Multiple Chemical Sensitivity Etiology
Airway Genetics and Ambient Combustion Aerosol
SPC 10 Kimata: Histamine Warning - Return to Masking
SPC 10 Kimata: Histamine Warning - Return to Masking
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)
SPC 10 Kimata: Histamine Warning - Return to Masking
Please choose the Incorrect Statement
SPC 10a)
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..."
SPC 10b)
SP (neuropeptide/transmitter substance P)
VIP (vasoactive intestinal peptide)
NGF (nerve growth factor)
H (histamine)
VOC (volatile organic chemical)
CTRL (25 control subjects)
ALLER (25 atopic excema dermatitis syndrome/allergy dust mites, pollen)
MCS (25 MCS)
b (baseline, before exposure to paint)
pa (after exposure to paint)
SP CTRL before 38 paint 39, ALLER b 75 pa 74, MCS b 105 pa 153
VIP CTRL b 10 pa 12, ALLER b 22 pa 21, MCS b 43 pa 68
NGF CTRL b 148 pa 156, ALLER b 889 pa 886, MCS b 1129 pa 1696
H CTRL b 278 pa 261, ALLER b 553 pa 565, MCS b 291 pa 563
"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..."
SPC 10c)
Histamine is often associated with the allergic response; allergen (antigen)-IgE (antibody) reaction.
Histamine release occurs more occasionally in MCS - upon sudden onsets or peaks in exposure sometimes giving an allergy-like outward appearance - as indicated in Kimata 2004 results.
SPC 10d)
"...Vasoactive intestinal peptide (VIP) is a 28-amino acid neuropeptide...
...The incubation of BEAS-2B cells (bronchial epithelial cell line) with VIP in concentrations...caused dose-related increases of IL-6 (98% increase above control, P<0.001)...
...These findings suggest that VIP can alter epithelial cell cytokine release and might be capable of modulating the airway inflammatory response in this manner..."
"...We investigated the effect of VIP on the secretion of interleukin-6 (IL-6) and interleukin-8 (IL-8), two pro-inflammatory cytokines, in TNF-alpha-activated proximal renal tubular epithelial cell line (HK-2) cells...
...These results strongly suggest that VIP synergistically enhances TNF-alpha-stimulated IL-6 and IL-8 synthesis via activating the NF-kB pathway in HK-2 cells..."
SPC 10e)
SAKAI 2004:
"...IL-6 stimulates multipotential cells, releases less mature PMNs (Suwa 2001, 2000, Patchen 1991), and accelerates monocyte differentiation (Jansen 1992, Bot 1989)). The association between band-formed PMN, monocyte counts, and IL-6 levels is consistent with previous reports (Suwa 2001, 2000, Jansen 1992, Patchen 1991, Bot 1989)..."
HOGG 2009:
"...We have reported that IL-6 accelerates the transit time of granulocytes through the bone marrow, releases them into the circulation, and promotes their sequestration in microvascular beds (Suwa 2001, 2000)...
...IL-6 stimulates the liver cells to produce acute phase proteins such as CRP, fibrinogen, and anti-proteases (Gabay 2007, Le 1987)..."
"...The results in this study show that a low level of atmospheric PM is associated with a decrease in bone marrow stimulation, which results in decreased circulating segmented PMN, band formed PMN, and monocyte counts...IL-6 levels were parallel with band formed counts...
...It is considered that the atmospheric PM level is one of the important factors affecting circulating leukocyte counts and basal inflammatory status...
...Multiple regression test showed that PM levels had more significant effects on segmented PMN, band formed PMN, and monocyte counts than cigarette smoking and type of work..."
SPC 10f)
MUKAE 2001:
"...We conclude that repeated exposure to PM-10 (particulate matter less than 10 microns in diameter) stimulates the bone marrow to increase the production of polymorphonuclear leukocytes (PMN) in the marrow and accelerate the release of more immature PMN into the circulation. The magnitude of these changes was related to the amount of particles phagocytosed by alveolar macrophages..."
"...alveolar macrophages, epithelial and other cells interact with the particles to produce a wide variety of cytokines and chemokines that generate a local inflammatory immune response. These mediators spill over into the blood to stimulate the bone marrow to increase the release of leukocytes from the marrow, and the liver to increase the production of a variety of acute phase proteins. This systemic response is associated with vascular activation and the progression of the atherosclerotic process..."
SPC 10g):
"...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..."
SPC 10h):
Neuropeptide VIP - elevated at baseline in MCS subjects (Kimata 2004) - is an integral player in the production of IL-6 (Huang 2012, Mullol 1997) which in turn stimulates the bone marrow - releasing less mature PMN (band cells) and accelerating monocyte differentiation - thereby increasing band formed PMN and monocyte counts (Hogg 2009, Sakai 2004) - the magnitude of increase in proportion to the amount of particles phagocytosed by alveolar macrophages (Mukae 2001) which - in addition to sensory neurons Veronesi 2001 and epithelial cells - are major in cytokine release.
IL-6 also stimulates the liver to produce acute phase proteins associated with progression of the atherosclerotic process ((Hiraiwa 2014, Hogg 2009, Goto 2004, Mukae 2001). Increased cardiopulmonary disease risk has been reported in a community based sample having odor intolerance (Baldwin 1998).
SPC 10i)
The MCS baseline picture and likely applicable to ME/CFS is clear: high IL-6 and other cytokines (Dantoft 2014, Maes 2012), elevated SP, VIP, and NGF confirmed in MCS (Kimata 2004) and indicators of immune activation PMN elastase, lysozyme, and neopterin in ME/CFS ( Maes 2012) - there is no other explanation but the ACA for this consistency of cause and effect - the ACA PM involvement with sensory nerves, alveolar macrophages, and epithelial cells - release of neuropeptide transmitters SP and VIP, growth factor NGF, and inflammatory cytokines including IL-6 - the activation of the immune system - release of less mature polymorphonuclear leukocytes (PMN) (band cells) and monocytes from the bone marrow - and the presence of lymphocytic infiltrates in the airway epithelium (Meggs 1997).
Exposure to paint in Kimata 2004 - raised SP, VIP, and NGF further above the already high baseline value and gave a temporary histamine spike - but eventually they left the freshly painted study room - all the while in continued exposure to the 24/7/365 ACA - promoter of illness, disability, and premature death.
SPC 10j)
When histamine subsides - but inflammation continuing as reflected by still high SP, VIP, and NGF at baseline among MCS patients - it can't sometimes contribute to mask of symptoms or belief that respiratory is not involved in MCS.
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)
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