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TOPIC: MCS ai Etiology: Highlights

MCS ai Etiology: Highlights 8 years 11 months ago #1

MCS ab Particulate Vector

GERDE 2001:

During combustion particles are generated and PAHs (polycyclic aromatic hydrocarbons) form in the gas phase. When the exhaust cools - PAHs adsorb or condense on the particles (Burtscher 1998).

rapidly desorbed PAHs "...are deposited, slowly absorbed, and extensively metabolized in airway epithelium at prolonged elevation of the local tissue concentration (Gerde 1997)..."

LI 2011:

"...DEP injures respiratory epithelia via a luminal -apical unloading mechanism of DEP organics delivered by carbonaceous nanoparticles...

...TRPV4-p19s, a human genetic polymorphism previously identified as a COPD susceptibility locus (Zhu 2009), increases MMP-1 activation via increased Ca-2+ influx, providing a mechanistic link between human airway epithelia signaling, airway disease and air pollution...

...our results imply that two human genetic polymorphisms are linked to respiratory health, TRPV4-p19s and MMP-1(-1607G/GG), thus highlighting the concept of disease susceptibility as a function of genetic "makeup" combined with environmental insults..."

MCS ad Naturally Sensitive

MCS 15 Airway Genetics

JUNG 1921:

Baynes Translation

"...the introverted intuitive...extraordinary dependence upon the sense impression...compensation to the thin upper air of the conscious attitude...hypersensibility of the sense organs..."

R.F.C. Hull Translation

"...extraordinary dependence on sense impressions...this compensates the rarified air of the intuitive's conscious attitude...hypersensitivity of the sense organs..."


"...the variable inflammatory sensitivity to PM observed in different mouse strains (ie Balb/C, B6) related to quantitative differences in the neuropeptide, VR1 receptors (now TRP) and acid sensitive pathways found on sensory neurons that innervate the nasal and upper pulmonary airway. Such data showed how genetically determined differences in sensory neural pathways could influence expressions of PM-induced airway inflammation...genetic differences are thought to underlie these variations and have been experimentally demonstrated for ozone (Kleeberger 1995, Zhang 1995), nitrogen dioxide (Holroyd 1997), and diesel exhaust (Ichinose 1997, Miyabara 1998)...

...conditions associated with chemical pollutants are characterized by damage to the epithelial barrier that lines the airways...

... Such damage not only results in the loss of critical neuropeptide deactivating enzymes (e.g. NEP) but allows the sensory fiber to physically extend closer to the airway lumen and in closer proximity to the inhaled PM particles...enhanced and prolonged inflammatory events...increased inflammatory response..."

MEGGS 1997:

....There are defects in the tight junctions between respiratory epithelial cells, focal desquamation of the epithelial cells in places, hypertrophy of glandular structures, lymphocytic infiltrates, and proliferation of sensory nerve fibers...tumor necrosis factor is produced by lymphocytes....

MEGGS 1999:

....The mechanism by which inflammatory conditions are provoked by chemicals is via chemoreceptors on sensory nerve C-fibers with the release of substance P and other mediators of neurogenic inflammation...progression of inflammation to organ damage is possible to those who continue to be exposed...

KIMATA 2004:

Substance P controls 38 and 39 MCS 105 and 153 Nerve growth factor controls 148 and 156 MCS 1129 and 1696 before and after exposure to paint

OSLUND 2008:

...substance P primes and activates human neutrophils for superoxide, H2O2, and nitric oxide production (Sterner-Kock 1999, Tanabe 1996)...


"...A number of studies have correlated responses to urban PM, including DEP (diesel exhaust particles) with activation of airway sensory neurons, particularly C and A beta fibers that express Transient Receptor Potential Ankyrin-1 (TRPA1), TRP Vanilloid-1 (TRPV1), and substance P (Hazari 2011, Teles 2009, Anand 2008, Nassenstein 2008, Kobayashi 2005)...

MCS ae Airway Reactivity


...transient receptor potential vanilloid 1 (TRPV1) and transient receptor potential ankryin 1 (TRPA1) are ion channels responsible for the action potential initiation in nociceptive nerves in response to a wide range of inflammatory mediators and noxious irritants (Bessac 2008)...

BESSAC 2008:

...The multiple chemical sensitivity of TRPA1...tissue injury may sensitize TRPA1 channels through inflammatory signaling pathways, thereby establishing prolonged hypersensitivity to multiple reactive chemicals (Bandell 2004, Bautista 2006, Dai 2007, Jordt 2004)..."


...our observations identify umbellone, via its selective TRPA1-agonism, as a trigeminovascular stimulator...for the headache-inducing properties of California bay laurel...a similar pathway may represent the underlying mechanism responsible for headache crises triggered in sensitive people by a series of compounds present in environmental pollutants and botanical perfumes/odours (Blau and Solomon 1985, Kelman 2007, Friedman 2009)..."

MCS af Central Sensitization


"...central sensitization...activity or use dependent form of functional synaptic plasticity that resulted in pain hypersensitivity...triggered by the activity evoked in dorsal horn neurons by input from c-nociceptors...chemical activation of nociceptors by irritant compounds...the TRPA1 channel...TRPV1 channels...

...The key features of acute activity-dependent central sensitization are that it is induced with a short latency (seconds) by intense, repeated, or sustained nociceptor inputs and typically lasts for tens of minutes to several hours in the absence of further nociceptor input...

...It generally requires activation of NMDA receptors for its induction, and these receptors contribute to its maintenance. Nevertheless, as reviewed above, multiple different triggers can contribute to the establishment of this form of central sensitization: glutamate acting on NMDAR, but also on AMPAR and mGluR, the neuropeptides substance P and CGRP, the kinin bradykinin, as well as BDNF and NO...


"...Neurocognitive deficits were found, particularly after chemical challenge, in MCS patients. The parietotemporal cortex, which has been related to MCS owing to electroencephalographic alterations found in this area (Bell 1998), is involved in the processing of complex aspects of attention and, in conjunction with the hippocampus, in the formation of memory (Bell 1996). Our finding of brain SPECT hypoactivity in these areas and also in frontal-subcortical circuits (Salmon 2001) could, in part, explain neurocognitive defects in MCS patients. Neurologic dysfunction observed prior to chemical exposure could point to persistent subclinical neurologic changes. In fact, basal SPECT brain cortical hypoactivity was found in our patients. In animal models, inflammation and permanent damage of the olfactory neuronal pathways could result from translocation of inhaled ultrafine particles to the brain (Elder 2006)..."


"...Breakdown of the nasal respiratory and olfactory epithelium and the BBB (Blood Brain Barrier) facilitates the access of systemic inflammatory mediators and components of air pollution to the central nervous system (CNS) (Calderon-Garciduenas 2004)...

...sustained exposures to significant levels of air pollutants including UFPM (ultrafine particulate matter) , PM2.5 (less than 2.5 microns), and PM-LPS produce brain neuroinflammation and neurodegeneration through at least four pathways:

1 Induction of upper respiratory, lung epithelial, and endothelial injury leading to persistent chronic inflammation in the respiratory tract and systemic inflammation. The systemic inflammation is accompanied by the production of pro-inflammatory cytokines such as TNF alpha, IL 6 and IL-1beta...these cytokines can activate endothelial cells in the BBB, disrupt the BBB...and trigger cascades...results in increased expression of nitric oxide synthase...and nitric oxide production that opens the BBB..."

2 We strongly support the importance of the olfactory pathway...since olfactory neurons are loaded with PM...will potentially translate into an abnormality in the limbic system...(Bedard 2004)...

3 The vagus/trigeminal (Lewis 2005) pathways are also crucial, given that PM enters the respiratory and digestive systems...

4 Direct access of UFPM to the brain, further accentuating an inflammatory response in the brain parenchyma...

... exposure to...air pollutants including UFPM and PM2.5 produces neuroinflammation and altered innate immune responses in crucial brain target anatomical areas...ultrafine PM could play a role in the enhancement rate of protein fibrillation affecting Abeta42 and alpha-synuclein (Linse 2007)...

...Long-term exposure to air pollution should be considered a risk factor for both Alzheimer's and Parkinson's diseases, and APOE beta 4 allele carriers could have a higher risk of developing AD if they reside in a polluted environment..."

MCS aa Not Always Visible

In combination with a genetic predisposition of the airway epithelium and its sensory innervation (Eberling 2009, Veronesi 2001, 2000, Roy 2000, Miyabara 1998, Jung 1921) -

MCS is usually caused by exposure to a continuous combustion byproduct aerosol - diesel and other exhaust, woodsmoke, and tobacco smoke - including particle agglomerates with adsorbed hydrocarbons and singlet nonagglomerated nanoparticles

(OSHA 2012, Deering-Rice 2011, Lucchini 2011, Taylor-Clark 2010, Baulig 2009, 2003a, Block 2009, 2004). Mohankumar 2008, Calderon-Garciduenas 2008, 2000, Inoue 2005, Veronesi 2005, 2003, 2002a, 2002b, 2001, 2000, 1999a, 1999b, Agopyan 2003, Oortgiesen 2000, Roy 2000, Pakkanen 2003, Schauer 2002, 2001, 1999, Kittelson 1998, Cadle 1999, Kleeman 1999 , Bonvallot 2001, 2000, Gerde 2001, 1997, US DOT FHA 2000, Miyabara 1998,1998a, Steerenberg 1998, Society of Automotive Engineers SAE 940233 1994)

Fine particles expected to reach the CNS via trigeminal and olfactory nerve pathways

Badolato MCS 11, Calderon-Garciduenas 2010, Genter 2009, Matsui 2009, Elder 2006, Lewis 2005

MCS 14 Genetics in Detox Enzyme Chemical Defense Usually Okay

DELUCA 2010:

"...Mckeown-Eyssen et al (2004) suggested also a possible gene-gene interaction between CYP2D6 and N-acetyl transferase 2 (NAT2), with rapid metabolizers for both enzymes showing a substantially elevated risk to develop MCS. The results concerning NAT2 alone or its combination with CYPs found no confirmation in later studies (Schnakenberg et al 2007; Weismuller et al., 2008; Berg et al 2010).

On contrast Schnakenberg et al (2007) suggested that individuals being slow acetylators, and those with homozygously deleted GSTM1 and GSTT1 genes, are significantly more likely to develop MCS syndrome. We did not confirm Schnakenberg's findings, as we did not find any significant differences in GSTs allele or genotype distribution between patients as compared with data previously published in healthy volunteers (table 4) (Garte et al., 2001)..."

Deluca 2010 found MCS people had nearly 3 times plasma cytokines IFN-y, IL-8, and IL-10, double the chemokine MCP-1, over twice growth factor PDGF, and 8 times VEGF - along with a 3 fold reduction in catalase activity, severe glutathione depletion, double nitric oxide, and a fatty acid profile of lipid peroxidation - increased SFA with losses in PUFA, N-6, N-3, arachidonic acid, and omega 3.

Deluca 2010 state: ..." dysfunction of two major antioxidant enzymes and depletion of glutathione leads to severe oxidative stress and impaired elimination of phase I oxidation metabolites. Excessive amount of hydrogen preoxide due to catalase deficiency will initiate a non enzymatic free radical driven chain reaction of lipid peroxidation implicated in a number of human pathologies. This kind of enzymatic oxidation could reasonably occur upon pro-inflammatory stimulation of blood cell populations with cytokines...

...there exist serious and multiple dysfunctions of chemical defensive systems in MCS patients. These dysfunctions may mainly depend not on genetic defects but on non-genetic modifications of metabolizing/antioxidant enzyme expression and/or activity, mediated by redox active agents such as NO and inflammatory cytokines, for example IFNgamma and IL-10..."

BERG 2010:

"In conclusion, based upon a considerable number of study participants, we were not able to confirm previous findings of substantial importance of gene variants in CYP2D6, NAT2, PON1, MTHFR, and CCK2R to MCS and self-reported chemical sensitivity...the current research into the genetic contribution to MCS and chemical sensitivity has yielded inconsistent findings, and no result seems to offer an etiologic explanation for a large proportion of patients. A recent finding that the heritability of respiratory symptoms related to perfume, a main complaint in MCS, was 0.35 (Eberling 2009), however encourages further research into the subject... "

MCS is usually genetic vulnerability in the airway epithelial cell population and its sensory innervation - including quantitative differences in neuropeptides, TRP receptors, and acid sensitive pathways critical to the homeostatic regulation of inflammatory neuroimmune response - which become altered to a proinflammatory condition - airway damage and exposed c-fiber nerves - in a continuous combustion byproduct aerosol including particle agglomerates with adsorbed hydrocarbons and singlet nonagglomerated nanoparticles - resulting in elevated plasma levels of neuropeptides, chemokines, cytokines, growth factors, and NO that mediate serious and multiple dysfunction of chemical defense systems.


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Bell I. Clinically relevant EEG studies and psychophysiological findings: possible neural mechanisms for multiple chemical sensitivity. Toxicol 111:101-17 1996


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MCS Etiology Mgt 104 Respirators: Particles and Adsorbed Hydrocarbons

MCS 9 Airway Origins: PM and a Defective Scrubber.

MCS 10 Credible Proof: The Study of all Studies.

MCS 11 PM: Trigeminal and Olfactory Pathways.

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