Aerotoxic syndrome, what is this about?

Contrary to what many people believe, Aerotoxic syndrome is not particularly related to airplane exhaust gases. Aerotoxic syndrome is related to fumes originating from engine lubricating oils. When such oils (which all contain organophosphates) come into contact with surface temperatures, shear forces and pressures above the design environmental envelope, a process called pyrolysis, will take place. This process triggers changes in the oil at a molecular level, and the creation of multiple new compounds. As the hot surfaces also induce evaporation, the fumes mentioned will enter the cabin air supply if bleed air offtake is used. These fumes trigger a wide range of effects on humans.

Who is affected?

Ca. 30% of people are poor detoxifiers. In other words their body has a hard time breaking down the toxines in the cabin air. This condition can be assessed by a costly DNA test. – This does not mean that other people may never suffer from Aerotoxic Syndrome. All is related to exposure, so even a good detoxifier might get ill after an acute fume event (i.e. high concentration over a short time) or chronically (low concentration over a longer time e.g. career or as frequent flyer).

What happens? = degeneration of neurological functions

So what are the actual mechanisms linked to polluted cabin air that cause health issues?

• White blood cells (T-Lymfocytes) attack the Myoline (i.e. the insulator around our nerves) causing electrical transmission problems. This is a clear indicator of Aerotoxic Syndrome (not present e.g. with multiple sclerosis). Problem: you can only check this condition post-mortem within 24h!
• Due to pyrolysis of oil in the engine, toxic organophosphates (TCPs) are formed. These are Acetyl and ButylCholineEsterase (AChE and BChE) inhibitors. AChE and BChE are enzymes that normally clear the receptor of nerve cells. If unable the electrical transmission in the nerves is blocked (causing e.g. numb fingers). Problem is that TCPs can also originate from other sources. So you would need to test people beforehand. Unfortunately you don’t know when you might have a fume event. Luckily, the SECURETEC test has established a baseline value, which can be used as a reference to assess TCP exposure after a fume event.
• Currently under study: metal dust nanoparticles (from the bearings) enter the brain via the nose ceiling and affect brain functions.

By the way: the fact that tricresyl phosphates (TCPs) are present, is undisputed. The real question is if and how these extremely low concentrations affects our health.

Why is there still no causality (exposure to toxines resulting in health issues) established?

• Research that’s done is biased and serves FUD (Fear/Uncertainty/Doubt) by the industry. According to Dr. Mulder, the chief editor of the Lancet was shocked by lack of peer-review in published studies regarding Aerotoxic Syndrome.
• No funding for independent research (money needed).
• Not well understood therefore often wrong diagnosis: multiple sclerosis, Alzheimer…

The air supplied to the cabin, where does it come from?

Historically, cabin air can be drawn from the engine compressor zone (bleed air offtake) or directly from the outside. Nowadays, practically all airliners use the bleed air offtake system. Boeing 787 is the exception.

Engine lubrication and lubricants

As any other engine and mechanical system, a jet engine needs lubrication of its moving parts. Moving parts comprise the axles on which the compressor and turbine are mounted.

What is cabin air contamination and where does it come from?

Any aircraft taking the air to pressurize (and ventilate) the cabin from the engine applies the “bleed air offtake” principle. In effect, air entering the jet engine will be tapped from one of the compressor stages, be fed to the air conditioning packs and thereafter into the cabin. The air mixture in the cabin will typically be a combination of “fresh air” and recirculated air.

Cabin air contamination of the type discussed in this article is about fumes originating from engine lubrication oil being subjected to temperatures, pressures or shear forces outside the design envelope. As the engine lubrication oil should be contained in its working space by seals, a leakage may be present. A “fume event” of the sort related to aerotoxic syndrome can take 2 forms:

• Slow leakage in low concentrations (seal leakage);
• High leakage in high concentrations (seal failure).

Does engine lubrication oil typically leak from its cavities of application?

Engine lubrication oils are enclosed in their space of function by seals. Typical seal types used: labyrinth seals and mechanical face seals. From an engineering perspective, one must understand that any seal is designed to leak. Indeed, designing a 100% isolating seal would be very costly in both design and implementation. Example: pilots on A32F check engine oil levels during the flight preparation. These levels continuously drop in flight and must thus be monitored. As oil does not just disappears it is not hard to link the seal design leakage with the presence of (pyrolysed) oil compounds. Pyrolysis will happen when oil leaking inside the engine encounters areas of temperatures above 250°C and /or high pressure/shear forces (measured up to 5000psi in jet engines). The reader no doubt realizes both conditions are continuously present in a typical jet engine operation.

Leakage of this kind is also heavily dependent on the engine regime. Reports indicate that fume events happen mostly during take-off (powering the engine from idle to take-off thrust) and final approach (going from flight idle to approach setting in full configuration). Moreover, some engines are more prone to leakage than others. The ones fitted on BAe146, AVRO and Boeing 757 are the most renowned when it comes to fume events, although it is an industry wide issue on all plane types.
A seal failure is of course an acute case and differs from the above because the design failed. Such cases are rare but any mechanical thing can always fail of course.

What is “pyrolysis”?

Pyrolysis will happen when oil leaking inside the engine encounters areas of temperatures above 250°C and /or high pressure/shear forces. The reader no doubt realizes both conditions are continuously present in a typical jet engine operation. Another way to name this is “lubricant degradation”.

Key fact: lubricants are often exposed to temperatures, pressures and shear forces well outside the design spectrum. This leads to lubricant breakdown.

Key question when discussing pyrolysis: which components break down and if so in what?

When engine oil undergoes pyrolysis, what kind of compounds are formed?

Many chemical components are present in engine oils subjected to design environmental conditions. However, the number of chemical components is being increased when subjected to pyrolysis. Of these many components resulting from pyrolysis, the following TCP-isotopes are typically found in highest concentrations: mmm-isotope (triggering paralysis) and mmp & mpp-isotopes (primarily influencing the nerve butts). All lubrication oils used today on modern airline turbofan engines are of the Organophosphate type and thus these TCP-isotopes. Important to know in this context is that engine lubricants are certified by performance specification, not composition specification. Actual content analysis is therefore virtually impossible given the chemical complexity of the lubricants by design. Pyrolysis further complicates the mixture as this is an uncontrolled process.

Are organophosphates and TCP-isotopes dangerous?

Engine lubricants are not the only substances in which organophosphates are used. For example, pesticides used to fight ZIKA & NILE virus (spread by mosquitoes) are also OP-based. Furthermore, nerve agents containing organophosphates can be weaponized. SARIN-gas is an example of this. Military findings indicate a remarkable similarity between the symptoms of SARIN-like nerve gas effects and aerotoxic syndrome.

What about the military?

Starting in the mid-50s, military (transport) aircraft have been using bleed air offtake systems much like civil airliners have. However, the military (based on information received from the USAF Human Factors Wing) have quickly spotted issues and have chosen to install cabin air filtration systems to safeguard the human element on board. Quoting Mr. G. Slusher, Research scientist of the 711th human performance wing USAF: “I am blown away that civil airliners have no cabin air filtration when using bleed air offtake”.
The military knows about the chemical and neurotoxic characteristics of Organophosphates as it is being applied in the form of nerve gases (e.g. SARIN).

Can TCP-levels be measured?

At present, we are not aware of any system available to measure TCP-levels in the cabin air. PALL-aerospace has communicated they will be launching a measuring system in 2018.

In human beings, e.g. after a fume event, it can be measured, but the detection process is very specific. The physician needs to know very well what to look for, which tests to do and specimen to collect. Also, the proper infrastructure needs to be present and available. Few medical centers are presently capable to do these tests. However, multiple tests are in development stage. Currently, it looks like the SECURETEC test (http://bit.ly/2sDPdmL) is the only one to have established a baseline value, which can be used as a reference to assess TCP exposure after a fume event using a standard blood sample.

For more information on proper testing on TCP-levels and aerotoxic syndrome, go to the GCAQE (Global Cabin Air Quality Executive): https://gcaqe.org.

Can TCP-levels be filtered?

PALL-aerospace will launch a filtration set for bleed air offtake aircraft in 2018. EasyJet has already decided (August 2017) to (retro)fit their entire fleet with such filters when they become available. No doubt, cabin air quality will quickly become not only a medical issue but also a commercial one.

Change of attitude?

The “aerotoxic syndrome” has received more and more coverage these last years. Ever more scientists, toxicologists, academics and universities start to focus on the subject. Still, only few real large-scale studies exist, and even fewer when only taking those studies not done by aviation rulemaking bodies (FAA, EASA…). All toxicologists, professors of health… present at the GCAQE Conference agreed on the fact that these rulemaking bodies are using faulty threshold values to establish whether organo-phosphate-concentrations measured in cabin air are harmful or not. The scientists hinted multiple times on the close relationship of these rulemaking bodies with the aviation industry and lobby.

The first large-scale study on aerotoxic syndrome has been done by Dr. Susan Michaelis and can be read in full via the following link: http://bit.ly/2saaBPH.

Is the Aerotoxic Syndrome considered as an occupational disease?

At the forefront of the present-day push of scientists striving for recognition of the “aerotoxic syndrome” is the research on it being an occupational disease or not. Put otherwise: if a person is subjected to cabin air possibly contaminated on a regular basis (like Crew Members on their daily flight duty…), does this lower the threshold for lasting neurological damage when exposed to higher concentrations in case of more severe leakage or seal failure? The aforementioned study by Dr. S. Michaelis clearly demonstrates a statistical significant indication this effectively being the case. More study is required. Finally, acceptance of this fact by the rulemaking bodies is far from becoming a reality.

The Belgian Ministry of Health has requested that the current studies on this topic be reviewed by a group of scientists in order to determine whether or not Aerotoxic Syndrome should be considered an occupational disease. BeCA has contacted the cabinet of Mrs De Block to offer our expertise. They are currently looking at the available studies and should get back to us at a later stage. We will keep you informed.