several months from April 1994 when she commenced work at TNL, she noticed the symptoms of nausea, myalgia, joint aches, mood changes, and abdominal discomfort. These symptoms became worse as her working week progressed. Catherine noted that her symptoms improved over the weekend, or with longer breaks away from work, but returned with commencing work at TNL. Catherine's work at TNL involved working at page set outs on computers, and comping. The comping area is next to two automatic photographic processors. Catherine was aware of the fumes from these processors, and over the time of her employment at TNL she noted increasing awareness of these fumes. For five months in the latter part of 1994, she worked for a Wanganui printer using computer graphics, and noted no health problems. She had no exposure to radiographic or printing chemicals. On her return in 1995 to work for TNL, her symptoms returned over a 2-3 week period." Her first symptoms of feeling unwell began soon after she commenced employment with TNL. She developed joint and muscle pain, nausea and sore itchy eyes; later muscle twitching, liver and kidney problems and reactions on eating various kinds of food. When she commenced work at TNL she had specified that she wished to avoid any environment with strong paint smells. It appears that she may already have had olfactory sensitivity but she had not experienced any consequential symptoms. In her employment with TNL she worked in an area into which two photographic processors vented. Dr Sprott later inspected the work environment. He said that the photographic chemicals contained agents such as diethylene glycol, hydroquinone, and acetic acid. Sulphur dioxide was released during film processing. The appellant suffered symptoms during her first period of employment. She ceased work with TNL because she was made redundant from her primary employment at Wanganui Hospital. She took another position in Wanganui where she was not exposed to any chemical smells and her symptoms abated. On returning to TNL she linked the onset of further symptoms directly with chemical smells in the workplace. She endeavoured to obtain medical treatment. Eventually she became sensitive to very low levels of fumes or odours and she experienced a worsening of symptoms even when she was re-deployed to another area in the building away from chemical processing. Her sensitivity developed to a stage where she reacted to air- conditioning, photocopiers or laser writers. Dr Sprott said: "Catherine presents with a cluster of symptoms and increasing sensitivity to work place chemical exposure. Her history is not consistent with allergic or irritant reaction, although irritation may have occurred initially. Her clinical assessment and investigations are normal. Catherine fulfils the criteria for that controversial diagnosis of multiple chemical sensitivity in that - - 3 - she has had known work place exposure to chemicals multisystem symptoms symptoms occur to very low exposure to chemicals and this is demonstrated recently when Catherine was redeployed in another area at TNL. Brief exposures to her old workplace lead to a reproduction of her symptoms . No objective test has demonstrated any abnormality" Dr Sprott provided a commentary on some of the literature relating to MCS. He said: "MCS is a controversial diagnosis that does not fit the established principles of toxicology. The four main theories regarding MCS are 1. MCS is a biologic/physical or psychophysiologic reaction to low level chemical exposures. 2. MCS symptoms maybe elicited by low-level environmental chemical exposures, but the sensitivity is initiated by psychologic stress 3. MCS is misdiagnosis and chemical exposure is not the cause. 4. MCS is an illness belief system; due to cultural influences on acceptable illness behaviour. The case definition of MCS relies on four principal characteristics: 1. MCS is acquired in relation to some documentable environmental exposure that may initially have produced a demonstrable toxic effect. 2. Symptoms involve more than one organ system and never abate in response to predictable environment stimuli. 3. Symptoms are elicited by exposure to chemicals that are demonstrable, but very low. These symptoms may occur to exposures significantly lower than would normally cause toxic or irritant effects in humans and typically involve chemicals of widely varied structural classes and different mechanisms of toxicological effect. 4. The manifestations of MCS are subjective. No widely available test of organ function can explain symptoms, and there is no objective evidence of organ system damage or dysfunction. The syndrome maybe severely distressing and functionally disabling." The respondents do not take issue with the diagnosis except to point out that it remains controversial. Nevertheless, the evidence before the Review Officer indicates the appellant suffers from a disabling hypersensitivity to a variety of stimulants which appear to be chemically related, that is to say the appellant's experience is that her symptoms occur after she has noticed chemical odours or after being in an environment in which some kind of chemical process has been undertaken. Rejection of the claim by the Corporation was based on an opinion of Dr Kelvin Bremner, Medical Adviser, Claims Processing Unit. He had referred in turn to opinions expressed by Dr Morris Cooke, Occupational Physician of Birmingham, Dr John O'Donnell of Christchurch, Dr Evan Dryson, Occupational Physician of . 4- Penrose, Auckland, and an article in the Health and Environmental Digest (US Freshwater Foundation). He referred in particular to a summary by Dr Dryson of an article by Sparks PJ et al. Multiple Chemical Sensitivity Syndrome: a clinical perspective. Journal of Occupational Medicine 1994; 36(7): 718-730. The extract to which Dr Bremner referred is set out in full because it deals with the variety of possible causes to which multiple chemical sensitivity could be attributed. "1. Allergic or immunological cause: controlled blinded studies have shown no difference in various measures of immune function between subjects and controls. The popular theory of allergy or sensitisation has not been substantiated 2. Inflammation from toxic free radicals due to deficiency of anti-oxidants. No scientific data available. 3. Neurogenic inflammation of URTI. Some experimental evidence to indicate- that low level environmental irritants e.g. cigarette smoke, may cause increased nasal resistance and URT symptoms possibly from release of cytokines and/or substance P from c-fibre neurones. Does not explain multisystem symptoms however. 4. Behavioural conditioned response to odour. Different odours produce symptoms through stimulus generalisation. No experimental evidence to support, but some clinical evidence. 5. Limbic kindling: postulates that symptoms are due to sub-convulsive kindling of the limbic system. Evidence that low level stimuli which at first do not produce a response eventually produce partial complex seizures. Odours and respiratory irritants may act similarly. Would explain time dependant sensitisation. No experimental data to support this theory as yet. 6. Odour triggered panic attacks. Odour produces autonomic arousal, may be amplified in people with predisposing susceptibility. Some experimental evidence to support 7. Cacosmia (subjective sense of altered olfactory function and feeling ill on exposure to chemical odours.) might also be associated with neurocognitive dysfunction. No difference between MCS subects and controls in one study. 8. Due to stress. Heightened sensitivity to odours or respiratory tract irritants results from some stressful event. (psychological, loss of self esteem, fear of harm from chemical exposure, physical illness) Some experimental evidence to support. 9. Misdiagnosed physical or psychological illness. Evidence of increased psychiatric disorders in MCS cases compared with controls. Evidence that such disorders predate (and not result from) MCS or history of chemical exposure. 10. Illness belief system. Belief in toxic damage promoted and perpetuated by some medical practitioners, support groups, media etc., cultural expression of psychosomatic illness. It is clear from the above that in the present state of knowledge it is not possible to ascribe the causation of MCS to exposure to chemicals whether in the workplace or not. There is a clear overlap between MCS and conditions such as chronic fatigue syndrome and chronic postviral illness. MCS may in fact be a subset of these with intolerance to chemicals being the distinguishing feature. - 5- Uncertainty over aetiology does not invalidate the diagnosis or the management offered to such people by occupational and other physicians, but it does have a bearing on the acceptability of ACC cover under section 7 of the 1992 Act." Section 7 of the Act contains the preconditions for a gradual process injury to qualify for cover under s 8. The relevant parts are as follows: 7. Personal injury caused by gradual process, disease, or infection arising out of and in the course of employment - (1) Personal injury shall be regarded as being caused by gradual process, disease, or infection arising out of and in the course of employment only if - (a) In respect of a period that ended on or after the Ist day of April 1974, the employment task performed by the affected person, or the environment in which it was performed, had a particular property or characteristic which caused or contributed to that personal injury by gradual process, disease, or infection; and (b) The property or characteristic is not found to any material extent in the non-employment activities or environment of that person; and (c) The risk of suffering that personal injury is significantly greater for persons performing that employment task in that environment than for persons who do not perform that task in that environment. (2) Nothing in subsection (1) of this section shall require that the property or characteristic be present throughout the whole of the person's employment. (3) For the avoidance of doubt, it is hereby declared that personal injury attributable to - (a) Air-conditioning systems; or (b) Passive smoking - shall be deemed not to have been caused by gradual process disease, or infection arising out of and in the course of employment for the purposes of this Act. Mr Wilton for the appellant submitted that the approach taken by the Corporation on the advice of Dr Bremner was simplistic and does not accord with the approach required by the legislation. He emphasised that s 7(1)(a) requires only that the work environment or the task contributed to the appellant's condition, so that even if the root cause is not clear, it may still be concluded that the work environment made such a contribution. The evidence in support of that includes the diagnosis of MCS and the appellant's history of worsening symptoms coinciding with periods when she was working for TNL and not occurring at other times. Therefore, the appellant submits, it is a reasonable inference that something related to working at TNL caused or contributed to the appellant's MCS. At the same time, the appellant submits, there is nothing in the evidence to suggest a stress related cause independently of the employment. The link with TNL is not simply temporal, but also is supported by two sources of evidence of airborne chemicals. The first is Dr Sprott's evidence that he visited the workplace on 30 June 1995 during a busy production run, and said that fumes were detectable in the - 6. comping room where two processors vented directly into the air. He did not identify the fumes but he referred to the chemicals which were being used as a likely cause of chemicals in the air. The second source of the evidence was a report of 17 August 1995 from Mr J T Sutton, Occupational Hygienist of Occupational Safety and Health Service. The report listed processor chemicals used in the work environment and listed the toxic effects on the human system. Mr Sutton said: "The chemicals present in film processing chemistry have the potential to cause serious harm and for this reason may be classified as significant hazards. Note: Although monitoring carried out did not detect chemicals in the air, it has been found that when more than one chemical is present then the health effects are more profound (synergism). Research in photographic laboratories have presented photographers with health symptoms at very low levels of chemicals." Mr Wilton recognised that the OSH inspection did not detect chemicals in the air, but he pointed to the remark about the effect of synergism, and another comment that OSH accepted that the appellant's problems had some links to the workplace. Mr Stevenson for the employer took issue with that analysis of the evidence. He submitted that the only possible basis for a gradual process claim causing multiple chemical sensitivity, could be that the appellant's condition was caused by airborne chemicals. He referred to a short passage in the appellant's evidence in which she attributed some exposure to sitting near an airconditioning vent close to a laser-writer. There is no evidence connecting that location with presence of airborne chemicals and it is a part of the evidence that does not assist the appellant. He dealt with Dr Sprott's report of his inspection of the premises in June 1995, and the OSH report. Both persons remarked on the obvious factor of presence of chemicals used in the developing process, but when it came to the important question of chemicals present in the air, both reports were negative. Dr Sprott said only that "fumes were not obviously detected near the computergraphics section, but that fumes were detectable in the comping room where two processors vented directly into the air." The OSH report found no fumes detectable in the monitoring exercise. Before dealing with the weight of evidence for and against the likelihood of airborne chemicals, it is as well to have regard to the requirement of's 7 of the Act. The Court has to be persuaded by evidence that the cause or contributory cause is a property or characteristic of the employment task or environment. In this case the question concerns the environment. It is then necessary to go on under s 7(1)(b) and compare the work environment with the claimant's non-work environment or activities to decide whether that same property or characteristic is found there to any material extent. Thus, a crucial part of establishing cover is to identify the property or characteristic sufficiently to judge the two important questions of firstly, causation and secondly whether the same property or characteristic is present in non-work activities or environment. - 7- The nature of the proof in this case is directed to the excluding of other possibilities so as to lead to a conclusion that workplace chemicals must have been the cause. I bear in mind the submissions of Mr Wilton which were put as follows: "The state of medical knowledge of MCS is not necessarily determinative of the issue. It is arguably analogous with the situations existing in the recent past in relation to the effects of exposure to asbestos; the effects of cigarette smoking; solvent-induced neurotoxicity; and the causes of occupational overuse syndrome (OOS). In each case the medical debate over precise causes continued long after there was general acceptance, on other evidence, that a real problem existed. The comparison with OOS is particularly apt. Even now there is no complete medical consensus on its cause, whereas it is accepted as being a gradual process injury originating in the workplace. MCS has been accepted as a ground for workers' compensation by appellate courts in New Hampshire, Oregon, California, Louisiana, Pennsylvania, Minnesota and Ohio, and by the state legislature in New Jersey (Clinical Toxicology (1995), 33(2), 111-113)." Counsel for the employer submitted that the appellant is unable to identify a particular chemical or group of chemicals, and there is no more than a suspicion of an airborne chemical agent, reinforced by a temporal coincidence in occurrence of worsening of symptoms. Further, the employer questions whether the symptoms suffered by the appellant are shown to have been caused in the manner defined or postulated for MCS, which is itself a controversial diagnosis. Submissions of counsel for the respondent followed a similar line of argument. Ms Hancock referred to a passage in an opinion by Dr Paul D Veitch, dated 26 November 1995, a consultant who examined the appellant at the request of the employer. Dr Veitch referred to the difference between association and cause, that is to say that although events may occur sequentially, they may not necessarily be linked in a toxicological causal sense. Dr Veitch could not find no causal link with a specific substance or substances in the workplace. I reach the conclusion that the respondents' submissions must be accepted. There is an attraction in fitting the circumstances of the case to the theory of multiple chemical sensitivity, but a decision favourable to the claimant must be based on reasonably persuasive medical opinion where the question at issue is a medical one. Where the diagnosis is controversial the Court must be guided by expert opinion rather than embarking on its own assessment of the claimant's medical condition. The function of the Court is not to make a diagnosis but to weigh the evidence. The medical literature is helpful in understanding the background to medical opinion, but it cannot have the same weight as qualified medical or scientific opinion directed specifically to the claimant's case. Although a condition of multiple chemical sensitivity can be accepted as the diagnosis, it is less evident that the diagnosis, together with circumstances of appearance of symptoms, can be used to predicate the cause. The uncertainty of aetiology leaves open other possibilities concerning the cause of the appellant's condition in the absence of acceptable evidence that she was exposed to airborne chemicals during some period of time in the course of her employment. - 8 - The difficulty in resolving the compensation question is perhaps caused by the apparently logical argument that if the symptoms became evident only in the workplace, and the presence of fumes provides a possible and apparently reasonable explanation of the cause of the symptoms, then the necessary criteria exist. The cautions that are expressed, in the unfavourable medical opinions and the literature concerning the collection of symptoms labelled MCS, are generally directed at the proposition that the diagnosis and attribution of causes are just not that simple. If the underlying condition of MCS exists, and if the symptoms have been exhibited in a particular environment, there is good reason to say that is not sufficient to establish the probable cause, or even a contributory cause. In this case, the conflict of medical opinion is divided on the question of identifying a specific chemical agent that fits the criteria for a diagnosis of multiple chemical sensitivity. Dr Sprott took the trouble to examine the workplace and he detected fumes. He found that one other employee suffered headache and nausea on Friday nights when more intensive processing was done. On the other hand, Dr Veitch and Dr Bremmer refused to make the link between airborne chemicals and multiple chemical sensitivity syndrome without first having some tangible evidence of exposure to a particular chemical or group of chemicals. The medical controversy does not necessarily prevent the Corporation or the Court from accepting a diagnosis of MCS and attributing the cause, or a contributory cause, to the workplace. A sufficient probability may well emerge in a particular case despite lack of agreement amongst medical experts. However, on the material available in this case, I find that there is insufficient evidence of a particular property or characteristic in the work environment to satisfy the specific tests under s 7 of the Act. For those reasons the appeal is dismissed. DATED at WELLINGTON this 22 day of April 1997 D A Ongley District Court Judge