Airway Genetics and Ambient Combustion Aerosol

SPC 24 Veronesi and Jung: A Perfect Match

SPC 24 Veronesi and Jung: A Perfect Match

Links: 35 CAR Test SPC Questions
CAR Warm Up
SPC 1 Introduction: South Pole CAR (SPC) - A Character Test
SPC 2 South Pole CAR: ACA PM, Band Cell, and Monocyte Drop
SPC 3 ACA PM and ME/CFS: Do We Hear An Echo?
SPC 4 ACA UFPM: In the RBC - Through the BBB
SPC 5 ACA UFPM: IL-1 beta, RBC, BBB, - MCS and ME/CFS
SPC 6 ACA UFPM: Nerve Penetration
SPC 7 ACA UFPM: Olfactory, BBB, AD, PD, MCS, and ME/CFS
SPC 8 ACA PM: Gastro-Inflammation, Immunity, Vagal Circuitry
SPC 9 Veronesi: Sensory Nerve Insight
SPC 10 Kimata: Histamine Warning - Return to Masking
SPC 11 Central Sensitization: Intense, Repeated, and Sustained Inputs

On CAR
SPC 12 Disease Conditions Begin: Airway Epithelial Injury
SPC 13 Exposed Sensory Nerves - TRPA1
SPC 14 Exposed TRPA1: Central Sensitization
SPC 15 ACA: Loud and Clear
SPC 16 Airway Cytokine Release: Principle Mediator of Systemic Inflammation
SPC 17 Calderon-Garciduenas: Airway to Systemic: Putting It Together
SPC 18 Airway Gaps - Exposed Nerves - UFPM to the CNS
SPC 19 ACA PM: Months and Years Residence Time
SPC 20 Airway Gaps: Reduced Detox Enzyme Intervention
SPC 21 Solvents and Pesticides Primary: Shoe Fits Glove?
SPC 22 Veronesi and Roy: Genetic Difference in Airway Sensitivity

SPC 23 Jung Was Right Sort Of
SPC 24 Veronesi and Jung: A Perfect Match
SPC 25 Tailpipe and Chimney Emissions: Horizontal Coning
SPC 26 How Far Symptoms Travel: 25 Years, 500 Locations, 22 States
SPC 27 Not Into That Kind of Entertaining
SPC 28 Does it Cost More Than Money?
SPC 29 Airway to Systemic: Dysfunction of Detox Enzymes - Terlecky
SPC 30 Airway to systemic: Dysfunction of Detox Enzymes - Khatsenko
SPC 31 Gerde and Stadler: Benzo[a]pyrene Forever?
SPC 32 Phase I and II Detox Enzymes Defined

Lifestyle Change
SPC 33 ACA Catastrophic Consequences
SPC 34 Impossibly Good City Design
SPC 35 South Pole CAR Test: Satisfaction Guarantee

MCS 3 Definition and Concensus Criteria

MCS 3a Criteria Amendment Research Points (CAR)

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

MCS 3b CAR References

SPC 24 Veronesi and Jung: A Perfect Match

Please choose the Incorrect Statement

SPC 24a)

Earlier studies - Schnakenberg 2007, Mckeown-Eyssen 2004, and Haley 1999 - are inconclusive when applied to a diagnosed MCS group (Berg 2010 ,Deluca 2010). Schnakenberg did not use diagnosed MCS patients - instead defined 52% of a general population sample as the chemically sensitive group based upon filling out a questionnaire. Mckeown-Eyssen cautioned against drawing conclusions from their results - stating that in view of the small numbers such an association must be viewed cautiously - and the Haley study involved Gulf war veterans rather than MCS patients.

SPC 24b)

DELUCA 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)..."

SPC 24c)

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... "

SPC 24d)

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.

The observation that sensitivity of the sense organs occurs along with an introverted intuitive cast of mind - both genetically determined (Jung 1921) - further supported by the relationship between genetic quantitative differences in neuropeptides, TRP receptors, and acid sensitive pathways on airway sensory nerves and contrasting inflammatory sensitivity of mouse strains (MCS 15, Veronesi 2001, 2000, Roy 2000) is consistent with heritability of respiratory symptoms related to perfume reported by Elberling 2009.

SPC 24e)
Jung's introverted intuition is one of 8 principle types - prevalence of MCS has been estimated 3.1-6.3% doctor diagnosed and 11-16% self reported (Caress 2005, Kreutzer 1999) - a large minority.

SPC 24f)

Greater genetic sensitivity of a large population subset suggests vulnerability rather than a defect - not prepared for hazardous chemical exposure 100% of the time - the continuous ACA and other chemicals.
It is best to dismiss MCS as a poorly understood sickness behavior or genetic deletion in metabolizing enzymes - even though evidence indicates otherwise.

Lifestyle Change
SPC 33 ACA Catastrophic Consequences
SPC 34 Impossibly Good City Design
SPC 35 South Pole CAR Test: Satisfaction Guarantee

MCS 3 Definition and Concensus Criteria

MCS 3a Criteria Amendment Research Points (CAR)

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

MCS 3b CAR References

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SPC 24 Veronesi and Jung: A Perfect Match

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