http://www.leagle.com/decision/199812720FSupp2d107_1111.xml/COFFIN%....

Criteria Amendment Research Points (CAR) are not intended for use in lawsuits. It is not recommended that an MCS person file suit - culpability usually cannot be assigned to a single entity or circumstance - usually unrealistic in the context of how MCS etiology develops.

Reference to Coffin vrs Orkin Exterminating 1998 is to show the difference in understanding implied by the 1999 Consensus Criteria for MCS compared to the 2015 MCS Consensus Criteria (CAR) documentation.

Consistent with the 1999 Consensus Criteria - Dr. Phillips on behalf of the plaintiff Marion Coffin stated the following:

Phillips Dep. at 31.

Dr. Phillips explains the symptoms of MCS as:
chronic, which is defined as being over four months in duration, sinus and/or upper respiratory symptoms as well as a sense of poor health such as fatigue, headache, loss of appetite, that occurs after exposure to VOC's that usually improves after they have been removed from the exposure; and then it recurs again with more exposure. And despite treating them for other possible diagnoses, they continue to ... have these chronic symptoms.

Phillips Dep. at 32.

Although the Court is aware of no uniformly accepted definition of MCS, another court has noted that "all proposed definitions include elements of (1) a multi-symptomatic disorder; (2) affecting multiple organ systems; (3) resulting from exposure to a diverse array of chemical compounds at levels tolerable by the majority of the population." Frank v. State of New York, 972 F.Supp. 130, 132 n. 2 (N.D.N.Y. 1997).

The 2015 MCS Consensus Criteria - with supporting CAR documentation - corrects Dr. Phillips as follows with special attention to Kimata 2004 below:

While leaving five of the six 1999 Consensus Criteria essentially intact - the 2015 Consensus corrects impression MCS is a syndrome in response to unrelated chemicals in a low level, commonly tolerated, non inciting background atmosphere. Amendment includes language more consistent with intent (2,3,4) and information - especially concerning the ACA (3,4). Pt 1 of the 1999 Consensus is not included because reproducibility of symptoms upon repeated exposure is effected by masking and overlap of continuous exposure to the ACA and other chemicals - saturating trigeminal and olfactory receptor sites and eliciting both immediate and delayed precipitation of symptomatology.

Multiple Chemical Sensitivity: 2015 Consensus Criteria

1) The condition is chronic

2) Levels of exposure to which most do not attribute symptoms result in precipitation of symptomatology

3) Symptoms may improve when incitants are removed - however exposure to the Ambient Combustion Aerosol (ACA) supporting the disease process is continuous

4) 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

5) Symptoms involve multiple organ systems

The 1999 Consensus: 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

KIMATA 2004:

"plasma levels of SP (substance P), VIP (vasoactive intestinal peptide), and NGF (nerve growth factor), but not histamine are significantly (p<0.01 by ANOVA) elevated in sMCS patients...

exposure to VOC further increased levels of SP, VIP, and NGF...exposure to VOC also increased plasma histamine levels...

these results indicate that sMCS patients may suffer from ongoing neurogenic inflammation which is aggravated by VOC..."

ORRIOLS 2009:

"...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)..."

It may seem incomprehensible - present in every breath since birth - exhaust saturated in the olfactory region - and along the entire nasal and upper respiratory tract of sensory receptors - fine particles with adsorbed chemicals - particulate vector and a prolonged residence time (Li 2011, Bonvallot 2001) stored in lung tissue and lymph nodes for months and years - desorption in 2 phases - initial rapid burst and extended gradual release (Gerde 2001, 1997) a physiological hijacking in a continual particulate shower - the ambient combustion aerosol - nearly all are rum dumb on this issue.

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.

DEERING-RICE 2011:

"...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..." Found elevated in MCS patients (Kimata 2004) (Hazari 2011, Teles 2009, Anand 2008, Nassenstein 2008, Kobayashi 2005)..."

1) There is a pre-existing genetic sensitivity of c fiber sensory nerve receptors and acid sensitive pathways resulting in a lifelong tendency to release more inflammatory mediators per exposure (MCS 15, Elberling 2009, Veronesi 2001, 2000, Roy 2000, Jung 1921).

VERONESI 2001:

"...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)...

2) Subsequent alteration by exposure - including a continous ambient combustion aerosol (ACA) - results in altered structure and function of the neuro-inflammatory system - especially beginning with alteration (damage) of the airway epithelium exposing the c fiber nervous system with its TRPA1, TRPV1, substance P producing (peptidergic) terminals (Nassini 2011, Taylor-Clark 2010, Caceres 2009, Bessac 2008, Veronesi 2001, 2000, Roy 2000, Meggs 1997).

MEGGS 1997:

Biopsy of MCS subjects

"...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..."

VERONESI 2001:

"...In normal physiological settings, the respiratory epithelial population and its sensory innervation act reciprocally to influence the growth, differentiation, and homeostasis of each other...These relationships are especially critical to the organism's inflammatory response...

...In all instances, sensory neurons release 10-200 fold higher levels of IL-6 (pro-inflammatory cytokine) relative to epithelial cells... Found elevated in MCS patients (Dantoft 2014)...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...

...BALB/c mice were deenervated of polymodal sensory c fibers by neonatal capsaicin treatment. Sensory neurons , dissected from the DGR (dorsal root ganglia) of these deenervated animals and exposed to various PM (50mg/ml) or prototype irritants failed to release IL-6 in response - implicating the sensory c fibers as critical to cytokine release in response to PM..."

3) A chronic symptomatology develops - less severe earlier - many not aware they have a disease condition and are vulnerable due to airway alteration having exposed the nerves.

4) In the example of Marion Coffin vrs Orkin - Marion's MCS was greatly worsened due to pesticides - Marion was aware of having sensitivity prior to the exposure - a condition supported by an ongoing underlying disease process - exposed peripheral nervous system in the airway - and continuous exposure to the ambient combustion aerosol (ACA) along with additional personal and incidental exposure - which depending on severity will worsen the condition - such as with solvents and pesticides.

5) The case was decided not in Marion's favor. Was it fair? That is a tough question - because in truth Marion may have just as well filed suit against Exxon, British Petroleum or General Motors. Or if parents had smoked in Marion's childhood home they might be held accountable. It could be that the majority of people were they exposed to Orkin's pesticides as Marion - would have been little effected.

6) This illustrates the importance of the Criteria Amendment - the condition does not resolve upon removal of inciting exposure - because exposure to the ambient combustion aerosol (ACA) never ends - this is reflected by the abnormal measures in MCS patients without study provocation and the relatively precise determination that has been made of the structural alteration, receptors, and metabolic pathways involved - evidenced in MCS 3b and supporting documentation.

Dr. Phillips also described Marion's condition as having gone from reversible to irreversible as a result of exposure to Orkin's pesticides:

"[Plaintiff] had developed reversible hypersensitivity to volatile organic compounds until she was exposed to the pesticide spraying. After the pesticide spraying she developed irreversible, permanent hypersensitivity to volatile organic compounds as well as to pesticide"

However, it has been shown that - rather than reversible - Multiple Chemical Sensitivity (MCS) is an ongoing neurogenic inflammation evidenced by respiratory cell tight junction defects, focal desquamation of epithelial cells, hypertrophy of glandular structures, lymphocytic infiltrates, and proliferation of nerve fibers (Meggs 1997) - high levels of nerve growth factor (NGF), substance P (SP), and vasoactive intestinal peptide (Kimata 2004), altered cytokine profile (Dantoft 2014), elevated nitric oxide (NO), severe glutathione depletion, catalase deficiency, and proatherogenic lipid changes (Deluca 2010, Baldwin 1998), SPECT hypoactivity (Orriols 2009), and electroencephalographic alterations - during time periods Dr. Phillips refers to as of reversibility. These study results show the MCS patient is continuously overwhelmed.

Therefore, something is driving the continuous underlying disease process - not the Easter Bunny - its the ambient combustion aerosol (ACA) Deering-Rice 2011, Hazari 2011, Costa 2010, Anand 2008, Nassenstein 2008, Kobayashi 2005.

The attitude of cars and trucks are fun to drive had better stop - the ACA is ultimately fatal to many (Pervin 2008, US DOT FHA 2000) an environmental free fall - extremely hard on the global environment - threatening mass extinction (Rogers 2011).

7) It is a moral responsibility to acknowledge the very significant and for many the largest lifetime exposure - the ambient combustion aerosol (ACA) which the Amendment is not claiming as cause in all cases - but conclusively the ACA has many components which support the underlying disease process of MCS (Deering-Rice 2011, Hazari 2011, Costa 2010, Anand 2008, Nassenstein 2008, Kobayashi 2005).

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