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Standard of Kindness

MCS Etiology is about Love and God

Preface: Is It Kind?

Preface Splash: Nutrition, Not Tradition

Expertise from the Most Prestigious Academic, Medical, and Government Research Facilities

MCS 2 The Etiology of MCS 

MCS 2a Etiology: TRPA1 Precision

MCS 2aa Etiology: Notes on References

MCS 3b CAR References

MCS 3h CAR Nutrition References

Carefully researched - fact and evidence based with no conflict of interest - MCS Etiology is the most advanced and credible statement on this subject. 

Multiple Chemical Sensitivity: 2021 Consensus Criteria 

Baseline, Diagnosis, Patient Rights, Etiology - 4 Parts:

I.   Baseline GSAA, ACA, SRPE

II.  Diagnosis, Patient Rights, Etiology

III. Baseline: Nutrition and Exercise

IV. Baseline: Nutrition and Exercise

Vegigram Max

VegiEnergiNutrigram

MCS Consensus Postscript Splash (these topics may be located last on the linked forum):

    I.   Ambient Combustion Aerosol (ACA) Composition

    II.  MCS, MECFS - Inflammatory Response to Air Pollution

    III. Macronutrients - Starch Preferred Energy

    III. Micronutrients - Vegetables Essential

    IV. ACA PM Gastro-Inflammation, Vagal Circuitry

Appendix: Added Splash I-III:

    I.  MCS 2aa Safdar 2011: To Run or Not to Run

    II.  MCS 2ab Etiology: Nasal Cytokines in Context

    III. MCS 3ac: Belpomme 2020, Lull 2010 - Ambient PM  Propagates the Cycle of Reactive Microgliosis

Appendix: IV, V:

    IV. MCS 2ac Etiology: Belpomme 2015 - Formula or Reality?

    V.  MCS 3ad: MCS Genetics - Likely a Neural Portrait

Appendix: VI:

    VI. MCS 3ae: Treatments Unsafe? Fermented Papaya (FPP) and Ginkgo Biloba

MCS Index: Consensus I, II

Nutrition Index: Consensus III, IV

USDA SR28

MCS 3ab: MCS Community - Unprofessional Conflict of Interest 

Principles apply also to pollution supported disease in general.

CALDERON-GARCIDUENAS 2008: 

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

Complete list of MCS and Management forums - in large easy to read print - are linked at right and in feature elsewhere. A select list is highlighted below. 

Careful Analysis:

MCS 3a Criteria Amendment Research (CAR) updated above

MCS 3a AKA Multiple Chemical Sensitivity:  2015 Consensus Criteria updated above

Clear, Concise Etiology and Definition: updated above

MCS 1 Etiology Narrative

MCS 2 The Etiology of MCS 

MCS 3 Definition and Consensus Criteria

MCS 3aa Etiology: Consensus Author CAR Test (SPC)

Highly qualified academic, medical, and government researchers:

MCS 3b CAR References

And Greetings from the President (smile):

Membership is free - and can read without joining. There are many links to important studies.

Please take the self study CAR Test and be a 2021 Consensus Author if you'd like.

More...

MCS 3c CAR Documentation

MCS 3d Etiology: CAR Case Example

MCS 3e Etiology: CAR Impossibly Good City Design

MCS 3f Criteria Amendment Q and A

MCS 3h CAR Nutrition References

Precision Etiology: Forums aa-af

Restatements...

MCS A-1 Etiology: Dantoft 2014

MCS ak Etiology: Words to the Wise

Environmental Dilemma:

MCS aj Impossibly Good

Mgt 101 Consume Less or Extinction  

Mgt 101a Impossibly Good City Design

Clean Diesel: Public Health Nightmare

180,000 people are added to the World every day

Consume Less or Extinction

 A Plan for Avoiding Extinction:

Mgt 101a Impossibly Good City Design

Better Morality

Population Stabilization

Low Speed, Injury Proof, Zero Emission Vehicles

Walk to School, Work, and Shopping

Thermostats 50 Degrees or Less

Engage Only Unwasteful Products and Activities

Consequences:

Love 201 Standard of Kindness

Nutrition: Mgt 110, 111, 112

 

Exercise: Mgt 109

"...Sensi-Clean is different. It contains no perfumes or brightening dyes. And its been proven to rinse completely clean leaving no chemical residue on your laundry. Because of this, Sensi-Clean is perfect for anyone with sensitive skin, or anyone who wants to avoid excess exposure to chemicals. Sensi-Clean also makes all of your fabrics look, feel, and perform like new..."

GS Filters for Electromagnetic Hypersensitivity

 

1) Most MCS people have genetically sensitive airway tissue (MCS 15, Veronesi 2001, 2000, Roy 2000, Jung 1921).

2) Experiments with mice confirmed genetic variability of the sensory innervation - including quantitative differences in neuropeptides, TRP receptors, and acid sensitive pathways - determine the degree of inflammatory response to environmental exposure (Veronesi 2001, 2000, Roy 2000, Miyabara 1998). Heritability of respiratory symptoms has been shown (Elberling 2009).

3) A sensitive airway is usually a physiological counterpart to an introverted intuitive psychological function type - all genetically determined and apparently occurring more frequently in women (Jung 1921).

4) The airway epithelium and its sensory innervation become altered to a proinflammatory condition

Deering-Rice 2011, Hazari 2011, Li 2011, Taylor-Clark 2010,  Baulig 2009, 2003a,  Calderon-Garciduenas 2008, 2000, Veronesi 2003, 2002a, 2002b, 2001, 2000, 1999a, 1999b, Agopyan 2003, 2003a, Bonvallot 2001, 2000, Gerde 2001, 1997, Oortgiesen 2000, Roy 2000, Chin 1998, Miyabara 1998,1998a, Steerenberg 1998, Meggs 1997, Bond 1988

usually by exposure to a continuous ambient combustion byproduct aerosol (ACA) - diesel, gasoline, propane and other exhaust, woodsmoke, and tobacco smoke 

Gillespie 2013, Block 2012, 2009, OSHA 2012, Pakkanen 2003, Schauer 2002, 2001, 1999, US DOT FHA 2000, Society of Automotive Engineers SAE 940233 1994 

including UFPM, PM2.5, and PM LPS - particle agglomerates with adsorbed hydrocarbons, singlet nonagglomerated nanoparticles, and acid sulfate resulting from catalytic converter transformation of sulfur dioxide

Lucchini 2012, Mohankumar 2008,  Inoue 2005, Kittelson 1998, Cadle 1999, Kleeman 1999  

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

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

5) MCS people have elevated levels of neuropeptides, chemokines, cytokines, growth factors, and nitric oxide (Dantoft 2014, Deluca 2010, Kimata 2004, MCS 7) that mediate serious and multiple dysfunction of chemical defense systems (MCS 13, Deluca 2010, Liptrott 2009, Oslund 2008, Kimata 2004, Chun 2002, Sterner-Kock 1999, Tinel 1999, Tanabe 1996, Tapner 1996, Nadin 1995, Stadler 1994, Khatsenko 1993).

6) Elevated cytokines are released by expression of the c-fiber sensory innervation of the nasal and upper pulmonary airway -including TRPA1 and TRPV1 irritant receptors

Deering-Rice 2011,Taylor-Clark 2010, Bessac 2008, Nassenstein 2008, Nilius 2007

Proinflammatory peptidenergic transmitters such as substance P, calcitonin gene related protein, and neurokinin A released by the sensory nerves interact with immune cells including lymphocytes, neutrophils, macrophages, and eisinophils exascerbating and perpetuating initial symptoms of inflammation with nitric oxide overproduction and amplification of immune response

Costa 2010, Oslund 2008, Mohankumar 2008, Calderon-Garciduenas 2008,  2000, Agopyan 2003, Veronesi 2001, 1999a, 1999b, Steerenberg 1998, Meggs 1997, Bascom 1992 MCS 6

7) Airway defects have been confirmed in MCS patients biopsied and rhinoscopied - conditions found were consistent with expectation of cytokine release and proliferation of nerve fibers was observed (Meggs 1997, 1996, 1993).

8) Reactive and measurable (Millqvist 2005, Nogami 2004, Lee and Pisarri 2001, Bonham 2001) - stimulation of c-fiber nerves may cause multiplication of nerve fibers to a 24-48 hour peak - not returning to baseline until 72-96 hours (Castranova 2002) accompanied with a rise in plasma vasoactive intestinal peptide, substance P, and nerve growth factor (Kimata 2004), ongoing flu-like symptoms attributed to cytokine release (Dantoft 2014, Bascom 1992 MCS 6), higher respiratory rate, increased nasal resistance (Doty 1994), secondary punctate hyperalgesia indicating facilitated central sensitization (Tran 2013, Holst 2011, Latremoliere 2009), head pain expected through increased trigeminal afferent activity from TRPA1 receptors on the exposed C fiber innervation of the nasal mucosa producing meningeal vasodilitation (Kunkler 2011, Nassini 2011) and connection to eye involvement through opthalmic branch of the trigeminal nerve in the olfactory bulb (Jordt 2011, Finger 1993).

9) Xenobiotic penetration and mediators of inflammation - activation and release involving TRPV1, TRPA1, substance P, CGRP, glutamate, NMDA, cytokines, and nitric oxide Deering-Rice 2011,  Costa 2010, Taylor-Clark 2010, Bessac 2008, Calderon-Garciduenas 2008, 2000, Mohankumar 2008, Nassenstein 2008, Oslund 2008, Nilius 2007, Agopyan 2003, Veronesi 2001, 1999a, 1999b, Steerenberg 1998, Meggs 1997, Bascom 1992 MCS 6) cause neurocognitive impairment, SPECT hypoactivity (Orriols 2009), electroencephalographic alterations (Bell 1998, 1996) sensitization - permanent neuronal damage and reduced inhibitory neuronal activity in the olfactory pathways to the orbito-frontal cortex and the limbic system.

10)  Endogenous production of electrophiles and oxidants result in an environment of oxidative stress - glutathione depletion and catalase deficiency - high levels of hydrogen peroxide and 4 HNE - lipid peroxidation with atherogenic implications (MCS 13,  Deluca 2010, Calderon-Garciduenas 2008, Yang 2008, Terlecky 2006, Kennedy 2005) -  increased cardiopulmonary disease risk  (Baldwin 1998), and disturbance in heme synthesis (porphyrin abnormalities) Daniell 1997, Hahn 1997. Elevated cytokine TNF alpha may cause gastrointestinal stasis experienced as queasiness or nausea via vagal circuitry (Emch 2000).

11) ACA PM induced release of inflammatory cytokines including IL-1 beta and IL-6 from alveolar macrophages, epithelial cells, and exposed sensory nerves in damaged airway epithelium - found elevated in MCS and ME/CFS (Dantoft 2014, Maes 2012) - stimulate the bone marrow to increase output of platelets and polymorphonuclear leukocytes (PMN), accelerate more immature PMN (band cells) into the circulation prone to sequestration in microvascular beds - and increase the liver output of acute phase proteins including fibrinogen, CRP, and C-reactive protein - all associated with vascular activation and the extent of atherosclerosis (Hiraiwa 2014, 2013, Hogg 2009, Goto 2004, Mukae 2001) - and indicated by elevated PMN-elastase, lysozyme, and neopterin confirmed in ME/CFS (Maes 2012).

12) Induction of upper respiratory, lung epithelial and endothelial injury leading to persistent chronic inflammation in the respiratory tract and systemic inflammation accompanied by the production of IL-6 and IL-1beta elevated in MCS and ME/CFS (Dantoft 2014, Maes 2012) may activate endothelial cells of brain capillaries opening the BBB (blood-brain barrier) involving upregulation of  COX-2 (cyclooxygenase-2), activation of NFkB (nuclear factor kB), and increased expression of iNOS (inducible nitric oxide synthase) found in ME/CFS ( Calderon-Garciduenas 2008, Maes 2007a, 2007b).

13) Because MCS people have airway defects there may be a sharing of at least some aspects of the following description (Block 2009, Calderon-Garciduenas 2008).

Airway breakdown occurs universally beginning in childhood among non-smoking residents of ACA PM 2.5, UFPM, and PM LPS - highly polluted Mexico City (MC) (Calderon-Garciduenas 2008, 2001) - and is accompanied by a closely investigated CNS pathology of neuroinflammation - subclinical early - but associated with eventual neurodegeneration due to ACA PM, adsorbed compounds, byproducts of ozone exposure (photochemical smog resulting principally from vehicle exhaust), and cytokines reaching the brain.

The CNS condition includes increased inflammatory markers iNOS (inducible nitric oxide synthesis), TNF alpha, Il-1beta, COX-2 (cyclooxygenase-2), and NFkB (nuclear factor kB) especially in frontal cortex, substantia nigrae, and vagus nerves (found systemically elevated in ME/CFS [Maes 2012]),

neuron damage or loss, microglial activation (innate immune system macrophages of the brain - their job to engulf and digest but with cumulative collateral damage) indicated by increase of HLA-DR surface antigen positive cells and CD-14 lipopolysaccharide (LPS) receptors - LPS a potent inflammatory cell wall component of gram negative bacteria (endotoxin) commonly adsorbed on DEP (diesel exhaust particles) ((Block 2004) - with resulting ROS (reactive oxygen species) and cytokine production, blood-brain barrier (BBB) dysfunction - changes in inflammatory , tight junction, and transport proteins of the cerebral vascular microvessels (3 to 8 micron diameter) that comprise the BBB - endothelial cell damage with increase in leukocyte adhesion molecules,

accumulation of Abeta-42 (42 amino acid form of amyloid beta) as neuronal, vascular and diffuse plaques, Abeta and alpha synuclein aggregation (associated with Alzheimers and Parkinsons Disease respectively) - CALDERON-GARCIDUENAS 2008:"...Both Abeta42 (42 amino acid-isoform of beta amyloid associated with Alzheimer's) and alpha synuclein ( an abundant brain 140-residue-protein linked to Parkinson's disease) are proteins capable of aggregation and misfolding (shown to occur more rapidly in conditions of PM exposure),  leading to progressive neurodegeneration that develops insidiously over the lifetime of the individual (McGeer 2006, Jellinger 2003, Nguyen 2002, Selkoe 2002, 2001)...",

lipid peroxidation (systemically confirmed in MCS people [Deluca 2010]), astrogliosis evidenced by enhanced glial fibrilliary acid protein (GFAP) expression, and DNA damage (Block 2009, Calderon-Garciduenas 2008).

In contrast, non-smoking residents of less polluted cities Veracruz and Tlaxcala - upon the same examination appeared in good shape during childhood - but four of the five oldest subjects age 27 and above - 27, 36, 40, and 45 demonstrated either dysruption of the BBB (blood-brain barrier) by confocal microscopy for tight junction abnormalities (Zonula Occlulens ZO-1) or Abeta42 (42 amino acid-isoform of beta amyloid) immunoreactivity by immunohistochemistry in olfactory bulb and cortical neurons of one subject - and in diffuse and mature senile plaques in another - a preAlzheimer's-like indicator of brain neuroinflammation (Calderon-Garciduenas 2008).

Although more is worse - there is no safe level of chronic and repeated exposure to combustion byproducts including vehicle exhaust.

14) Studies involving large diagnosed MCS groups found no significant differences in allele and genotype frequencies of CYP's, UGT, GSTM, GSTT, and GSTP (Deluca 2010) - and CYP2D6, NAT2, PON1, MTHFR, and CCK2R (Berg 2010) comparing the MCS and control groups - with the conclusion that multiple dysfunction of chemical defense systems in MCS patients mainly does not depend on genetic defects in chemical defense but instead modifications by redox active agents such as NO and inflammatory cytokines found higher among MCS patients in the Dantoft and Deluca studies.

16) GSTM1 and GSTT1 - objects of the Deluca and Schnakenberg studies - concern the activation of Phase II enzymes known as GSH S-transferases (GST) which catalyze the reaction of glutathione (GSH) with electrophiles - a broad class of xenobiotic and endogenous compounds - including environmental toxins and reactive oxygen species (Block 2011, Manfredi 2009, Hayes 2005, Wu 2004, Griffith 1999).

Over 50% of the population have one or both of the GSTM1 and GSTT1 deletions (Piacentini 2011,  Block 2011, Ginsberg 2009, Hayes 1995).

 

17) In a condition such as MCS GSH depletion may be inevitable - regardless of deletions - either by excess utilization in spontaneous or GST catalyzed reactions resulting in loss of cysteine - one of the amino acid precursors for the resynthesis of glutathione - or by suppression of synthesis such as with high levels of NO production (Lu 2009, Oslund 2008, Darmaun 2005, Wu 2004, Canals 2003, Griffith 1999, Sterner-Kock 1999, Tanabe 1996).

 

18) In apparent sudden onset of MCS from a large toxic exposure, usually the disease pre-existed as a genetic disposition (Eberling 2009, Veronesi 2001, 2000, Roy 2000, Jung 1921)

in a continuous environment of combustion byproduct fine particle aerosol - with airway epithelial cells and the sensory innervation already altered proinflammatory (Veronesi 2001, Meggs 1997, 1996) 

mediating dysfunction of chemical defense systems (Deluca 2010, Liptrott 2009, Oslund 2008, Chun 2002, Sterner-Kock 1999, Tinel 1999, Tanabe 1996, Tapner 1996, Nadin 1995, Stadler 1994, Khatsenko 1993)

and facilitating access of systemic inflammatory mediators and components of air pollution to the central nervous system (Calderon-Garciduenas 2008, 2004).

19) Because MCS - and environmentally caused disease in general - usually involves permanent proinflammatory alteration in the structure and function of the airway epithelium and its sensory innervation - there is no cure (Calderon-Garciduenas 2008,  Veronesi 2001, Meggs 1997).

Though chemokines, growth factors, cytokines, and NO are elevated, glutathione depleted, catalase deficient, fatty acid profile altered indicating lipid peroxidation, and CNS changes measurable (Dantoft 2014, Tran 2013, Holst 2011, Deluca 2010, Orriols 2009, Millqvist 2005, Kimata 2004, Bell 1999, 1998) laboratory tests may have no utility for the patient - therefore mandatory testing is unethical and immoral.

20) If cause and effect were isolated - one breath of exhaust would exceed in reactivity all personal exposures of a careful person over several days - and yet the exhaust is continuous. Failure to recognize the effect of combustion byproduct particulate with adsorbed incompletely combusted gasoline and diesel fuel hydrocarbon - inhaled at every breath - has been a grand illusion.

Perhaps impossible to express delicately - but the point needs to be made - worrying about a smell in the refrigerator or other perception is missing it - those exposures are relatively minor. They are riding on a continuous horizontal coning (Chapter 4) of tailpipe, chimney, and smokestack combustion particulate with its adsorbed hydrocarbon component - obviously the most significant cumulative and ongoing exposure (Block 2009). For that there is billions in health care costs (Pervin 2008, US DOT FHA 2000) and need for a non-combustion way of life.

21) We should be together in addressing the crisis of unrestrained growth and consumption that is threatening life on earth (Rogers 2011). Consequences are catastrophic - geopolitical turmoil, overpopulation: 1960/2015 - 3 to 7.4 billion in just 55 years (Worldometers 2015), resource loss, climate change, ocean acidification, mass extinction, speed, violence, pollution, injury, illness, and premature death.

It is to evaluate one's own attitude, character, behavior, and motives - and admit that all are of a grand scheme to destruction so long as the lifestyle of unrestrained growth, consumption, fast pace, preoccupation with competition and violence, and engagement of wasteful products, activities, and traditions persist - including billions of people taking a 4000 lb machine everywhere they go - rather than the healthful effort of walking - drawing upon thousands of years physical development and thoughtful reflection - a moral exertion - strength and integrity - choosing honesty, goodness, kindness, and love - to slow down and live environmentally consistent with those values.

With 1 billion people added to population in 15 years taught that unrestrained growth, consumption, and combustion fueled activity is okay - this world will not support all movement at 25-300 MPH - recognized is a need for Impossibly Good City Design - to slow down, walk more, change to non combustion vehicles, turn down thermostats, reduce population and consumption - using good moral judgement to protect a supporting environment.

There is perhaps more than enough study - there is a need to apply morality - and learn to be impossibly good.

A slower paced, reduced consumption, non combustion lifestyle is needed or human beings will go extinct due to loss of environment and resources.

MCS 3b Etiology: 1, 2, & 3 References