Multiple Chemical Sensitivity Etiology

Airway Genetics and Ambient Combustion Aerosol

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g) Top researchers in the world conclude that conditions associated with chemical pollutants begin with induction of airway epithelial injury (Calderon-Garciduenas 2008, Veronesi 2001) - tight junction defects, focal desquamation, and proliferation of nerve fibers found in biopsy of MCS patients (Meggs1997) - coherent pathways - exposed c-fiber nerve receptor (nociceptor) inputs and central sensitization (Latremoliere 2009, Bessac 2008) inflammatory mediator release and systemic oxidative stress (Dantoft 2014, Deluca 2010, Kimata 2004) pollutant penetration and more oxidative events (Gillespie 2013, Block 2012, 2004, Calderon-Garciduenas 2008).
h) It can't be that simple - exposed sensory nerves in damaged airway epithelium - activated by the ACA and other chemicals - by physiological definition the other things will happen. There is genetic and exposure variation among individuals - but a fundamental picture emerges - causal relationships that can't be abridged. Better happy than acknowledge the ACA - combustion fuel vehicles, oil refineries, fireplaces, woodstoves, geopolitical turmoil, overpopulation: 1960 to 2015 - 4.4 billion added in 55 years, resource loss, climate change, ocean acidification, mass extinction, speed, violence, pollution - injury, illness, and premature death

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a) TRPA1 expressing peptidergic terminals, c fiber nerves, sensory receptors, nociceptors, primary afferents, unmyelinated c fibers - synonymously referring to the initiating point of inflammatory response. Peptidergic includes release of neuropeptide (neurotransmitter) inflammatory mediator substance P.
b) Once MCS is established - airway damage - permanent alterations - exposed TRPA1 expressing sensory receptors - whether from the continuous ACA or other exposure - at that point - activation of TRPA1 supports the disease process - an equal opportunity receptor to a broad range of chemicals.
c) MCS response is often masked - continuous exposure including the ACA - lacking distinction - the baseline upon which other exposures are judged - straws on the camel's back - perception of relative significance can be turned backwards. A smoker diagnosed MCS - as with the continuous ACA - has overlooked thousands of chemicals - many adsorbed on PM - potent stimulators of TRPA1 - supporting the MCS disease process.
d) The most qualified researchers in the world have shown that deenervation, genetic deletion, or pharmacological channel inhibition of TRPA1 impairs inflammatory release (Nassini 2011, Caceras 2009, Bessac 2008, Bautista 2006, Veronesi 2001) and the ACA has PM and gas phase components that potently stimulate TRPA1 - releasing cytokines and neuropeptides upon which the multiorgan systemic inflammatory process of MCS depends (Deering-Rice 2011, Taylor-Clark 2010, Andre 2008, Bessac 2008, Escalera 2008, Bautista 2006, Inoue 2005, Dinis 2004, Symanowicz 2004, Veronesi 2001).
e) People like fireplaces, woodstoves, and combustion fueled transportation - it is best to present MCS as a syndrome in response to unrelated chemicals in a non inciting background atmosphere. It is not preferable to worry about ACA catastrophic consequences - geopolitical turmoil, overpopulation: 1960 to 2015 - 4.4 billion added in 55 years, resource loss, climate change, ocean acidification, mass extinction, speed, violence, pollution - injury, illness, and premature death.


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f) The ACA cannot support the MCS disease process - including central sensitization - by activating exposed TRPA1 expressing peptidergic sensory receptors in damaged airway epithelium - releasing proinflammatory neuropeptide substance P.


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b( Something is supporting the ongoing neurogenic inflammation - evidenced in biopsies, plasma tests, SPECT, and electroencephalograms - all at baseline.
c) Its not the energizer bunny that keeps going and going.
d) Its not a well managed MCS household!
e) Its not the Ambient Combustion Aerosol (ACA) - its Superman!


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f)  Veronesi evidenced the critical role of airway sensory c-fibers initiating the MCS disease process.

g) Conclusions of top researchers disregarded - MCS people do not have airway inflammatory cytokine release - systemic implications - in response to PM of the ACA.

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d) ACA CO2 - climate change, ocean warming, receding ice, acidity rising, reduced generation of shells and reefs, threatening mass extinction - doesn't slow us down - and neither should expert evidence - we like our cars. MCS is a dubious diagnosis - a poorly understood sickness behavior or form of depression.

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