Is there something in the (cabin) air?

In early 2013, the death of a BA Pilot (Richard Westgate) hit the headlines following claims that he may have been suffering from symptoms related to occupational exposure to neurotoxic chemicals. Specifically, there was speculation about whether his death may have been the result of repeated exposure to contaminated cabin air. Due to the obvious impact that toxic cabin air might have in terms of public safety, the Senior Coroner for the County of Dorset (Sheriff Stanhope Payne) was charged with investigating these claims, and at the time of writing this blog in June 2015, this inquest is still ongoing.

In February this year (2015), Richard Westgate’s death hit the headlines again when Sheriff Payne was compelled to issue a Regulation 28 report out of concern for public health. These reports are only written when a coroner determines a possible cause of death that could have a wider impact on others – when it is felt further deaths could result from the same cause and that preventative action could and should be taken. In this case, Sheriff Payne cited organophosphate (OP) exposure as a probable cause of death and he issued the report to both British Airways (BA) and the Civil Aviation Authority (CAA), calling for urgent action to be taken to minimise any future risk of harm. Two months later, both of these organisations issued their formal responses to this report stating that the evidence on which the Sheriff based his conclusions was ‘selective’ and that no link between exposure to contaminated cabin air and long-term health effects has been established – although they acknowledge that such a link cannot be excluded.

Despite these claims, in June 2015 the BBC reported that at least 17 individuals are now seeking legal action against British airlines citing exposure to toxic cabin air as the cause of their ill health. Whether or not they will be successful in their claims remains to be seen, but at least one precedent has been set: in 2010 a former flight attendant was awarded compensation for respiratory damage sustained as a result of exposure to on-board neurotoxic chemicals (including OPs).

What are organophosphates and why are they harmful?

OPs are a type of neurotoxic compound which have a number of different properties and uses. ‘Neurotoxic’ essentially means that they can interfere with nervous system functions, resulting in cognitive, emotional and/or behavioural problems. This interference can take place via a number of different mechanisms, but the main biological actions seem to be through (1) interrupting the normal process of neurotransmission (particularly with regard to the neurotransmitter acetylcholine) and (2) as a result of damage to parts of the neurons themselves, specifically axons and myelin (Abou Donia, 2010).

The fact that OPs can directly interfere with the nervous system is not a new discovery. In fact, some OPs have been used as nerve gas agents since World War II – both Sarin and Soman are types of OPs. However, their use is not confined to areas that are quite so controversial or necessarily harmful. Since the 1950s OPs have been engineered to have lower toxicity to mammals, and some have selective toxicity to specific organisms, such as insects. In this form, OPs make up the vast majority of the world’s pesticides/insecticides and are extensively used to control insects in both domestic and public contexts, agriculture, horticulture and veterinary medicine. However, while these versions of the compounds have been modified to make them less harmful to humans, this does not necessarily mean that they are harmless. Indeed the immediate effects of high level exposure to OPs have been well documented and a plethora of evidence exists to support the view that acute OP poisoning can cause ill health and neuropsychiatric symptoms. However, considerable controversy still surrounds the issue of whether exposure to lower levels of OPs is harmful (see Alavanja et al (2004)  and Mackenzie-Ross et al (2013) for reviews).

But why are these compounds on a plane? The reason is that in addition to acting as pesticides, OP compounds have a number of chemical properties that make them very useful in a number of different contexts. For example, the OP tricresyl phosphate (TCP) has anti-wear and flame retardant properties which allows it to work as a lubricant under extreme pressure. As such, TCP is a very useful additive in jet engine lubricants and hydraulic fluids. In fact, it is exposure to TCP that a number of aircrew are particularly concerned may be the cause of their ill health.

What are the reported effects of OP exposure?

Airline crew and passengers have been reporting ill-health following exposure to contaminated air for many years (see Mackenzie-Ross et al (2012) for more information). The immediate effects of exposure include eye and skin irritation, breathing difficulties, headaches, nausea, dizziness, fatigue and cognitive impairment (e.g. disorientation, confusion and memory problems). These effects tend to occur soon after exposure and resolve when the person moves away from the source of OPs. However some exposed individuals report more persistent symptoms lasting months or even years after their last exposure to OPs. In these more chronic cases, a wide array of physical and psychological symptoms may be experienced, including cognitive impairment (memory, word finding, multitasking difficulties), lack of coordination, nausea/vomiting, diarrhoea, respiratory problems, chest pains, severe headaches, light-headedness, dizziness, weakness and fatigue, paraesthesias (pins and needles or tingling sensations), tremors, increased heart rate, palpitations (pounding heart), irritation of ear, nose and throat, muscle weakness/pain, joint pain, skin itching, rashes, blisters, hair loss, signs of immunosuppression (being more prone to illness) and chemical sensitivity. Although a debate is ongoing in the UK about the causation and diagnosis of these long-term effects, OP exposure remains a possibility.

The uncertainty about a causal link between OP exposure and these chronic symptoms lies in the difficulty we have with establishing an accurate estimation of exposure. For example, given the absence of routine on-board air quality monitoring on commercial aircraft, it is impossible to determine what chemicals enter the cabin or in what quantities. In addition, self-report measures of exposure are notoriously problematic as they rely on people’s memory of events and their capacity to detect noxious substances (both of which vary in reliability enormously). As such, before a causal relationship can be established the mechanisms through which exposure might occur and the level of the exposure need to be better established. So first, let’s consider how someone on a plane might become exposed to OPs.

How does exposure occur?  

The issue here comes from how air is supplied throughout the aircraft to allow crew and passengers to breathe. When on the land, we are used to breathing in air that is an average of 15°C and a pressure of 14.7 psi. (in the UK at sea level). However, at an altitude of 35,000 feet the air pressure is only 3.46 psi with temperatures lower than -50°C. Fresh air is pumped into the plane from outside the aircraft, but it first needs to be warmed and pressurised to a safely breathable level.

As part of the propulsion process, airplane engines heat and compress air before fuel is added and combusted. On some aircraft this air is then ‘bled off’ and pumped into the aircraft, unfiltered. Ordinarily this process is safe, however occasionally faulty seals can result in contamination by allowing engine oil fumes to escape into the airflow.

The incidence of these ‘fume events’ is difficult to quantify, as commercial aircraft are generally not fitted with equipment for monitoring on-board air quality. There is also significant under-reporting of exposure: for example, the Committee on Toxicity of Chemicals in Food, Consumer Products and the Environment (CoT) have estimated that fume events occur on approximately 0.05% of flights. However, a survey by the British Airline Pilots Association (BALPA) found that up to 96% of the contaminated air events that pilots experience may go unreported to the CAA (Michaelis, 2003), possibly due to lack of awareness, commercial pressure and the perception that exposure to such contaminants is normal and part of their everyday job.

In 2000, to better establish the incidence and outcome of fume events, CoT recommended that the UK DfT commission (1) an air monitoring study of affected aircraft types and (2) a cross-sectional epidemiological study examining neurological outcome in pilots. In 2008 Cranfield University were chosen to undertake the first of these studies. They monitored a total of 100 flights, measuring the levels of several chemical compounds that were present in the cabin during various stages of flight. A number of chemicals were detected over the course of this study, including the organophosphate TCP, carbon monoxide and toluene; all levels were reported to be within safe limits – although it is of note that no aircraft safety standards actually exist with regard to TCP. While this may be reassuring for routine flight safety, no fume events were observed on any of the flights that were monitored (which is not overly surprising given the sample size and the relative rarity of cabin air contamination). As such, the possible exposure that passengers and aircrew may face during a fume event remains unclear.

So what evidence is there?

Without accurate measures of exposure, it’s very difficult (if not impossible) to reliably establish whether or not there is a relationship between ill-health and exposure to fume events. However, there is some supporting evidence. For example, symptom surveys (e.g. Michaelis, 2003) and case studies of passengers and crew who have been involved in known contamination events (as confirmed by mechanical report) have demonstrated deficits consistent with OP exposure (e.g. Murawski, 2011). Indeed, my own work (in collaboration with colleagues at UCL) has found a cognitive deficit profile in airline pilots similar to that seen in OP exposed farmers (Mackenzie-Ross et al, 2012). In addition, biological markers of possible neurotoxicity have been found in some individuals with these symptom profiles (e.g. Abou-Donia et al, 2013) and at post-mortem (Abou-donia, 2014). However, while these studies may provide evidence consistent with OP exposure, it is still very difficult to claim causation; mainly due to the small sample sizes and correlational findings.

So it seems there is still a large amount of scientific uncertainty regarding the long term effects of inhaling pyrolysed engine oil on human health. However, with the growing pressure from lobbyists (like the Aerotoxic Association), potential legal suits and inquests it seems like we may soon have a more definitive answer to this question. At the end of 2014, the European Aviation Safety Agency launched a Preliminary Cabin Air Quality Measurement Campaign, which should allow for the funding and development of instruments that may be able to monitor air quality in real time. In addition, biomarkers for exposure to TCP have recently been developed by researchers from the Universities of Washington and Nebraska. Given these advancements, we may not be far away from establishing a valid and reliable measurement of exposure. Once that has been achieved, establishing whether a potential link between ill health and exposure truly exists should be the logical next step.

Gini Harrison, The Open University