Commentary
Personal injury claims are being brought by approximately 220 pilots and cabin crew at the High Court in London on the grounds of aerotoxic syndrome (ATS). This group of claimants includes 51 claims which were issued by Thompsons in March 2019 involving pilots and cabin crew working for EasyJet, British Airways, Thomas Cook, Jet2 and Virgin Atlantic. These two claims are not included in these ongoing English collective proceedings. These were claims by two pilots who lost the chance of bringing successful claims as a result of the admitted negligence of a Scottish law practice.
Although the central medical issue in this case was aerotoxicity, it is important to bear in mind that what the court did not have to decide whether the pursuers, airline pilots, had proved causation on the balance of probabilities. Rather, it was required to value the chances of success in their underlying claims that they lost as a result of the solicitors’ admitted negligence. It is therefore important not to see this as a "trial within a trial". However, experts instructed in the collective proceedings will be greatly assisted by this judgment because it identifies the nature of the expert evidence that will be needed, it reveals how the credibility of experts may be challenged and how their evidence is likely to be tested by the adverse parties and judged by the court.
Case
These were two separate actions. Both actions were brought by former pilots as clients against a firm of solicitors. Both pursuers were interested in pursuing claims for damages against their former employers. Ultimately, no such claims were brought by the defender on behalf of the pursuers. In each of the present actions, the pursuer sued the defender for breach of contract and reparation for the loss of a chance to have brought personal injury claims against their former employers.
In each case, the pursuer claimed that he suffers from a number of chronic symptoms which had prevented him from continuing his work as a pilot. Specifically, each pursuer claimed to suffer from aerotoxic syndrome (ATS). This is a controversial diagnosis. The condition is not recognised in the International Classification of Diseases and there are no generally accepted or validated diagnostic criteria for it. Each pursuer maintained that his condition had been caused by exposure to toxic fumes on a daily basis while he was employed as a pilot.
Mr Gough
Mr Gough first became aware of health issues during a skiing holiday in Canada in early 2003. He began to suffer from shortness of breath and ultimately collapsed. He was exhausted. He was taken to a first aid centre where it was discovered that his blood oxygen level was very low. He was immediately rushed to hospital. He underwent a series of tests but nothing could be found to indicate what was wrong. Prior to this, Mr Gough had enjoyed good health and had led an active life.
Following his return to work, Mr Gough felt better again. He did notice that he had begun to take long gasping breaths during flights but otherwise seemed to be fine. However, in August 2003, Mr Gough suffered another incident where he experienced severe pain in his left arm and hand. Mr Gough missed 2 days of work but the problem disappeared in 2 days. In mid-April 2004, Mr Gough suffered from a severe headache. Following a visit to the GP, he was admitted to hospital. Tests were carried out but the results were inconclusive. Mr Gough remained in hospital for 2 days and was unwell for a number of weeks thereafter. As a result, his medical certificate was suspended until later in July 2004. In 2005, Mr Gough began to see flashing lights while flying. He began to feel nauseous during flight. Mr Gough also noticed that when his body temperature increased he would suffer temporary blindness in his left eye.
Eventually, having dealt with the symptoms for a period, Mr Gough sought medical treatment in the summer of 2005. Having been seen by both optical and nerve specialists, he was informed that he either had multiple sclerosis or a virus in the optic nerve or optic centre of the brain. Mr Gough's certification of medical fitness to fly was suspended and he ceased flying. Following further testing and treatment by a neurological consultant, Mr Mark Roberts at the Alexandra Hospital in Cheadle, Mr Gough was informed in November 2005 that he had the early presenting features of what might become multiple sclerosis
Mr Gough continues to suffer from a number of symptoms both mental and physical including disturbed vision, balance issues, migraines, depression, mental and physical fatigue, and nausea. In particular, Mr Gough's evidence was that he could become very tired, both physically and mentally, very suddenly. When these symptoms arise, Mr Gough has found that it is best to give in to them and to rest.
Mr Gough first became aware of ATS following a conversation he had with his friend, Mr Montague-Trenchard. Mr Montague-Trenchard had a former colleague who had not flown for a number of years as a result of ill health. This colleague had made Mr Montague-Trenchard aware of the issue of toxic cabin air. Following this conversation, Mr Gough began to look into ATS himself.
Mr Gough first became aware of having a potential personal injury case against his former employer in 2012. Again, that was as a result of speaking to Mr Montague-Trenchard. In August 2012, Mr Gough travelled with Mr Montague-Trenchard and two other former pilots to the Netherlands. One of the other former pilots was Mark Atherton. This trip was for certain DNA tests to be carried out relating to the detoxification of organophosphates together with brain activity tests as well as a specific EEG test. The tests were carried out by Dr Michel Mulder. Dr Mulder was himself a former pilot who had been medically retired. Mr Gough received his test results in September 2012. Mr Gough understood that the DNA test results showed that he fell into a part of the population which do not detoxify organophosphates, resulting in them being stored in body fat. Mr Gough dated his own certainty that his symptoms were as a result of ATS from his receipt of the test results.
Lee Montague-Trenchard
Mr Montague-Trenchard's evidence was that he was frequently unwell after he started work for Airtours. This consisted mainly of chest and stomach infections which were treated with antibiotics. He also noticed that his sleep pattern started to become interrupted and that his athletic performance decreased sharply after more intensive blocks of work. However, it was notable that his wife, Rachel Cox, who first met him at this time, thought he appeared to be a normal energetic guy.
During the brief period between jobs in 2003/4, Mr Montague-Trenchard noticed a general resurgence in his health. However, while working for Etihad, Mr Montague-Trenchard felt that his health really began to deteriorate. He began to suffer from diarrhoea and bad headaches during flights. He continued to suffer from multiple infections. He developed coping strategies to try to address the symptoms he was suffering from including keeping a very careful check on what he ate and drank and monitoring his sleep. Although with the benefit of hindsight, he considered it should have been obvious that the flying was causing his ill health, Mr Montague-Trenchard felt that at the time he was in denial as to the cause. As his symptoms worsened, Mr Montague-Trenchard was off sick for periods. This was attributed to "burn out".
In January 2012, Mr Montague-Trenchard completed his final flight. It lasted only 20 minutes and was internal to the UAE but afterwards his chest hurt and felt tight. He subsequently developed acute sinusitis and bronchitis which incapacitated him for 3 months.
Following a meeting with the Etihad company doctor, Mr Montague-Trenchard's fitness to fly was withdrawn. At this point, a dispute arose between Mr Montague-Trenchard and Etihad. Mr Montague-Trenchard felt that the company doctors were not helping him recover. Mr Montague-Trenchard was also subject to disciplinary procedures because his attendance record was bad. In the end, Mr Montague-Trenchard chose to return to the UK at the beginning of April 2012. He never returned to Abu Dhabi
On his flight home to the UK in April 2012, Mr Montague-Trenchard wore a brand new white shirt. After the flight, the shirt was tested and organophosphates were detected. Mr Montague-Trenchard considered that his health significantly declined from 2009 until 2012 when he stopped flying. His symptoms included frequent severe headaches, vision problems, numbness, reduction in mental processing and problem-solving ability, permanent diarrhoea, long-term chest infections and chronic fatigue.
Since 2012, Mr Montague-Trenchard has made considerable efforts to address and rectify his health problems by taking supplements and modifying his diet and lifestyle. His headaches and migraines have reduced in frequency. The issues with both his digestive system and his susceptibility to infection appear also to have improved. His chronic fatigue has improved to some degree. However, he is unable to remain active either mentally or physically for prolonged periods. If he attempts to do too much, he tends, subsequently, to have a bad day. He was formally diagnosed with chronic fatigue syndrome in April 2018.
Mr Montague-Trenchard traced his first knowledge of ATS to a meeting he had had in Malaysia towards the end of 2011 with his friend Andrew Birtle, a former pilot. Mr Birtle had failed his medical certification and had had to retire in his late 40s. Although Mr Birtle's symptoms seemed similar to his own, at that time Mr Montague-Trenchard did not think it could be his job which was causing his ill health.
Later, in early 2012, Mr Montague-Trenchard was in contact with another medically retired former pilot, John Hoyte, who was part of an organisation called the Aerotoxic Association. This was both a campaign group that was trying to obtain wider recognition for ATS and a support group for those who had the condition. Mr Hoyte put him in touch with Dr Mulder. Through these contacts, Mr Montague-Trenchard was put in touch with Mr Cannon as Mr Cannon was in communication with Mr Hoyte. Along with Mr Gough and others, in August 2012, Mr Montague-Trenchard travelled to the Netherlands so that tests could be undertaken by Dr Mulder. Mr Montague-Trenchard considered that the results of the tests carried out in the Netherlands were a "diagnosis" of ATS.
Separately, Mr Montague-Trenchard also had tests carried out by a Dr Jenny Goodman in London. Dr Goodman conducted a battery of tests including multiple blood tests, a fat biopsy and a cognitive interview. Following these tests, in November 2012, Mr Montague-Trenchard received a diagnosis from Dr Goodman that his illness was caused from exposure to engine fumes.
Expert evidence
The pursuers led evidence from Professor Mackenzie Ross, a clinical neuropsychologist and chartered clinical psychologist. She had studied the long-term effects of low-level exposure to organophosphates. From 1998, she had been retained by a firm of solicitors to investigate the potential toxic effects of pesticides on people. While carrying out this work, she had reported to a number of government bodies, including the Committee on Toxicity. She had been commissioned by DEFRA to carry out research into low-level exposure to organophosphates.
In around 2006, she had been approached by BALPA who raised concerns about ATS. She had assessed a number of pilots and found what she thought was alarming evidence of cognitive impairment among them. As a result, she had approached the Department of Transport and the Civil Aviation Authority (CAA).
Professor Mackenzie Ross had interviewed and assessed the pursuers. She had subsequently prepared a report in respect of each of them. The focus of her reports was the cognitive functioning and mental health of each pursuer. In respect of both Mr Gough and Mr Montague-Trenchard, Professor Mackenzie Ross' assessment did not find evidence of global intellectual decline. However, in each pursuer, her testing revealed patchy under-functioning in tests of auditory memory and verbal fluency. In Mr Montague-Trenchard's case, there was also evidence of under-functioning in respect of processing speed.
Professor Mackenzie Ross considered that it was difficult to draw firm conclusions in relation to causation based solely on performance in psychometric testing. The results of this testing had to be considered in the context of the clinical information acquired from other sources and other medical tests. However, Professor Mackenzie Ross noted that neurotoxic conditions were frequently misdiagnosed or not diagnosed at all. She attributed this to the fact that few healthcare professionals received training in toxicology. She considered that neuropsychological assessment was the most sensitive means of examining the effects of toxic exposure. But she also recognised that, given the wide range of factors that can influence performance, caution was required in the absence of corroborating results from other medical disciplines.
Professor Mackenzie Ross sought to apply the Bradford Hill criteria to assist in the interpretation of the pursuers' cases. These criteria were formulated by Sir Austin Bradford Hill and are used in the public health field to establish epidemiological evidence of a causal relationship between a presumed cause and effect. In considering the pursuers' cases, Professor Mackenzie Ross noted that each gave a history of repeated and continuous exposure to engine oil fumes. In both cases, that exposure was connected in time with their initial symptoms of ill health. She considered that in the case of both pursuers their reported symptoms and neuropsychological profiles were consistent with those which had been reported in previous studies of aircrew. These included respiratory, cardiovascular, gastrointestinal, eye, nose and throat irritation, dermatological, systemic symptoms (fatigue, arthralgias) and neurological problems (sensory changes and cognitive impairment), following exposure to contaminated air.
Professor Mackenzie Ross recognised the fact that the studies of cabin air quality which had been carried out to date had not detected chemicals at levels which were considered to be a concern from an occupational medicine perspective. However, she considered that there were methodological weaknesses in the studies which had been carried out. She noted that none of the cabin air studies had captured a so-called "fume event". Furthermore, she also pointed out that consideration of particular chemicals had not taken account of either the effect of combining the chemicals which had been identified or the fact that those chemicals had been preheated to a very high level.
In her view, one also had to be very careful comparing the unique hypoxic environment of an aircraft cabin with other working environments. Professor Mackenzie Ross highlighted the fact that the cabin air studies did not, in her opinion, consider the risk to health posed. They did not look at the effect of cumulative low-level exposure and they did not seek to correlate the data with health effects.
On this basis, and in light of her research, Professor Mackenzie Ross considered that it would be premature to conclude that aircraft cabin air did not pose any risk to aircrew. However, she recognised the limits of her expertise. In the cases of the pursuers she considered that the opinions of both a clinical toxicologist and a neurologist should be sought.
Professor Mackenzie Ross was asked about the diagnosis of the pursuers by the consultant neurologist, Dr Davenport. His view was that both of the pursuers were suffering with chronic fatigue syndrome. So far as Professor Mackenzie Ross was aware, this diagnosis was more of a description of the symptoms each pursuer had. It did not assist with identifying the cause. However, Professor Mackenzie Ross did recognise that the results of her testing of both pursuers might also be found in someone who had been diagnosed with chronic fatigue syndrome.
The defender led evidence from Dr Richard Davenport, consultant neurologist, who had prepared two reports in respect of each of the pursuers. In each case, Dr Davenport examined the pursuers in person before preparing his first report, dated June 2021. He subsequently had an online consultation with each pursuer before preparing supplementary reports in January 2024. Dr Davenport did not undertake a detailed cognitive assessment of the pursuers. The carrying out of such an assessment would, in Dr Davenport's experience, be something carried out by a neuropsychologist.
In relation to Mr Montague-Trenchard, Dr Davenport's primary diagnosis was that he was suffering from chronic fatigue syndrome. Dr Davenport could not find a specific neurological diagnosis to account for Mr Montague-Trenchard's neurological symptoms. Dr Davenport explained that chronic fatigue syndrome is considered a "functional" disorder, meaning that there is no identifiable structural disease to explain the symptoms. Its diagnosis does not imply any known underlying definitive mechanism. In relation to the other symptoms of which Mr Montague Trenchard complained, such as the irritation of the lower gastric tract, Dr Davenport considered that these symptoms would also be recognised as being consistent with a functional disorder
In relation to Mr Gough, Dr Davenport had, when preparing his first report, diagnosed Mr Gough as suffering from a functional neurological disorder along with both a migraine disorder and a mental health disorder. Dr Davenport did not consider that Mr Gough was suffering from multiple sclerosis. Dr Davenport considered that Mr Gough's visual symptoms were being caused by migraines albeit he considered that the way in which the migraines manifested themselves was unusual. Subsequently, in preparing his second report, Dr Davenport altered his opinion. He considered that chronic fatigue syndrome was the best explanation for the fatigue from which Mr Gough was suffering and which appeared to be his dominant symptom. Dr Davenport stressed that there were overlaps in these diagnostic areas which should not be regarded as silos.
Dr Davenport was of the view that Mr Gough's case was more neurologically complex than that of Mr Montague-Trenchard as could be demonstrated from the many interactions with neurologists which Mr Gough had had during the course of his treatment.
Dr Davenport accepted that chronic fatigue syndrome was a descriptive term and that its cause was not known. However, he considered that it remained a meaningful diagnosis. Although, ultimately, Dr Davenport had diagnosed both pursuers with chronic fatigue syndrome, he considered that it would be slightly circular to regard this as a pattern.
Although the principal disabling problem was the same in both cases, there were important differences between them. Furthermore, chronic fatigue could be seen to affect a very wide group of individuals from many different areas of employment and backgrounds.
As to ATS, Dr Davenport noted that the condition had yet to be accepted as a condition, was not recognised by most doctors and did not feature in the International Classification of Diseases. Dr Davenport also noted that, so far as he was aware as a neurologist, there were no accepted diagnostic criteria for this syndrome. Insofar as criteria had been put forward, these were very broad and, in any event, it was not apparent to Dr Davenport that either pursuer satisfied these criteria. Overall, Dr Davenport considered that there was insufficient evidence in the medical literature to support the notion of a specific aerotoxic syndrome. However, Dr Davenport was careful to accept that, in the future, it might be that ATS would become a recognisable and accepted diagnosis.
Dr Davenport did not recognise the use of the term "diffuse encephalopathy" as Professor Howard had used that term to describe the condition of both of the pursuers. Dr Davenport considered that this descriptive term would be used in situations where there was an alteration in mental state, disorientation, confusion evolving into coma if the cause was not corrected. It could be caused by a broad range of conditions: infectious disorders, metabolic disorders, toxic causes, and sometimes specific neurological conditions.
In respect of both pursuers, Dr Davenport had in his first reports considered that they would be able to work in a flexible, part-time role. Dr Davenport clarified that, based on his experience, he recognised the difficulties in working regular, routine hours experienced by those who suffered from chronic fatigue because of the tendency of such people to suffer from unexpected periods of fatigue. He did not seek to cast doubt on the accuracy of the pursuers' account of their symptoms. He also was careful to make clear that he did not consider that he was really in a position to comment in detail on either of the pursuers' residual earning capacity.
Each party put forward an expert witness speaking to the issues of toxicology: Professor Vyvyan Howard for the pursuers and Professor Jim Bridges for the defender. Each of these witnesses had prepared a number of reports which they adopted and the two witnesses gave their evidence concurrently.
Professor Howard is emeritus professor of bioimaging at the University of Ulster. He has been a fellow of the Royal College of Pathologists since 1999.
In respect of ATS, Professor Howard had first come across the issue when asked to give a presentation at a BALPA conference in 2005. Subsequently, in 2017, he had been asked to examine a number of pilots who were complaining of ill health. As a result of his examination of these pilots, his view was that the symptomology was very diffuse. There were no localising signs typically used by neurologists to indicate lesions or structural damage within the nervous system.
Professor Howard had prepared three reports. The first, dated 22 June 2018, was described as his generic report. In this report, Professor Howard set out his understanding of a number of matters, including: the way in which cabin air is heated and pressurised; the ways in which there is a pathway for oil droplets or fumes to enter the cabin air supply as a result of the design of the seals and the operation of the engines; the ways in which "fume events" occur and how they might be avoided; the recognition within the aviation industry that low-level leakage of oil and other fluids does occur as a normal function of using the bleed air system; the composition of synthetic jet engine oils; the effect on the oil of exposure to high temperatures within the engine resulting in it being subject to thermal degradation (pyrolysis).
Professor Howard was cross-examined as to the basis upon which he had the relevant expertise to include this material within his report. In response, Professor Howard did not dispute these areas fell outwith his field of expertise. His position was that he was seeking to set out the basis of his understanding by extracting material from publicly available sources.
Professor Howard also set out the results of the cabin air studies carried out to date which showed that included among the substances identified as being present, was tricreysl phosphate or TCP, and that the amounts of these substances was well below any applicable "Occupational Exposure Levels" or OELs.
Professor Howard noted that classical toxicology has been developed to test individual chemicals one at a time. Accordingly, classical toxicology is not good at addressing mixtures of chemicals and non-straight line dose responses. As such, classical toxicology tends to assume that the effect of chemicals in a mixture is simply additive. That assumption requires the toxicity of each individual component in the mixture to be known. Professor Howard considered that an assumption of additivity was unfounded when considering cabin air. He pointed to studies which highlighted unexpected synergistic interactions arising from mixtures. For these reasons, Professor Howard considered that there was no merit in trying to apply OELs or other equivalent regulatory limits to the cabin air situation. In particular, Professor Howard considered that this was the case in relation to TCP and tri-ortho-cresyl phosphate (TOCP). The isomers of TCP were acknowledged to be neurotoxic
Professor Howard did not consider that it was possible, safely, to divide exposure into fume events and non-fume events. He considered that the available data showed that there were a number of different factors that required to be taken into account including: individual susceptibility both in terms of genetics and length of prior exposure and the number and mixture of different chemicals involve.
In terms of considering the method of exposure of pilots and cabin crew to toxins, Professor Howard considered that inhalation both of fumes and ultra-fine particles represented the principal route. He noted that there was a lack of inhalation studies in respect of jet oils and TCP. In relation to the ultra-fine or nano particles, research indicated that these could be composed of pure engine oil. This suggested that exposure levels may be higher than previously thought.
As to the mechanism whereby exposure causes injury, Professor Howard accepted that the precise mechanism was not defined. The main impediment to this was the complexity of the mixture of chemicals involved. He emphasised the length of exposure which pilots and cabin crew would experience over many thousands of hours. Professor Howard noted that in its report into cabin air, the UK Committee on Toxicity had focussed only on TOCP in the context of organophosphate-induced delayed neuropathy (OPIDN). It was acknowledged that OPIDN required a high level of exposure to organophosphates. Other research had identified the toxicological effects of repeated dose exposures to low levels of organophosphates. Professor Howard referred in particular to papers published by Professor Alvin Terry of the Department of Pharmacology and Toxicology, Medical College of Georgia, Augusta University, Georgia, USA. Some of the effects described in that research were irreversible and, therefore, cumulative in their pathogenic action.
On the basis of this research, Professor Howard considered that there was evidence that exposure to organophosphates interfered with axonal transport, the process by which information was communicated between nerve cells. This led Professor Howard to the conclusion that cabin crew and pilots would be more susceptible to neurological harm than passengers following an acute high-dose fume event. Professor Howard considered that this conclusion was borne out by a comparison of hospital attendance rates by passengers and aircrew following fume events.
In Professor Howard's opinion,
"on the balance of scientific and medical probability, exposure to the low level
fumes in engine bleed air is causally related to the signs and symptoms known
collectively as 'Aerotoxic Syndrome'."
His opinion was that ATS is caused by continual low-dose exposure rather than that the severity of symptoms is affected by the amount of toxic cabin air to which an individual has been exposed. This was confirmed by the fact that, in the article Howard, C & Michaelis, Susan & Watterson, Andrew. (2017). The Aetiology of ‘Aerotoxic Syndrome’- A ToxicoPathological Viewpoint. Open Access Journal of Toxicology, Professor Howard and his co-authors went on to identify three complications in understanding the issue of causation: (i) the complexity of the mixture to which the aircrew are exposed; (ii) the wide variability between individuals' ability to metabolise and detoxify OP compounds; and (iii) the fact that low-dose repeated exposure can increase the vulnerability of neurons to a subsequent high-dose event.
Professor Howard also prepared a further report in respect of each of the pursuers. These reports were prepared following a desktop review and did not involve a physical examination.
Professor Howard did not agree with the conclusion of Dr Davenport that there was no organic basis for Mr Gough's observed symptoms. Professor Howard considered that research had demonstrated the mechanisms by which harm could be caused by repeated low-dose exposure to organophosphates. These mechanisms included the inhibition of axonal transport, neuroinflammation and organophosphates binding to amino acids. Professor Howard's view was that these mechanisms could cause what he described as a "diffuse encephalopathy" giving rise to the spectrum of signs and symptoms associated with ATS. He accepted that the diffuse nature of the symptom spectrum presented difficulties for diagnosis. Accordingly, Professor Howard was of the view that Mr Gough had suffered organic damage to his nervous system as a result of chronic and acute exposure to aircraft engine bleed air over his flying career and that Mr Gough's symptoms are consistent with a diagnosis of ATS.
In respect of Mr Montague-Trenchard, Professor Howard reached a similar conclusion. He again noted the results of Professor Mackenzie Ross's assessment of Mr Montague-Trenchard and disagreed with the conclusion of Dr Davenport that there was no organic basis for Mr Montague-Trenchard's observed symptoms. Professor Howard noted that, on the basis of Mr Montague-Trenchard's recollection of his symptoms, there was an association between those symptoms and his flying. Professor Howard considered that this was a strong indicator that Mr Montague-Trenchard's illness was associated with exposure to a factor in his place of work the cockpit. Accordingly, Professor Howard was of the view that Mr Montague-Trenchard had also suffered organic damage to his nervous system as a result of chronic and acute exposure to aircraft engine bleed air over his flying career and that his symptoms are consistent with a diagnosis of ATS.
Professor Bridges is emeritus professor of Toxicology and Environmental Health Professor Bridges had not published at all in respect of ATS. As he explained in evidence, this was a conscious choice of his to avoid areas of public controversy.
Professor Bridges had prepared two reports in respect of each of the pursuers.
Professor Bridges' starting point was to highlight the fact that pilots, as all individuals in normal life, will be exposed every day to many thousands of different chemicals. In the case of the great majority of those chemicals, the level of exposure will be very low. Professor Bridges pointed to the results of research in 2017 which attempted to model the interaction of the mixture of chemicals thought to be relevant to ATS. This research found only minimal changes in the effect of the mixture. Professor Bridges recognised that the science in this area was not complete, but, in his view, low-level exposure to a wide range of chemicals did not lead to obvious toxicity. Human beings were exposed every day to many thousands of chemicals without noticeable significant adverse effects on their health.
Professor Bridges noted that the assumption in the majority of studies of ATS appears to have been that TOCP is the sole or the most important toxic component of cabin air. TOCP, an isomer of TCP, is an organophosphoric chemical. Professor Bridges questioned this focus. Since 2017, ultrafine particles had also been considered.
In terms of the level of exposure, Professor Bridges highlighted that there were many different factors to be considered and it was difficult to assess the effect of exposure. However, Professor Bridges emphasised that it is an established principle of toxicology that for each chemical there is a level of exposure below which no adverse effect will arise. This principle has been used for many decades as the basis upon which safe exposure levels have been set. The setting of these levels is based upon data derived from, among other things, toxicity studies and human epidemiology. The precautionary principle is then applied and levels are set substantially below the estimated "no adverse effect" threshold. This process results in the setting of OELs.
Professor Bridges also considered that, of the chemicals identified as "aerotoxic", none were likely to be sufficiently persistent to build up in the body during normal flights. He considered that a significant contribution from other psychological, physical or biological stressors would be required. Organophosphates were generally not regarded as bioaccumulative, so exposure to very low doses does not generally result in significant quantities accumulating within the body.
Professor Bridges recognised that the appropriateness of applying OELs in the context of ATS was disputed. However, he could find no studies which provided scientific evidence to justify why pilots and cabin crew should be regarded as uniquely susceptible.
Professor Bridges considered that for a member of air crew to be diagnosed as suffering from ATS, exposure levels should be comparable at least to the OELs of the chemicals of interest. However, the available studies of cabin air showed TCP levels which were very low, if present at all. The measurements were well below the relevant OELs. This was true even if the OELs were reduced ten-fold. Professor Bridges considered that the measured levels were far too low to have caused any adverse health effects. So far as Professor Bridges was concerned this was also true of the short-lived "fume events" which had been measured.
Professor Bridges considered that the available published studies suffered from one or more of the following problems: a lack of reliably objective criteria to characterise the symptoms; unreliable data; non-random selection; poor information on exposure to the "aerotoxic chemicals"; wide variability in the symptoms; and a failure to take into account other stressors. Inevitably, the main source of information was self-reported symptoms.
In respect of both pursuers, Professor Bridges considered that there were three principal challenges in concluding that their ill health was attributable to ATS: first, there were no measurements of the exposure to chemicals of either; second, the pattern of symptoms of both pursuers was not characteristic of organophosphates; and third, no specific events had been correlated with the development of their symptoms.
In Professor Bridges' opinion, the pursuers' estimated exposure to cabin air chemicals did not support the conclusion that either Mr Gough or Mr Montague-Trenchard suffered from ATS. Although as yet unidentified chemicals could not be ruled out, Professor Bridges thought that the likelihood was that their levels would be extremely low.
Expert disagreement
The judge introduced this section of the judgment:
It is fair to observe that there was little by way of a meeting of minds between the two professors. In particular, it was notable that Professor Bridges refused even to accept that Professor Howard was qualified to express an opinion on toxicology. Apparently for similar reasons, Professor Bridges had considered there would be no value in his meeting with Professor Howard in advance of the proof to prepare a joint statement.
One of the principal areas of disagreement between the two professors concerned the use of OELs. Professor Howard had a number of concerns with the use and application of OELs in the context of cabin air. As a starting point, Professor Howard noted that OELs were not intended to apply to an environment in which the general public would be present. Furthermore, of the substances which had been detected in cabin air, the great majority of the chemicals had not even been identified, so the toxicology of these substances was unknown. The complexity of this mixture also meant that it was difficult to isolate and assess the numerous chemicals contained within it. Second, Professor Howard questioned whether OELs were applicable to the high altitude, high pressure and hypoxic (low oxygen) environment of the cabin. Nerve cells were highly metabolic. It was also known that if hypoxia were induced, the toxicity of a number of toxicants was increased.
Professor Bridges accepted that a different standard should be used where the general public were concerned. But in considering the pursuers in their workplace, he considered that this required to be seen in context. Humans are exposed to thousands of airborne chemicals every day. It was necessary to determine the particular chemicals to be concerned about. You could never be absolutely sure that you had not missed something but experience indicated that this did not happen commonly. This approach was the common approach that was adopted in relation to the fixing of OELs.
The fact that a mixture of chemicals was found in the cabin was not unique to aircraft. Professor Bridges was also of the view that synergistic effects were relatively rare. He pointed out that two chemicals could also interact in an antagonistic way where the effect of one blocked another. As to the lower level of oxygen experienced in the aircraft, Professor Bridges did not consider that the lower level would be likely to affect the toxicity of the chemicals being considered.
The experts also disagreed about the extent to which there was evidence that low-dose exposure to organophosphates would have an adverse effect. Professor Bridges had considered the papers published by Professor Terry referred to by Professor Howard.
However, he considered that it was important to distinguish between a change caused by exposure and whether this was, in fact, adverse.
For Professor Bridges, the key issue was to quantify the dose of any toxin which was being considered. For him, the cabin air surveys showed that the likely dosage was far below the relevant OELs for, in particular, organophosphates. Whereas for Professor Howard, it was important to recognise the patterns of symptoms which were being reported by the pilots and cabin crew affected. That is what he, amongst others, had done in the paper he had published in the WHO publication Panorama in 2017. Identifying the dose would require more research and access to testing in aircraft. Professor Bridges responded that the symptoms referred to were very varied. He questioned whether enough consideration had been given to other possible causes such as the other stresses biological, physical and psychological to which pilots were exposed.
The law
The pursuers stressed that much guidance could be taken from the observations made by Lord Prosser in Dingley v Chief Constable of Strathclyde Police 1998 SC 548 (IH) (at 602 and following). The pursuers took two propositions from Lord Prosser's observations. First, that when the court is determining a question of medical causation, the court requires to approach this question on the basis of the evidence before it and determine the question on the balance of probabilities. Second, self-evidently, that approach would clearly be quite different from the approach which would be adopted by clinicians.
A claimant in English law was entitled to recover damages for personal injury caused or materially contributed to by the defendant's negligence. The court does not need a full scientific account of exactly how exposure caused a particular injury (McGhee v National Coal Board [1973] 1 WLR 1. However where there is a lack of medical literature creating an association between chemical exposure and the injury sustained, causation may not be established if there are other factors which could have caused the injury (Wood v Ministry of Defence [2011] All ER (D) 66.
Submissions
The defender focussed on four fundamental issues which it contended the pursuers would require to address in order to be successful in their claims : (1) foreseeability of injury; (2) the harmful substance to which the pursuers have been exposed; (3) breach of duty; and (4) causation.
The defender argued that parts of Professor Howard's generic report fell outwith the scope of even his self-professed expertise. Second, the defender argued essentially that as Professor Howard was neither a toxicologist, toxico-pathologist nor a clinician, his opinion on these matters was not admissible. Finally, the defender argued that Professor Howard was not independent as he was, essentially, advocating for his theories in respect of aerotoxicity. He was, so contended the defender, part of a small group of "believers" in ATS.
The defender submitted that the problems identified under each of the four headings were so significant that the court should conclude that the pursuers' claim would have been bound to fail.
Decision
The judge considered that the defender's argument failed to appreciate the important distinction drawn out by Lord Prosser in Dingley (at 602 to 604) between the requirement of legal proof in a civil action namely, the balance of probabilities on the one hand and the ordinary use of "establishing" or "proving" that something is the case in any other context, particularly a medical or scientific one. As Lord Prosser put it:
"But speaking very generally, I think that the civil requirement of a pursuer that
he satisfy the court that upon the evidence his case is probably sound would in
ordinary language be regarded as very different from, and less stringent than, a
requirement that his case be established or proved. More importantly in the context
of a case such as the present, the fact that the two concepts are distinct in ordinary
language, but the same in this legal context, seems to me to give rise to a risk of
ambiguity or misunderstanding in the expressed opinions of expert witnesses."
Reformulating the defender's argument to take into account Lord Prosser's distinction, one can see that there might be significant force in the proposition that without identifying the particular substances involved, it would be impossible for the pursuers to demonstrate that their condition had been caused by exposure to toxic cabin air as a matter of scientific proof. However, as Lord Prosser makes clear, that is not the appropriate approach in the context of civil litigation. Of course, even though the judge rejected this part of the defender's argument, he still required to consider the defender's arguments in relation to causation which he did in the next section.
Under the heading of causation, it was necessary to consider two discrete arguments raised by the defender. The first concerned the issue of causation in general and was, essentially, whether the problems in respect of causation were so significant as to mean that the pursuers' chances of success were negligible. The second concerned the specific question of the divisibility or otherwise of ATS as a condition. This argument related, in particular, to Mr Montague-Trenchard.
The majority of the evidence that was heard was focussed on the issue of causation. In particular, this included evidence from four expert witnesses: the neuropsychologist, Professor Mackenzie Ross; the consultant neurologist, Dr Davenport; the toxicological pathologist, Professor Howard; and the toxicologist, Professor Bridges.
Distilling the pursuers' case on causation to its essentials, it could be summarised as follows:
1. Aeroplane cabin air is contaminated by air "bled" from the aircraft engines.
2. As well as occurring at a low level, this contamination is evident in one-off "fume events".
3. The contamination includes both fumes and particles from jet oil which is known to comprise, among other things, organophosphates.
4. The contamination is capable of causing harm. This can be seen from:
- The documented effects of fume events; and
- The research which identified the toxicological effects of repeated exposure to
low levels of organophosphates.
5. The pursuers had each been exposed to contaminated cabin air including fume events.
6. The development of neuropsychological symptoms by both of the pursuers was consistent with those reported by other aircrew and was consistent with the pursuers' history of exposure. The defender submitted that the problems with the pursuers' cases were so significant as to render negligible any chances of success which they had lost. The starting point for the defender's position was to highlight that the pursuers were seeking to establish causation in the absence of a medical consensus as to any causal relationship between the contaminated cabin air and the symptoms suffered by the pursuers.
The court then referred to the experts in turn:
Professor Howard
The defender challenged the admissibility of Professor Howard's evidence on three grounds. The court was not persuaded that it should sustain any of the defender's objections.
First, the defender argued that parts of Professor Howard's generic report strayed beyond even his self-professed expertise as a toxicological pathologist and, therefore, Professor Howard's opinion on these matters was not admissible. But the court did not understand Professor Howard to be holding himself out as an expert in these matters. Rather, Professor Howard was clear that in these parts of his report, he was simply setting out his understanding of the relatively complex factual background to his opinion based on publicly available and referenced documents.
Second, and more fundamentally, the defender objected to Professor Howard's evidence on matters of toxicological pathology on the grounds that he was not appropriately qualified and, therefore, his evidence was inadmissible. To sustain the defender's objection would require the court to be satisfied that Professor Howard's knowledge and expertise fell below the threshold of admissibility. The defender's objection appeared to proceed on a very narrow definition of the field of toxicology and to stem from Professor Bridges' views on this matter. However, it appeared to the court, on the basis of the evidence which it heard from, in particular, Professors Howard and Bridges, that the field of toxicology involves a number of different professional disciplines and subjects including those of medicine, pathology, analytical chemistry, neuropsychology, public and occupational health. Having considered Professor Howard's qualifications, his publications, his professional memberships and his experience, not least, in serving on public committees the court had no hesitation in repelling this objection.
Finally, the defender objected to Professor Howard's evidence on the grounds that he was not truly independent. This objection was based on the assertions that, first, Professor Howard had "...spent his recent professional life trying to convince others of his theories on aerotoxicity..." (defender's written submissions) and, second, that Professor Howard did not present competing or alternative positions in any of his reports. The defender asserted further that it was not open to the court to admit evidence and address the issue of independence or impartiality in terms of the weight ascribed to that evidence.
Dealing with the last point first, the court considered that the defender's argument was not consistent with the opinion of the UK Supreme Court in Kennedy v Cordia (Services) LLP [2016] WLR 597. Their Lordships are clear that independence and impartiality is an issue of admissibility as opposed to being "merely" one of weight. However, the court did not read their Lordships as restricting the court, once it is satisfied that the threshold of admissibility has been crossed, from taking account of any remaining issues in relation to a witness' independence and impartiality in the weight ascribed to that witness' evidence.
In any event, having considered Professor Howard's reports and having listened to his evidence, the court considered that the defender's objection was unfounded. It is fair to observe hat Professor Howard has, in recent years, involved himself in research and publishing in the undoubtedly controversial area of aerotoxicity. However, the court considered that Professor Howard's response when his independence was challenged in cross-examination was equally fair: "... I am not an activist. I am just putting my scientific thoughts into the literature with co-writers, co-authors and that's where it stands." In the reports he prepared in respect of each of the pursuers, he addressed the opinion of Professor Bridges and explained his reasons for not agreeing with it. Accordingly, for these reasons, the court repelled the defender's objections to the admissibility of Professor Howard's evidence.
Instead, to carry out that exercise of valuation, the court required, first, to consider whether the pursuers' chances of success can be rejected as negligible or speculative. On the basis of Professor Howard's evidence, the court did not consider that the pursuers' chances could be so described. Taken as a whole, Professor Howard's evidence established a basis for inferring that the pursuers' symptoms could have been caused by contaminated air to which they were exposed.
The court did not consider that, properly understood, the evidence of Professor Bridges negated that basis. Rather, Professor Bridges' evidence raised a series of factors which cast doubt on the drawing of the inference of causation. These factors include the following:
There was little or no evidence of the chemicals to which the pursuers were
actually exposed in the cabin.
Insofar as chemicals have been identified in cabin air, these do not appear to
be unique to that environment.
Furthermore, the estimated exposure of the pursuers to the chemicals identified appeared significantly lower than the levels currently thought to be capable of causing an adverse effect using current well-established methodologies.
The fact that humans are exposed to many chemicals at low levels each day
indicates that additive and synergistic effects must be uncommon in practice.
The fact that low-dose exposure to organophosphates has been shown to produce
a change does not, in itself, show that any such change was adverse.
There does not appear to be a recognised or accepted pattern of symptoms
reported by those who claim to suffer from ATS.
The court did consider that these factors do gave rise to significant doubts in respect of causation. These doubts require to be carried forward into the overall assessment of the pursuers' chances of success.
Professor Mackenzie Ross
The defender's submission in respect of Professor Mackenzie Ross was that, in short, her evidence as a neuropsychologist did not, in fact, support the pursuers' case on causation. She had been careful to make clear that the tests she performed on the pursuers do not, in themselves and in the absence of other evidence, allow conclusions to be drawn in relation to the cause of the pursuers' symptoms. She had concluded that it was premature to conclude that cabin air does not cause any risk to aircrew, but her evidence left open the opposite conclusion: namely, that it was premature to conclude that cabin air does pose such a risk. The defender contrasted the evidence of Professor Mackenzie Ross with that of Dr Davenport who had concluded that there was insufficient evidence to conclude that ATS was the cause of the pursuers' symptoms.
The court accepted the thrust of the defender's argument. It agreed that Professor Mackenzie Ross' evidence, on its own, would not provide a sufficient basis to infer that the pursuers' symptoms had been caused by toxic cabin air. However, that was not the pursuers' case. As the court understood their position, they principally relied on Professor Mackenzie Ross' evidence in two respects: first, to show that each of the pursuers presented the neuropsychological symptoms which her psychometric testing had revealed; and second, that those symptoms were consistent with previous studies of aircrew and appeared to show a temporal relationship with the pursuers' exposure. The pursuers relied upon this evidence to connect the symptoms suffered by the pursuers with their exposure to toxic cabin air as explained by Professor Howard.
Dr Davenport
The court did not understand there to be any real conflict between his evidence and that of Professor Mackenzie Ross. He had diagnosed each of the pursuers with chronic fatigue syndrome. He did not consider that there was sufficient evidence in the medical literature to support the notion of a specific aerotoxic syndrome. Further, he highlighted that based on what had been published to date, it was not clear to him that the pursuers would satisfy the criteria. However, it was clear that he remained open-minded. He did not seek to deny the possibility that at some point in the future ATS might become a recognised and accepted diagnosis.
Accordingly, the court did not consider that the defender's submissions in respect of the pursuers' reliance on the evidence of Professor Mackenzie Ross undermined the pursuers' case on causation. The pursuers' chances of success could not be described as negligible or speculative on this basis. The court carried forward Dr Davenport's doubts to the overall consideration of the pursuers' chances of success.
Overall assessment
The court considered that the pursuers had a real and substantial chance of success in their claims against Thomas Cook which was calculated to be a 40% chance. By "success" the court meant the achievement of a substantial payment in respect of their claims whether following a fully contested litigation or following an extra-judicial settlement.
Taking into account the assessment of each pursuer's lost chance at 40%, the court concluded that Mr Gough's loss was £24,762.80 and that of Mr Montague-Trenchard £1,159,094.74.
References
Cannon F. (2016) Aircraft cabin air contamination and aerotoxic syndrome a review of the evidence. Nanotechnology Perceptions 12: 1-27.
Howard, C & Michaelis, Susan & Watterson, Andrew. (2017). The Aetiology of ‘Aerotoxic Syndrome’- A ToxicoPathological Viewpoint. Open Access Journal of Toxicology. 1. 10.19080/OAJT.2017.01.555575.