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How clean is the air we breathe when we fly?

Air travel has become ubiquitous and more affordable in the last decade. In 2014 alone, global passenger traffic rose nearly six percent, which was higher than the 10-year average growth rate and the previous year’s, according to the International Air Transport Association (IATA). IATA predicts that passenger traffic will more than double over the next 20 years despite current global economic uncertainties.

As globalisation in trade and travel put more people in the air, cabin air quality is increasingly becoming a more  important issue.

“Cabin air contamination may well be an emerging public health risk and must be taken seriously,” said Michael Hubel, head of unit of health programme and diseases, Directorate General for Health and Consumer Affairs (DG SANCO) of the European Commission. Susan Michaelis is an advocate and authority on cabin air quality and has been working to bring attention to the issue of air quality for pilots and cabin crew. “Anyone outside can clearly see that breathing heated synthetic jet engine oils and fluids cannot be good, particularly when there is an engineering mechanism that explains how low level oil leakage is a part of the engine cycle and completely normal,” she said.

Michaelis, who has a doctorate on workplace safety science, was a commercial pilot and is head of research of the . Although it is a fact that Michaelis and other pilots and cabin crew have suffered from aerotoxic syndrome, a disease caused by occupational exposure in the airplane, there are those in the aviation industry who refuse to acknowledge it as an occupational hazard. Others prefer to use different diagnoses for health problems due to exposure to cabin air contamination, such as organophosphate-induced chronic neurotoxicity (OPICN), organophosphate-induced neuropathy (OPIDN) or reactive airway disease.

Lawsuits such as that filed by four Alaskan Airlines flight attendants against Boeing recently for illness due to a toxic air leak from the engine during a 2013 flight is just one in a slew of similar cases that have been litigated. Terry Williams, a former American Airlines flight attendant, agreed to an out-of-court settlement with Boeing in 2011. In 2010, Joanne Turner won her case in Australia. The death of a 43-year old, previously healthy, British pilot who suffered severe neurologic symptoms in 2012 even led to an inquest in 2015 “to prevent future

“We are having more effect outside the aviation industry, but we are getting heard within the industry bitby- bit, but all behind closed doors,” said Michaelis. ”In fact, at a meeting with the major aviation regulator in Europe, it was acknowledged that they took virtually all their information from the manufacturers, with other sources being secondary.”

Capt. Tristan Loraine, former airline captain and director of "A Dark Reflection," a film about aerotoxic syndrome.
Capt. Tristan Loraine, former airline captain and director of “A Dark Reflection,” a film about aerotoxic syndrome.

What is the problem? 

Most aircraft currently use engine air compressors that “bleed” air into the cabin deliberately to supply cabin ventilation and conditioning. Auxiliary power units (APU) can also be used while on the ground and sometimes during takeoff or landing, which can also cause contamination. Most jet engines use synthetic oils that contain an array of potentially toxic substances when pyrolysed and inhaled. The majority of the literature focuses on tri-aryl phosphates (TAP), in particular tri-cresyl phosphate (TCP) and its 10 isomers, although N-phenyl-alpha-napththylamine (PAN) is also of concern and carbon monoxide can be present in the deadly cocktail of toxic cabin air leaks. The likelihood of fume events and contamination is further exacerbated when engine operate at very high temperatures. However, studies have shown there is a risk of exposure, even absent obvious fume events.

TCP, an anti-wear additive present in most jet engine oils and hydraulic fluids, generally makes up one to three percent of many formulations with varying amounts of ortho, meta and para isomers of TCP. Organophosphate poisoning from insecticides is quite well known, but in the case of tri-ortho cresyl phosphate (TOCP), one of the ortho isomers of TCP, its human neurotoxicity was established after the poisoning outbreak in the 1930s when tens of thousands of people suffered from what was labeled as the Ginger Jake paralysis.

Other ortho isomers, mono-ortho cresyl phosphate (MOCP) and di-ortho cresyl phosphate (DOCP), are even more toxic than TOCP, five and ten times respectively.

Because of the known toxicity of TOCP it is used sparingly in jet engine oil formulations. It is classified as a hazardous chemical by the U.S. Occupational Safety and Health Administration (OSHA) and the Material Safety Data Sheet (MSDS) specifically cautions against breathing in its dust, fumes, gas, mist vapor or spray. In case of inhalation, a person is advised to move to fresh air and in case of accidental release, adequate ventilation is advised aside from use of personal protective equipment (PPE). These measures are hard to follow in case of an airplane leak, except perhaps the use of PPE if there is the obvious fume or “dirty sock smell.”

TOCP is the only TCP isomer with an established OSHA permissible exposure limit (PEL) of 0.1 mg/m3 for general industry, not specifically for the aviation industry or enclosed spaces such as an aircraft. Although meta and para isomers are supposedly completely inactive, results of some studies on oil formulations that had low levels of TOCP yet showed consistent neurotoxicity seem to put that into question.

Trixylyl phosphate (TXP) is another tri-aryl phosphate used and is on the European REACH substance of very high concern (SHVC) list due to reproductive toxicity effects, meaning it may cause harm to the unborn or impair fertility, and is on the first phase of the REACH process of substitution.

Health effects: real or imagined?

In 2000, Winder and Balouet published “Aerotoxic Syndrome: Adverse Health Effects Following Exposure to Jet Oil Mist During Commercial Flight.” They coined the term aerotoxic syndrome, which encompasses consistent neurologic, gastrointestinal, respiratory and other symptoms that they documented immediately after exposure and post-flight with some symptoms lasting for longer than six months.

However, some argue that it is not a true syndrome nor is it exposure-related. Common symptoms include disorientation, blurring of vision, memory impairment, shaking tremors, nausea, vomiting, dizziness, confusion, numbness, loss of balance, shortness of breath, palpitations, eye and nose irritation. Longer term sequelae include cognitive problems, headaches, fatigue and tremors, to name a few.

Robert Harrison, senior attending physician of occupational medicine at the University of California inmedicine at the University of California in San Francisco, is the lead author of the 2010 “Exposure to Aircraft Bleed Air Contaminants Among Airline Workers: A Guide for Health Care Providers.” The project, which was funded by the Federal Aviation Administration (FAA) Office of Aviation Medicine, was the collaborative effort of several agencies.

The document addresses the issues and recognises that pyrolysed jet engine oil or hydraulic fluid may contaminate the air inside the cabin and as such, affect cabin air quality and consequently affect the people inside the airplane. The term aerotoxic syndrome is not used in this guide, although the symptoms described by Harrison overlap those reported by Winder and other publications that use the term.

A case series is presented with exposure events, acute symptoms and supporting physical examination tests and some laboratory tests. The comprehensive document goes on to establish a case definition of acute health problems due to bleed air contamination, as well as health risk and exposure assessments.

The United Kingdom’s Committee on Toxicity (COT) acknowledged in their 2013 position paper, that  “contamination of cabin air by components and/or combustion products of engine oils, including triaryl phosphates, does occur, and peaks of higher exposure have been recorded during episodes that lasted for seconds.”

Susan Michaelis
Susan Michaelis

Furthermore, “episodes of acute illness, sometimes severely incapacitating, have occurred in temporal relation to perceived episodes of such contamination and there are a number of air crew with long-term disabling illness, which they attribute to contamination of cabin air by engine oils or their combustion products.”

However, the committee almost immediately backtracked on their statements by stating that these could all be due to a “nocebo effect”, which means just the suggestion of possible harm (from exposure) will bring actual negative effects or physical symptoms.

“I believe that my patients exhibited their symptoms due to direct or indirect toxicity secondary to their exposure and that it is not due to a nocebo effect,” Harrison said when questioned about the COT’s explanation.

Don’t ask, don’t tell or don’t want to know? 

For most ardent advocates of the issue, there is a high level of frustration due to the catch-22 scenario. There is no strict and real-time continuous monitoring of air quality during flight, which means contamination within the cabin is poorly documented. Although any fume event is supposed to be reported by law in the U.S. and other countries, it seems that it is underreported. Incidence rate of leaks or fume events are extrapolated from data based on airline crews’ self-reporting of events and from studies with relatively small sample sizes looking into traces of TOCP and other isomers after a normal flight.

In addition, the absence of real-time monitoring to document exposure makes it hard to directly correlate the onset of illness to a specific exposure event. Lastly, the absence of an accepted gold standard laboratory test or even a reliable and accepted test to determine exposure to TCP (isomers) and other potentially toxic substances right after or soon after exposure and later when symptoms develop makes it difficult for those affected to prove their case.

Bleed air diagram courtesy of documentary "Welcome Aboard Toxic Airlines."
Bleed air diagram courtesy of documentary “Welcome Aboard Toxic Airlines.”

Solving the problem with engineering controls 

“More electric/bleed-free systems (i.e., a separate electrically driven-environmental control system or ECS compressor) will remove any chance of cabin air pollution as the air is taken from a separate inlet well away from the engines. This also allows the ECS operation to be better matched to the flight cycle and allows higher cabin pressures and air flow rates,” said Peter Malkin, professor of electric power systems at Cranfield University’s School of Aerospace, Transport and Manufacturing in Bedfordshire, UK.

“Unfortunately, despite much work in Europe, only Boeing’s 787 Dreamliner has adopted this technology. This is despite the fact that 787 has shown that such systems also save fuel for many flights. It is disappointing that Airbus has not adopted this technology despite many millions of funding from the EU,” Malkin said. “There are some technical issues which make a 787-style system difficult to scale for various aircraft sizes but these can be solved.”

Heiko Stolzke, Airbus’ media relations manager, countered that Airbus cabins are designed to prevent air
contamination under normal operating conditions and the air on board is safe, clean, oxygen-rich and almost sterile
during flight. According to Stolzke, the latest studies show no evidence of concentrations of TCPs in an aircraft cabin. Airbus aircraft (and its cabin air systems) are certified by the European Aviation Safety Agency (EASA) and FAA and comply with airworthiness requirements and industry standards, she said.

The Boeing 787 Dreamliner’s no-bleed systems were clearly heralded by Boeing as a major improvement, in the matter of saving fuel and enhancing operational efficiencies, but it avoids any mention of the health and safety benefit of the new aircraft. When asked about th and safety impact of the new no-bleed systems, Boeing did not offer any comment on the subject.

There has been research into developing procedures and reliable tests for monitoring cabin air contaminants, including TCP and its various isomers, to better document its presence. One of them was a 2012 published report by the Airliner Cabin Environment Research (ACER) entitled “Sensors and Prognostics to Mitigate Bleed Air Contamination Events,” where the authors mentioned that a prototype of a wireless sensor network has been “successfully tested in a Boeing 767 mock-cabin.” Of course, this technology is not yet proven and has not been tested to detect all the substances of concern, but at least there is hope.

Less toxic alternatives 

Nyco, which is based in France, has a line of commercially available aviation jet engine oils which are TCP-free. Nyco has used isopropylated triphenylphosphate (TIPP) in the formulation, instead of TCP since the 1970s, when TCP was added to the list of chemicals that can cause occupational diseases in France. Turbonycoil 640 has received U.S. military specification MIL-PRF-23699 HTS approval and was added to the Qualified Products List (QPL) at the end of December 2014. It can be used in hot to very hot engines in military and civil aircraft. In 2015, Embraer has qualified NYCO’s Turbonycoil 600, synthetic standard turbine oil, on the Embraer-jet family (E170/E175/E190/E195) powered with GE CF34-8E and GE CF34-10E turbofans.

The development of a safer anti-wear additive is an on-going effort by some manufacturers and researchers like Clement Furlong, professor of medicine, Division of Medical Genetics & Genome Sciences, at the University of Washington in Seattle, Wash., U.S.A. Furlong and his colleagues have done in vivo and in vitro tests to determine potentially less toxic additives with encouraging results, such as the tert-butylated isomers of TAPs that produced less butyrylcholinesterase (BChE) inhibition than the other 18 TAPs they tested.

Testing for TCP exposureTesting for TCP exposure 

With recent on-going research, there is the possibility that affected pilots and cabin crew could prove they are not imagining the correlation between exposure and disease and that they are not just suffering from the “nocebo effect.”

“After attending two conferences on this issue, I decided that the first and most important issue was to develop a blood test to document exposure,” said Furlong. “We are still working on this test, but getting much closer. The methods that we have developed so far allow us to detect as little as 2% modification of the active site of plasma cholinesterase by organophosphorus insecticide from a blood sample as small as a blood spot on a filter paper.”

Interestingly, the researchers also published a 2011 study wherein six out of 12 subjects (aircraft passengers) tested positive for low levels of plasma phosphorylated BChE. None of the six exhibited any overt symptoms. After re-evaluation of those passengers three to seven months after their last flight, four tested negative for BChE.

Furlong and his colleagues have also investigated acylpeptide hydrolase (APH), which is present in red blood cells, as a biomarker for TCP exposure.

“A second question regarding the differential sensitivity among people is being addressed by identifying the cytochromes P450 that convert TCP into very toxic metabolites. We have made significant progress on this issue and are working on a manuscript describing this work,” he said.

Furlong is also working on addressing the question of the conversion of the pre-toxins to potent toxin metabolites in the brain.

Other researchers are working actively to provide answers as well, looking at other possible markers. A 43-year old pilot was never diagnosed as having OPICN when he was alive, but had a subcutaneous biopsy about six months after his last flight (but prior to his passing), which showed organophosphate metabolites. Mohamed Abou-Donia et al conducted further studies postmortem. Histopathologic studies were consistent with OPIDN. Furthermore, increased autoantibodies against neurofilament proteins (NFP) and other brain specific proteins were consistent with OPIDN or OPICN.

Furlong said that in the Cranfield II conference, there was a suggestion to follow the health issues of passengers on flights where the pilots and crew have suffered documented neurological damage. “Many or most times of fume events, the passengers are sent on their way with no explanation of the nature or significance of an exposure that they’ve just experienced. A good epidemiological study of passengers on such flights would be very informative,”
he said.

Hopefully, studies like these will be undertaken and researchers like Furlong will receive support from all sectors. Real regard for health and safety is needed and all stakeholders should work together, instead of against each other, to make aviation safer for the crew and for their customers, the flying public.