My case fits all clauses of the 1999 Consensus Criteria and I think the Criteria is good - almost! I agree with the practicality of the Criteria in arriving at a "definition" for diagnosis purposes without involving tests.

Of course , I worsen with exposure to the broad range of substances and improve when the exposure stops - the big however is that horrendous symptoms continue all the time from the continual exhaust - only when I go very remote in very unusual circumstances do the symptoms stop. That is why I'm saying - people are rum dumb about the exhaust. That makes Pt 4 misleading. Its just the fact that by not bringing light to it - this dangerous unawareness continues.

But - for emphasis here - I do think the 1999 Consensus Criteria is good - but with the exception I just mentioned.

I would think there is a broad range of gray - there are so many factors and variables - so many individuals - I think there are similar overlaps but distinct differences - one common denominator is the dysregulation of neurogenic inflammation in the tissue involved.

I agree that a key part of someone having MCS is the "abnormal" hypersensitivity - I agree just paraphrasing what you said.

I think if I had perfume to inhale continually I could call that "supporting the underlying disease process". But if I'm careful I don't inhale perfume. The ambient exhaust/smoke is relentless - continually "supporting the underlying disease process" - it really can't be doing anything else - its the rum dumb under-recognized continual "perfume".

You said "sustaining cause" - that is not the phrase I proposed for Pt 4 - because "cause" is individual - exposure histories vary so much. I referred to the aerosol as principle in promotion and cause but I used the word "principle" - it does not exclude other substantial or even more significant causes among individuals. Given the enormous chemical inclusiveness of exhaust and smoke it is major among contributing causes.

You specified in this answer that it be relative to personal experience not interpretation of literature - I would say I really can't tell original cause subjectively.

I might think it was the pack a day Mom - or the nail polish Mom - but my brother doesn't have the problem. As big a factor as any is genetic. I am the classic "introverted intuitive" psychologically who C.G. Jung in his monumental Psychological Types observed were the ones with "hypersensitivity of the sense organs". It is major insight concerning MCS. It puts origin of cause in the position of peripheral sensitivity and vulnerability. When you combine that with Veronesi's (EPA lab) observation that mice who can't stand air pollution have more sensitive pathways from birth in the sensory innervation of the airway epithelium (Roy 2000, Veronesi 2000) - that is MCS.

Those sensitive pathways generate more inflammation per every exposure from birth - and inflammation equals damage. That is strong information indicating that MCS really doesn't develop overnight. An individual might think it has - but that is often a subjective error - they had long taken themselves as normal - but had the genetic predisposition and a subsequent gradual alteration and damage taking place. The port of entry is the airway epithelium - it has a great capacity for metabolizing these toxics of concern - if that tissue isn't functioning as it should the whole organism can go down.

Origin of cause would be a coming together of the genetic - Jung speculated it was "hypersensitivity of the sense organs with an extraordinary dependence on sense impressions to compensate for the rarified air of the intuitive cast of mind". That could be most MCS in a nutshell at origin of vulnerability. It seems almost everyone I meet with MCS is "introverted intuitive" and that would be vulnerable genetically sensitive sensory and olfactory tissue from birth. The canaries...

It seems that the "elementary my dear Sir Watson" conclusion (Calderon-Garciduenas 2008, Veronesi 2001, Meggs 1997) is that MCS involves permanent alteration of the airway epithelium exposing the critical TRPA1 receptors. So therefore if an MCS person has reached the point of meeting the 1999 Consensus Criteria then the issue of "cause" has become history. It has become a done deal.

If the MCS person could reach a position of no pollution whatsoever and maintain that for a long time they still would not heal. An exposure out of nowhere would result in start up of the disease process - so the issue once a person has MCS - meets the Criteria - is simply what is "supporting the underlying disease process". For that there is another line of conclusive understanding - the indispensable TRPA1 multiple chemical receptor (Bessac 2008). Its simply this: any chemical that is a TRPA1 agonist will turn on MCS. Bessac called it the MCS receptor because it responds to such a wide range of chemicals.The Ambient Combustion Aerosol contains so many TRPA1 agonists that it is a simple fact that it has to turn on and support the underlying disease process.

The chemical characteristic of perfume is that it is also a TRPA1 agonist. But again the "cause" is already established - alterations of the airway epithelium - such as tight junction defects exposing the sensory nerves and more precisely the TRPA1 receptors which are thought to be co-located on "peptidergic" terminals ((Materazzi 2013, Battacharya 2008 ) - those that release neuropeptides such as substance P found very elevated in MCS people (Kimata 2004). TRPA1 appears to be essentially or coincidentally involved in substance P release.

And its all wired to the CNS - the excessive TRPA1 inputs alter the neural circuitry - Latremoliere 2009 calls it "neural plasticity" and it eventually results in central sensitization multiplying the pain. There are of course lots of other physiological players involved but I'm not encyclopedic about it - to appreciate you just have to look at there work on this subject - they have it down to increased precision.

So I guess if I seem so "certain" as you mentioned earlier - its just look at the precision. The agonists in exhaust and smoke (the ambient combustion aerosol) set off TRPA1 - they have to - and that by precise understanding must have the effect of "supporting the underlying disease process" (Deering-Rice 2011, Bessac 2008).

Concerning perfume - Nassini 2011 stated the TRPA1 importance in the reaction of sensitive people to botanical odors and perfume - having experimentally determined that blocking TRPA1 from agonist influence prevents the reaction - experiment involving odor produced by the "headache tree" which causes "headache crisis" - smile - inhale near this tree and get a headache crisis - wow! But even milder trees put out a lot of chemical - pine aren't all that great for MCS people - lots of agonists (Goldstein 2001, 2000, Guenther 2000, Schade 2000, Geron 2000, Fantechi 1998, Benjamin 1996) but not nearly bad as exhaust - unless the pine is burning - then its worse than exhaust! Light the perfume on fire if it will burn - then you have exhaust - chemicals of the perfume then adsorbed on fine particles for a longer residence time in tissue...supporting the underlying disease process (Bonvallot 2001, Gerde 2001, 1997).

MCS A-1 Etiology: Dantoft 2014

MCS A-1 Etiology: References

MCS 2 The Etiology of MCS

MCS 3 Definition and Concensus Criteria

MCS 3a Criteria Amendment Q and A

MCS 3b Criteria Amendment Research Points (CAR)

MCS 3c CAR References

MCS 3d CAR Documentation

MCS 3e Etiology: CAR Moral Responsibility

MCS aj Impossibly Good

Mgt 101 Consume Less or Extinction

Mgt 101a Impossibly Good City Design

References

Bessac B. & Jordt S. Breathtaking TRP channels : TRPA1 and TRPV1 in airway chemosensation and reflex control. Phys 23:360-70 2008

Bonvallot V. et al. Organic compounds from diesel exhaust particles elicit a pro-inflammatory response in human airway epithelial cells and induce cytochrome P450 1A1 expression. Am J Resp Cell Mol Biol 25: 515-21 2001

Calderon-Garciduenas L. et al. Long-term air pollution exposure is associated with neuroinflammation, an altered innate immune response, disruption of the blood brain barrier, ultrafine particulate deposition, and accumulation of amyloid beta-42 and alpha-synuclein in children and young adults. Tox Pathol 36: 289-310 2008

Deering-Rice C. et al. Electrophilic components of diesel exhaust particles (DEP) activate transient receptor potential ankyrin-1 (TRPA1): a probable mechanism of acute pulmonary toxicity for DEP. Chem Res Tox 24;6:950-9 2011

Gerde P. et al. The rapid alveolar absorption of diesel-soot adsorbed benzo[a]pyrene: bioavailability, metabolism, and dosimetry of an inhaled particle-borne carcinogen. Carcinogenesis 22;5:741-49 2001

Gerde P. et al. Benzo{a}pyrene at an environmentally relevant dose is slowly absorbed by, and extensively metabolized in, tracheal epithelium. Carcinogenesis 18:1825-32 1997

Jung C.G. Psychological Types. Princeton University Press and in the Portable Jung Viking Press 1921

Kimata H. Effect of exposure to volatile organic compounds on plasma levels of neuropeptides, nerve growth factor, and histamine in patients with self reported multiple chemical sensitivity. Int J Hyg Env H 207:2 159-63 2004.

Latremoliere A. & Woolf C. Central sensitization: a generator of pain hypersensitivity by central neural plasticity. J Pain 10;9:895-926 2009

MCS aa Etiology: Not Always Visible

MCS 3 Definition and Concensus Criteria

Meggs W.J. Hypothesis for induction and propagation of chemical sensitivity based on biopsy studies. Env H Perspect 105(2): 473-78 1997

Nassini R. et al. The 'headache tree' via umbellone and TRPA1 activates the trigeminovascular system. Brain doi:10 1093/brain/awr272 2011

Roy et al. Susceptibility to pollutant-induced airway inflammation is neurogenically mediated. EPA EIMS Metadata report 59754 2000

Veronesi B. et al. Vanilloid capsaicin receptors influence inflammatory sensitivity in response to particulate matter. Tox Appl Pharm 15;169(1): 66-76 2000

Biogenic:

Benjamin M. et al. Low-emitting urban forests: a taxonomic methodology for assigning isoprene and monoterpene emission rates. Atmos Env 30;9: 1437-52 1996

Fantechi G. et al. Mechanistic studies of the atmospheric oxidation of methylbutenol by OH radicals, ozone, and NO3 radicals. Atmos Env 32;20: 3457-3556 1998

Geron C. et al. A review and synthesis of monoterpene speciation from forests in the United States. Atmos Env 34: 1761-81 2000

Goldstein A.H. and Schade G.W. Whole ecosystem measurements of biogenic hydrocarbon emissions. Final Report ARB award no. 98-328. State of Cal Air Resources Board 2001

Goldstein A.H. and Schade G.W. Quantifying biogenic and anthropogenic contributions to acetone mixing ratios in a rural environment. Atmos Env 34:29-30: 4997-5006 2000

Guenther A. et al. Natural emissions of non methane VOC, CO, and NOx from North America. Atmos Env 34: 2205-30 2000

Schade G. et al. Canopy and leaf level 2-methyl-3-buten-2-ol fluxes from a ponderosa pine plantation. Atmos Env 34: 3535-44 2000

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