(This is a repost of an article written by Khaly Castle with Erik Johnson, and originally published on CFSUntied.com Blog on 9/21/2011.)
Aerotoxic Syndrome is a fairly recent term, to describe a fairly recent phenomenon – long or short term illness that is attributed to cabin air that has been contaminated with atomized chemicals.
According to Wikipedia, with the exception of the Boeing 787, the air in a jet or turboprop cabin is supplied by “bleed air” from the aircraft’s engines. By most accounts, the air is approximately half bleed air, and half recirculated air. Although most aircraft cabins have filters for the recirculated air, the bleed air is not filtered.
Bleed air has the potential to be contaminated by a multitude of chemicals, not the least of which is TCP (tricresyl phosphate), from the synthetic lubricant oils used. This can happen when there is a seal leak, or when reservoirs are overfilled. TCP is an organophosphate, deemed to be linked to neurological damage when ingested.
According to a 2009 article in the Wall Street Journal titled “Up in the Air: New Worries About “Fume Events” on Planes” the FAA recorded over 900 “fume events” between 1999 and 2008. “But some airline-worker unions believe that contamination events are underreported by airlines and pilots.”
In the last blog post, (And Now For Something Completely Different) we talked about the toxin potential to human health that appears to be inherent in nanoparticles. Basically, the surface excitability of a material that is reduced to nanosize is greatly enhanced, giving nanoparticles the ability to “glom onto” biotoxins and other particles, and transport them to the human brain.
We talked about “Steering Immunostimulation By Particle’s Size: Nanoparticles and Human Health”, which deals with the idea that the human immune system differentiates between viral and bacterial pathogens based on size, and as a result, pathogens or toxins that are introduced to the system in nanosize are treated to a viral immune response.
We also talked about the fact that molds can act as nanoparticle factories, metabolizing nanoparticles and then spitting out plumes of even smaller nanoparticles, and in some cases how the mold toxins themselves have been attached to the new smaller nanoparticles.
This makes toxic mold a particularly compelling model for this hypothesis, as not only is it adding its own toxic elements to the nanoparticle soup, it is actually capable of breaking nanoparticles down to even smaller size and emitting them in plumes, even further increasing the potential for this dynamic.
But let’s bypass the mold factor completely for a moment. It’s an added factor that makes the nanoparticle delivery system even more confounding and dangerous, but even without it,…. Houston, we have a problem.
There are numerous studies out there that one can pull up regarding nanoparticle content in aircraft engine emissions. Most agree that, as one study put it, “aircraft engines emit a considerable amount of insoluble sub-0.1 μm sized combustion aerosol particles” Petzold, Aviation Particle Emissions and Airport Air Quality, June 14, 2005.
That being the case, let’s bang that against the 2007 annual report issued by The Committee on Toxicity, a committee that evaluates chemicals for their potential to harm human health, for various government departments and regulatory authorities in the UK. This report covers a variety of toxic topics, including nanoparticles, the COT addendum to joint statement of the committees in Toxicity, Mutagenicity and Carcinogenicity on Nanomaterial Toxicology.
Item number 11 is of particular interest:
For pharmaceuticals it has been shown that incorporation into nanoparticle formulations can greatly influence the biodistribution (and hence toxicity) of included chemicals. Indeed the intention behind many such formulations is to facilitate drug delivery across tissue barriers. There is little evidence that the biodistribution of other chemicals not physically included in the original formulations, but accidentally present in the body at the same time as the nanoparticles, can be so influenced.
However there is at least a theoretical possibility that freshly generated nanoparticles with reactive surfaces could significantly bind and alter the biodistribution of other xenobiotics. Such effects would not represent nanoparticle toxicity per se, but would represent a consequence of co-exposure.
”Reactive surfaces could significantly bind and alter the biodistribution of other xenobiotics”
This is exactly what we’ve been talking about. If, for instance, TCP would normally have to be ingested in quantity in order for its neurotoxic effect to establish damage in the human body, but instead was delivered directly to the brain via binding to nanoparticles, then we are talking about a whole new and potent delivery system of xenobiotics – One that would not require “massive quantities” to see effect.
So while it may not appear that enough xenobiotics were being introduced into your airplane cabin via the “bleed air”, the fact that nanoparticles can grab these toxins and upload them to the brain, bypassing normal avenues of immune response, changes the game completely.
This is the exact same mechanism that we were talking about in the last blog, except that we were talking more about biotoxins from mold. As Erik Johnson pointed out in one of his communications to the W.H.O., the Saratoga Springs manual noted surges of fungal pathogenesis that could not match what they knew about mycotoxins. Dr. William Croft called the effects “radiomimetric”. In the case of Aerotoxin illness, we have a different toxin possibly being subjected to the same hypothesis of delivery to the human brain as we did with mold toxins in the last article.
Dr. Sarah Myhill, CFS/ME expert in the UK, is also the medical advisor to the Aerotoxic Association. She goes into more detail in her paper Aerotoxic Syndrome – The Poisoning of Airline Pilots, Cabin Crew, and Passengers, that is possible on any airflight, where she discusses the effects of bleed air and its contamination with not only TCP, but an accompanying range of volatile organic compounds and heavy metals from the engine itself.
All of this is dire enough. What we are proposing is simply the additional nanoparticle factor. If we take what we already know about fume events and factor in the nanoparticle delivery-mechanism potential, we may be looking at a ready explanation for why toxic assault is happening at such increasingly devastating levels.
Again, this paradigm is not being proposed “instead of” XMRV, or instead of any other current pathogen trail. There is no reason to think that there is only one dynamic at play here.
But Erik Johnson observed the effect of transcendent-toxic-pathogenesis at the inception of CFS, noted its uncanny similarity to Aerotoxic syndrome, and the application the nanopathology hypothesis appears to possess potential to demystify at least some portion of these otherwise inexplicable phenomena.
This effect still screams for research. It may be a dynamic that reaches far beyond CFS and encompasses a new look at human health issues on a very broad scale.