Comparing the MCS 2021 Consensus to the MCS 1999 version

[michael edward badolato jr]

This forum is dedicated to Judith, and July 30, 2021 will be forever known as Judith Day, an MCS National Holiday; unless of course, every day is a Holiday. Judith Day honors the day, Judith became Commander and Chief of MCS Etiology.

Contents:

I. The MCS 1999 Consensus Criteria

2. The MCS 2021 Consensus Criteria

The 1999 Consensus authors were somewhat drunk when voting on the language, many are even totally delusional while sober. A few were reading comic books, while others were sleeping through the hearing phase.

The 1999 version, especially criteria 3 below, leaves it wide open as to whether it is a physiological disease or psychological syndrome, and perhaps leaning toward the latter; and providing little clue as to physiology and etiology of the disease. 

The 1999 Consensus Criteria  mcsrr.org / Bartha P. et al. Multiple Chemical Sensitivity: a 1999 Consensus. Arch Env H 54:147-49 1999:

1) symptoms are reproducible with repeated exposure

2) the condition is chronic

3) low levels of exposure [lower than previously or commonly tolerated] result in manifestations of the syndrome

4) symptoms improve or resolve when the incitants are removed

5) responses occur to multiple chemically unrelated substances

6) symptoms involve multiple organ systems

The MCS 2021 Consensus, while brilliant, has one problem: the MCS community of gangster-like big wigs refused to support it. Consequently it is a "consensus" of data from the most prestigious academic, medical, and government research facilities; such as Yale, Harvard, and the US EPA NHEER, who were somehow widely ignored by the "club".

II. MCS 2021 Consensus Criteria 

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

IIA. Diagnosis 9a-g

9. MCS 2021 Consensus Criteria

a. Genetically susceptible acquired alteration (GSAA): ambient combustion aerosol (ACA) and subjectively recognized personal exposure (SRPE) - at levels to which most do not attribute symptoms - result in precipitation of symptomatology involving multiple organ systems.

b. A chronic condition - symptoms may improve when incitants are removed (SRPE relieved) - however, exposure to the ambient combustion aerosol (ACA) supporting the disease process is continuous.

c. Responses occur to multiple chemicals - usually those having greater acidic, electrophilic, oxidizing, or solvent properties [toxicity] - increased further if instilled by particulate vector as in the ACA .

italics above from: mcsrr.org / Bartha P. et al. Multiple Chemical Sensitivity: a 1999 Consensus. Arch Env H 54:147-49 1999

d. Particulate matter including diesel exhaust particles - and numerous acidic, electrophilic, and oxidizing components of the ambient combustion aerosol (ACA) - to which all are continuously exposed - activate airway sensory c fiber nerves that express TRPA1, TRPV1, and substance P (Deering-Rice 2011, Hazari 2011, Costa 2010, Taylor-Clark 2010, Caceres 2009, Anand 2008, Bessac 2008, Nassenstein 2008, Bautista 2006, Inoue 2005, Kobayashi 2005, Veronesi 2001).

Therefore, the ACA and SRPE support the underlying disease process - including central sensitization from excessive nociceptor inputs (Latremoliere 2009).

TRPV1 is activated by chemical irritants, inflammatory mediators, and tissue damaging stimuli - most famously capsaicinoids and has been referred to as the capsaicin receptor (Veronesi 2006). Observing a lower cough threshold among MCS patients compared to controls when exposed to capsaicin - Nogami 2004 suggested such provocation as a diagnostic test for MCS. However, TRPA1 may be the major reactive irritant receptor (Bessac 2008).

TRPA1 is activated by formaldehyde, acetaldehyde, tear gas agents, and industrial isocyanates (Bessac 2009, Brone 2008, Bang 2007, McNamara 2007), smoke constituents - methacrolein, methyl vinyl ketone, and croton aldehyde (Andre 2008, Escalera 2008), and oxidizing agents including hypochlorite (Bessac 2008a).

Almost all oxidizing and electrophilic agents effect TRPA1 function (Bessac 2008).

Endogenous agonists include reactive oxygen species (ROS), hypochlorite, lipid peroxidation products, cyclopentenone prostaglandins, and isoprostanes (Bessac 2008).

The volatile organic chemical monoterpene ketone umbellone - outgas agent from the California Bay Laurel "headache tree" - stimulates the TRPA1 channel activating the trigeminovascular system. TRPA1 deficient mice failed to have the trigeminal response to umbellone. Nassini 2011 concluded that TRPA1 agonism may be responsible for headache crisis in sensitive people after exposure to environmental pollutants and perfume.

BESSAC 2008:

...TRPA1 can be locked into a constitutively active state, indicating saturation of a reactive site (Hinman 2006)...

...three cysteine residues were crucial for channel activation (Macpherson 2007)...activation of TRPA1 by covalent modification through reactive irritants...dose response relationships and activation kinetics of TRPA1 do not conform to standard pharmacological paradigms and are highly dependent on the chemical status of the cellular and tissue environment...

...TRPA1 agonists show wide divergence, sometimes one or two orders of magnitude...TRPA1 agonist activity will depend on the reversible or irreversible nature of the chemical bonds formed and on agonist membrane permeability...

 ...since most TRPA1 agonist can react with thiols, cellular and extracellular reduced glutathione levels will affect the reach and potency of inhaled airway irritants. Once glutathione is depleted, either as a consequence of disease or during extended exposures, TRPA1 may respond more strongly (Deluca 2010 found MCS people have severe glutathione depletion). With each breath more reactive agonist is delivered, leading to an increase in covalent modifications and heightened TRPA1 activity...robust TRPA1 induced irritation even at low subacute exposure levels...once irreversibly modified channels may remain active for extended periods of time even when the irritant stimulus is removed...(Bessac 2008a)...

...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)..."

e. Provocation tests are not appropriate - confounded by ambient conditions and 48 hour acute phase response from prior ACA and SRPE (Castranova 2002, Bascom 1992). 

f. GSAA (genetically susceptible acquired alteration) - MCS is not a psychological illness.

g. MCS - not an allergy - involves immunoglobulin G (IgG) - the most prominent type of serum antibody which protects against bacteria, viruses, and toxins - distinctly different from the bridging of two IgE molecules by allergens causing a release of chemical mediators from mast cells - including histamine - the allergic response (Merck 1999).

MERCK 1999:
"...Histamine is widely distributed in mammalian tissue. In humans the highest concentrations are in skin, lungs, and GI mucosa...The release of histamine from the mast cell storage granules can be triggered by physical tissue disruption, various chemicals (including tissue irritants, opiates, and surface active agents), and most prominently by antigen-antibody interactions..."

Kimata 2004 found the IgE driven allergy people had plasma H (histamine), NGF (nerve growth factor), SP (substance P), and VIP (vasoactive intestinal peptide) all elevated at baseline: 553, 889, 75, 22 but unchanged by exposure to the toxins of paint: 565, 886, 74, 21.

MCS people had NGF, SP, and VIP higher at baseline due to GSAA (genetically susceptible acquired alteration), ACA (ambient combustion aerosol), and prior SRPE (subjectively recognized personal exposure): 1129, 105, 43 further elevated by the paint to 1696, 154, 74 - markers nearly double that of allergy: 886, 74, 21.

MCS people had histamine similar to controls at baseline but elevated 291 to 563 after exposure to paint because mast cell degranulation and histamine release may occur as noted above - either by allergic bridging or as in MCS - upon sudden increase of chemical exposure.

Controls were nearly unaffected by paint and had far lower levels at baseline except close to MCS on histamine: H, NGF, SP, VIP before and after paint: controls 278,261; 148,156; 38,39; 10,12 compared to MCS 291,563; 1129,1696; 105,154; 43,74.

In summary, much like controls MCS people tend to be unaffected by allergens; and allergic people not acutely reactive to toxins.