Multiple Chemical Sensitivity Etiology
Airway Genetics and Ambient Combustion Aerosol
Multiple Chemical Sensitivity: 2021 Consensus Criteria Part I Baseline GSAA, ACA, SRPE
Multiple Chemical Sensitivity: 2021 Consensus Criteria
Baseline, Etiology, Diagnosis, Patient Rights
Part I Baseline GSAA, ACA, SRPE
Expertise from the most Prestigious Academic, Medical, and Government Research Facilities
Consensus Amendment Research, TRPA1 Precision
Outline
I. Baseline GSAA, ACA, SRPE 1-8
II. Diagnosis, Patient Rights, Etiology 9-14
III. Baseline: Nutrition and Exercise 15-31
A. SJF, LE 15-20
B. Whole Food Nutrition 21-31
IV. Baseline: Nutrition and Exercise 32-38
C. Suboptimal Actors 32
D. Maintaining Bone Density 33-37
E. Preventing Atherosclerosis 38
I. Baseline GSAA, ACA, SRPE 1-8
1. ACA Basal Inflammation
2. GSAA Amplified Response
3. MCS Genetics: Likely a Neural Portrait
4. GSAA (Genetically Susceptible Acquired Alteration)
5. Olfactory Dysfunction: MCS, AD, PD
6. ACA and SRPE
7. Cerebral Hypoperfusion, Atherogenicity
8. Herbal Antiplatelet Activity
Abbreviations
GSAA: Genetically Susceptible Acquired Alteration
ACA: Ambient Combustion Aerosol
SRPE: Subjectively Recognized Personal Exposure
1. ACA Basal Inflammation
During combustion particles are generated and PAHs (polycyclic aromatic hydrocarbons) form in the gas phase. When the exhaust cools - PAHs adsorb or condense on the particles (Burtscher 1998).
There are two principal fractions of adsorbed PAHs: one is quickly desorbed - and the other retained on particles for a long time (Gerde 1991, Burtscher 1986, Adamson 1982, Natusch 1978).
Over 5 months later particles in the lung and lymph nodes had only 37 and 59% of B[a]P desorbed - mostly during the initial rapid release - with the exception of more desorption from particles translocated to the lymph nodes - possibly due to environment within macrophages (Nyberg 1989, Harmsen 1985, Lundborg 1984).
Approx 80% of rapidly desorbed PAHS are deposited on the thin alveolar type 1 epithelium deep in the lung (Yeh 1996) and become systemic quickly with blood concentration peaking in several minutes.
3/4 of blood activity from the rapidly absorbed B[a]P (benzo[a]pyrene) used in Gerde 2001 ceased in 10 minutes - nearly all within 30 - and by one hour completely leveled - mostly into conjugated phase ll metabolites (Fung 1999, Thompson 1989, Molliere 1987).
However, approximately 20% of initially desorbed chemical from PM (particulate matter) of the ACA (ambient combustion aerosol) is deposited, slowly absorbed, and extensively metabolized in the thick upper respiratory and nasal epithelium at prolonged elevation of the local tissue concentration (Gerde 2001, 1997).
In airway epithelial cells, DEP (diesel exhaust particles) via chemicals desorbed from the carbonaceous core involve a complexity of transduction and transcription factors (NFkB, MAPK, XRE, ARE, NrF2) and modification of cellular redox - with the secretion of inflammatory cytokines and induction of Phase I and II gene expression including CYP1A1 and NQO-1 (Baulig 2003a) - from a point of view excluding the sensory innervation.
This activity is with cost - the carbonaceous core of ACA PM considered a vector leading to sustained stimulation of the cells (Bonvallot 2001, 2000, Boland 2000, 1999, Baeza-Squiban 1999, Bayram 1998, Kumagai 1997, Thomas 1997) - inhalation of combustion byproducts living on the edge - with the generation of reactive oxygen species, depletion of antioxidant defenses (Ziedinski 1999), DNA strand scission of plasmidic DNA (Stone 1998), and apoptosis of epithelial cells (Apogyan 2003a, Chin 1998).
Instead of a more localized expression of metabolizing and antioxidant enzymes in solid airway epithelium protecting the nervous system - exposed nerves of damaged and inflamed epithelia result in activation of the TRP channels - elevated inflammatory mediators including substance P and cytokines - involvement of the immune system and increase of NO - endogenous products of inflammation to burden and suppress 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). Symptoms of MCS are often of a flu like pattern (Dantoft 2014, Bascom 1992) with increased congestion (Doty 1994) and hyperalgesia (Tran 2013, Holst 2011, Latremoliere 2009).
It is impressive - the complex metabolism taking place in both the nasal and tracheal bronchial epithelium (Block 2012) in close proximity to the critical c fiber sensory nerve receptors with their TRPA1 expressing peptidergic terminals.
Once airway alteration is established - the nervous system more vulnerable - subsequent exposure to substances such as solvents and pesticides may greatly increase the disease - especially concerning the CNS.
Particulate matter air pollutants - particle agglomerates with adsorbed hydrocarbons, singlet non agglomerated nano particles, and acid sulfate - result of catalytic converter transformation of sulfur dioxide (Lucchini 2012) - carbonaceous cores coated with thousands of chemicals and heavy metals - many hazardous (Li 2011) - principle components of the ambient combustion aerosol (ACA) - diesel, gasoline, and other exhaust, woodsmoke, and tobacco smoke (MCS aa, OSHA 2012, Schauer 2002, 2001, 1999, Society of Automotive Engineers SAE 940233 1994) - induce upper respiratory, lung epithelial, and endothelial injury, persistent chronic inflammation in the respiratory tract, and systemic inflammation accompanied by the production of proinflammatory cytokines such as TNF alpha, IL-6, and IL-1 beta (Calderon-Garciduenas 2008, 2003, 2001, 2000) - found elevated in MCS patients (Dantoft 2014).
Many hundreds of studies depict the harm of ACA components - annual cost estimate in the US for premature death and illness due to air pollutants associated with motor vehicle use range in the hundreds of billion dollars with 95% attributed to ambient PM - principle component of the ACA (Pervin 2008, USDOTFHA 2000).
2. GSAA Amplification
With GSAA (genetically susceptible acquired alteration) - inflammatory response to the ACA is amplified (Hogg 2009) - fundamental to the MCS disease process - neurogenic inflammation, oxidative stress, severe multiple dysfunction of exenobiotic metabolizing and antioxidant (detox) enzymes, electroencephalographic alterations, SPECT hypoactivity, cerebral hypoperfusion, and autonomic dysregulation - baseline MCS subjects - before or without study provocation - chemokines, growth factors, cytokines, and NO elevated, glutathione depleted, catalase deficient, fatty acid profile altered indicating lipid peroxidation, and CNS changes measurable (Belpomme 2015, Dantoft 2014, Tran 2013, Holst 2011, Deluca 2010, Orriols 2009, Milqvist 2005, Kimata 2004, Bell 1999, 1998, Meggs 1997, 1996, 1993).
The extent ACA is principle supporter depends on individual circumstances. Each exposure in a bubble is followed by a 48 hour acute phase response - reactive and measurable (Milqvist 2005, Nogami 2004, Bonham 2001, Lee and Pisarri 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 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). The real world presents overlap - a rum dumb condition. For a person careful to eliminate SRPE (subjectively recognized personal exposure) all the more ACA takes on principle significance.
SRPE often spikes histamine up from normal (Belpomme 2015), Elberling 2007, Kimata 2004) - and further raises already elevated markers.
"...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..."
3. MCS Genetics: Likely a Neural Portrait
There is no evidence genetic deficiency in detox enzymes accounts for the majority of MCS (Caccamo 2013, Berg 2010, Deluca 2010, Schnakenberg 2007, Mckeown-Eyssen 2004). For example, over 50% of the population have one or both of the GSTM1 or GSTT1 deletions (Block 2011, Piacentini 2011, Ginsberg 2009, Hayes 1995) - found to correlate with intolerance of chemicals in 52% of a general population sample (Schnakenberg 2007) - percentages not applicable to MCS - and PON1 deletion was associated with Gulf War Syndrome (Haley 1999). MCS GSAA may have such deletions involved - however 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 2014 and Deluca 2010 studies.
A candidate gene approach is limited because cannot take into account all the potential modifiers of environmental toxicants (Block 2012) however there is likely a neural portrait - greater dependence on sense impressions and hypersensitivity of the sense organs compensates rarified air of the intuitive conscious attitude (Jung 1921) - likely determined by genetic quantitative differences in neuropeptide release, TRP receptors, and acid sensitive pathways that innervate the nasal and upper pulmonary airway epithelium (Veronesi 2001, 2000, Roy 2000).
"...In conclusion, we found an increased familial occurrence of perfume-related respiratory symptoms where 35% of phenotypic variation was due to additive genetic effects and 65% was due to individual specific environmental effects..."
4. GSAA (Genetically Susceptible Acquired Alteration)
MCS genetic susceptibility and cumulative exposure translates into acquired neuroinflammatory alterations - airway epithelial tight junction - olfactory, sensory, trigeminal, central - then symptoms are attributed to SRPE (subjectively recognized personal exposure).
"...Tight junctions are critical barrier features in tissues throughout the body. In the olfactory epithelium, tight junctions are found at the apical surface of cells, adjacent to the nasal airways..."
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 ..."
"...after capsaicin provocation the patients showed a significant increase in NGF which was related to capsaicin cough sensitivity...SHR (sensory hypereactivity) is real and measurable, demonstrating a pathophysiology in the airways of these patients compared to healthy subjects..."
"...The findings of the present study indicate that the mechanisms underlying MCS may originate in the sensory nervous system..." - MCS cough occurring in response to capsaicin at concentrations far less (.150) than both the control group (1.120) and the chronic cough group (.630).
"...Although the neuronal architecture of the olfactory and trigeminal systems differ , the fact that both have sensory receptors within the nasal epithelium and project directly to the CNS suggest that similar pathways for toxicant entry may exist ...
...These data support the conclusion that a similar pattern of uptake may occur within the trigeminal system as has been observed in the olfactory system...
...into the CNS in concentrations greater than those found with systemic distribution and without penetrating the blood-brain barrier...
...These data underscore the importance of considering routes of toxicant entry that allow for bypassing of the protection afforded by the blood brain barrier, and the importance of understanding the conditions under which these pathways are operative..."
"...The results obtained support that nano-sized DEPs (diesel exhaust particles) do in fact translocate to the central nervous system through the olfactory nerve..."
Central sensitization is a form of functional plasticity resulting in pain hypersensitivity triggered by the activity evoked in dorsal horn neurons by input from chemically activated c-nociceptors (airway c fiber sensory receptors) including TRPA1 expressing peptidergic terminals. Latremoliere 2009 described central sensitization as a constantly changing mosaic of alterations in membrane excitability, reductions in inhibitory transmission, and increases in synaptic efficacy, mediated by many converging and diverging molecular players in a background of phenotypic switches and structural alterations.
Intense, repeated, and sustained inputs from exposed airway sensory nerves involve TRPA1, TRPV1, substance P, CGRP, NKA, cytokines, NO, BDNF, bradykinin, glutamate, NMDAR, AMPAR, and mGluR (Latremoliere 2009).
5. Olfactory Dysfunction: MCS, AD, PD
Similarly, olfactory dysfunction - usually indicating airway breakdown and penetration of pollution components via neural pathways to the CNS - precedes recognition of Alzheimers (AD) and Parkinsons (PD) onset - in the latter symptoms don't show until nearly 50% of dopaminergic neurons are destroyed.
"...The nasal olfactory pathway is believed to be a key portal of entry, where inhaled nanoparticles have been shown to reach trigeminal nerves, brainstem, and hippocampus (Wang 2008, 2007)...particulate matter has been observed in human olfactory bulb periglomerular neurons and particles smaller than 100nm were observed in intraluminal erythrocytes from frontal lobe and trigeminal ganglia capillaries (Calderon-Garciduenas 2008)...air pollution components reach the brain (Peters 2006), even penetrating deep into the parenchyma...
...Alzheimer's (AD) and Parkinsons Disease (PD) share early pathology in the olfactory bulb, nuclei, and pathways, with olfactory deficits being one of the earliest findings in both diseases (Doty 2008)..."
"...The clinical symptoms of PD, manifest as the loss of initiation and control of movement and appear only after a substantial loss of dopaminergic neurons (50-60%) in the substantia nigra pars compacta (SNpc) in the midbrain (Pakkenberg 1991)..."
6. ACA and SRPE
Genetically susceptible acquired alteration (GSAA) - MCS, ME/CFS, RADS, COPD, AD, and PD - cumulative environmental exposure - air pollution exerts an insidious neurodegeneration (Calderon-Garciduenas 2008) - tailpipe and chimney emissions - horizontal coning and layering - the ambient combustion aerosol (ACA) is always present. MCS is not a subjectively recognized personal exposure (SRPE) occurring in a vacuum.
BLOCK 2009:
"...Major sources of PM2.5 include oil refineries, metal processing facilities, tailpipe and brake emissions from mobile sources, residential fuel combustion, power plants and wildfires (Muhlfeld 2008, Rothen-Rutishauser 2008, Valavanidis 2008).
However, UFPM is widely implicated in PM-associated pathology, as their nanometer size makes these particles the most effective size for lung deposition, penetration, and effects extending beyond the respiratory tract (Craig 2008). The primary contributors to UFPM are tailpipe emissions from mobile sources (motor vehicles, aircraft, and marine vessels) (Muhlfeld 2008)...
...Alarmingly, UFPM levels are unmonitored and unregulated in the USA, but exposure is estimated to be high..."
"...The major components of PM include transition metals, sulfate and nitrate ions, organics, minerals, adsorbed gases, and biocontaminants (e.g., endotoxins, mold, pollen), attached to a core of carbonaceous material. The size of the particulates found in PM has been inversely related to its inflammatory damage (Pedata 2010, Valavanidis 2008, deHaar 2006, Oberdorster 1996) with smaller, ultra fine size particles being more toxic to the target tissue...
...Numerous clinical and experimental studies have...identified the brain to be neurochemically and neuropathologically affected by various types and sizes of PM air pollution (Gerlofs-Nijland 2010, Campbell 2009, 2005, Calderon-Garciduenas 2008, 2007, Sunyer 2008, Zanchi 2008, Sirivelu 2006, Block 2004)...
...In the central nervous system (CNS), oxidative stress is largely mediated by microglia, which are macrophage-like, phagocytic cells that are activated by a broad range of stimuli, including PM (Sama 2007, Block 2004) and nanoparticles (Long 2006). Once activated, the microglia produce multiple reactive oxygen species (ROS) such as hydrogen peroxide, hydroxyl radicals and peroxynitrites (Block 2007, Fariss 2005) that can diffuse from their plasma membrane and damage nearby neurons..."
7. Cerebral Hypoperfusion, Atherogenicity
Cerebral hypoperfusion might be end game - confirmed in up to 50% of MCS subjects (Belpomme 2015) - autonomic dysregulation - if not, atherogenicity due to systemic inflammation (Deluca 2010, Baldwin 1998).
"...cerebral hypoperfusion in one or two of the hemisphere in 50.5% of the cases...
...We serially measured the brain blood flow (BBF) in the temporal lobes of each case with pulsed cerebral ultrasound computed tomosphygmography (UCTS). Both disorders (MCS and EHS) were associated with hypoperfusion in the capsulothalamic area, suggesting that the inflammatory process involves the limbic system and the thalamus..."
"...MCS patients present brain signal photon emission computed tomography (SPECT) and psychometric scale changes...
In comparison to controls, cases presented basal brain SPECT hypoperfusion in small cortical areas of the right parietal and both temporal and fronto-orbital lobes. After chemical challenge, cases showed hypoperfusion in the olfactory, right and left hippocampus, right parahippocampus, right amygdala, right thalamus, right and left Rolandic and right temporal cortex regions (p<0.01)...
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)..."
"...a single exposure to particulate matter (PM) or gaseous air pollutants has the potential to "sensitize" the heart to subsequent arrhythmogenic stimuli, which is further worsened by the presence of underlying cardiovascular disease (Hazari 2009)...
...the airways are innervated by sensory nerves bearing transient receptor potential (TRP) channels; namely, member A1 (TRPA1), and member V1 (TRPV1), which detect different types of noxious chemicals, including many of those found in the complex mixtures of common air pollutants such as DE. Activation of these nerves by airborne irritants such as ozone or acrolein causes centrally mediated autonomic "imbalance", which produces ventilatory, pulmonary, and cardiovascular function changes (Bessac 2008, Ghelfi 2008, Bautista 2006)..."
"...the MCS group perceived the n-butanol exposure as being more intense, more unpleasant and rated symptoms to be of greater magnitude compared to controls...additionally, individuals with MCS had higher than normal pulse rate and lower than normal pulse rate variability...indicating abnormal regulation of the sympathetic branch of the autonomic nervous system during the exposure..."
HIRAIWA 2013:
"...PM-2.5 and UFPM (ultra fine particulate matter less than 0.1 micron median aerodynamic diameter) are primarily derived from direct emissions from combustion processes such as vehicle use of fossil fuel products, wood burning, and coal burning (Bernstein 2004)...several studies have shown that PM 2.5 and UFPM have the strongest association with adverse cardiovascular effects (Franck 2011, Stolzel 2007 ), which is a direct consequence of the systemic response induced by these particles (Nemmar 2002, Nemmar 2001)..."
Those familiar with MCS and CFS might find it nearly inconceivable that all could originate as a chain reaction due to airway defects - but coherent pathways have been elucidated (Latremolier 2009, Calderon-Garciduenas 2008, 2000).
Substance P - elevated in MCS patients (Kimata 2004) primes and activates human neutrophils for superoxide, H2O2, and nitric oxide production (Oslund 2008, Sterner-Kock 1999, Tanabe 1996).
Dysfunction of chemical defense systems in MCS patients are mediated by redox active agents such as NO and inflammatory cytokines (Deluca 2010, Liptrott 2009, Oslund 2008, Chun 2002, Sterner-Kock 1999, Tinel 1999, Tanabe 1996, Tapner 1996, Nadin 1995, Stadler 1994, Khatsenko 1993). Depletion of phase II glutathione leads to severe oxidative stress and impaired elimination of phase I CYP metabolites. Catalase deficiency results in accumulated hydrogen peroxide leading to lipid peroxidation (Deluca 2010, Terlecky 2006).
Deluca 2010 found MCS patients have 3 fold reduction in catalase activity, severe glutathione depletion, double nitric oxide, and a fatty acid profile of lipid peroxidation - increased SFA with losses in PUFA, N6, N3, arachidonic acid, and omega 3.
MCS and ME/CFS patients have a lipid profile and oxidant biology that is consistent with cardiovascular disease risk because atherosclerosis is mediated in large part by inflammatory and oxidative mechanisms including lipid peroxidation (Yang 2008, Kennedy 2005).
Lipid peroxidation includes decomposition of PUFA to form aldehydes such as 4-HNE, and losses of arachidonic acid may translate to increased lipid mediators of inflammation such as prostaglandins and leukotrienes (Deluca 2010).
Glutathione-s-transferases (GSTs) protect against oxidative damage to vascular endothelium from aldehydes such as 4-HNE, yet MCS patients have glutathione depletion and and a trend to high 4-HNE (Deluca 2010).
Peroxidized lipids such as prostaglandins may strongly contribute to platelet activation or vasoconstriction of the peripheral vasculature (Kennedy 2005, Fontana 2001, Sametz 1999).
Lipid peroxidation may also result in higher levels of oxLDL and lower HDL associated with the development of atherosclerosis (Kennedy 2005, Nordin Fredrickson 2003).
Baldwin 1998 found increased cardiopulmonary disease risk in a community based sample having odor intolerance.
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).
8. Herbal Antiplatelet Activity
Platelets are important for blood coagulation and platelet plugging - repairing thousands of normally occurring tiny vascular ruptures each person every day. In electrohypersensitivity subjects (EHS) where fermented papaya preparation (FPP) restored blood flow to temporal areas of cerebral hypoperfusion - other areas were elevated to over twice normal - antiplatelet blood thinning?
At the time of subject inclusion prior to treatment - using Ultrasonic Cerebral Tomosphygmography (UCTS) - pulsatility index (PI) was measured for 12 brain temporal lobe areas with 6 registering lower than normal PI indicating inflammatory conditions and cerebral hypoperfusion - reduced brain blood flow (BBF). The purpose of the clinical trial was to determine the safety and efficacy of FPP in improving BBF, lowering inflammatory conditions, and alleviating symptoms (Irigaray 2018b, contributing data Irigaray 2018a, and FPP further recommended in Belpomme 2020).
"...we showed that natural products such as fermented papaya preparation (FPP) and ginkgo biloba can restore brain pulsatility in the various middle cerebral artery-dependent tissue areas of temporal lobes.."
"...we have no clear explanation how FPP can restore normal mean PI values and how it can increase mean tissue PI values in comparison with normal values at T3/T6 in the superficial MCA, cortical-subcortical and carotidian areas of the left and right temporal lobes..."
Carotidian (C), Subcortical (SC), Superficial MCA (SMCA) of both the right and left brain temporal lobe areas were raised to abnormally high - nearly 2-4 times normal value:
Rounded data from Irigaray 2018b
BF (before FPP treatment), AF (after 3 or 6 months FPP), Normal (values of historical controls)
Right
C BF 12, AF 23, Normal 13
CS 5, 9, and 2
SMCA 7, 13, and 5
Left
C BF 15, AF 23, Normal 13
CS 5, 9, and 2
SMCA 9, 13, and 5
Could FPP and Ginkgo Biloba have dangerous antiplatelet effects? What is responsible for the FPP induced above normal PI in 6 temporal areas of Irigaray 2018b?
"... herbal supplements that are known to possess antiplatelet activity (ginkgo, garlic, ginger, bilberry, dong quai, feverfew, ginseng, turmeric, meadowsweet and willow)...
those containing coumarin (chamomile, motherworth, horse chestnut, fenugreek and red clover) and with tamarind, enhancing the risk of bleeding...
Ginkgo (Ginkgo biloba L.)...ginkgolides (particularly ginkgolide B) have also been shown to inhibit the binding of platelet activating factor (PAF) to its receptors on platelet membranes, resulting in reduced platelet aggregation...
It is believed that bilberry’s medicinal properties stem primarily from the anthocyanins, which also exert antagonism of platelet aggregation (9, 15, 21)..."
"...Platelets (also called thrombocytes) are minute discs 1 to 4 micrometers in diameter. They are formed in the bone marrow from megakaryocytes, which are extremely large cells of the hematopoietic series in the marrow; the megakaryocytes fragment into the minute platelets either in the bone marrow or soon after entering the blood, especially as they squeeze through capillaries. The normal concentration of platelets in the blood is between 150,000 and 300,000 per microliter...
The platelet-plugging mechanism is extremely important for closing minute ruptures in very small blood vessels that occur many thousands of times daily. Indeed, multiple small holes through the endothelial cells themselves are often closed by platelets actually fusing with the endothelial cells to form additional endothelial cell membrane. A person who has few blood platelets develops each day literally thousands of small hemorrhagic areas under the skin and throughout the internal tissues, but this does not occur in the normal person...
When a sharp-pointed knife is used to pierce the tip of the finger or lobe of the ear, bleeding ordinarily lasts for 1 to 6 minutes. The time depends largely on the depth of the wound and the degree of hyperemia in the finger or ear lobe at the time of the test. Lack of any one of several of the clotting factors can prolong the bleeding time, but it is especially prolonged by lack of platelets..."
I. Baseline GSAA, ACA, SRPE 1-8
II. Diagnosis, Patient Rights, Etiology 9-14
III. Baseline: Nutrition and Exercise 15-31
A. SJF, LE 15-20
B. Whole Food Nutrition 21-31
IV. Baseline: Nutrition and Exercise 32-38
C. Suboptimal Actors 32
D. Maintaining Bone Density 33-37
E. Preventing Atherosclerosis 38
Appendix: Added Splash I-VI; MCS Etiology: 2021 CAR References
MCS 2021: CAR Nutrition References; Index: MCS, Nutrition, Top Article
MCS Consensus Postscript Splash:
I. Ambient Combustion Aerosol (ACA) Composition
II. MCS, ME/CFS - Inflammatory Response to Air Pollution
III. Macronutrients - Starch Preferred Energy
III. Micronutrients - Vegetables Essential
IV. ACA PM Gastro-Inflammation, Vagal Circuitry
MCS Consensus I Postscript Splash: Ambient Combustion Aerosol (ACA) Composition
The following are subsets - the ACA includes thousands of chemicals and metals - much adsorbed to particulate matter carbonaceous cores - 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.
C1-32 organic compounds from gasoline powered motor vehicles
6 branched alkenes including isobutene; 1 alkyne: ethyene
10 saturated cycloalkanes including methylcyclopentane
1 unsaturated cycloalkene; 2 tricyclic terpanes; 3 hopanes
48 aromatic hydrocarbons including benzene, toluene, ethylbenzene, m- and p-xylene, p-ethyltoluene, m-ethyltoluene, 1,2,4-trimethylbenzene, naphthalene, 2-methylnaphthalene, 1-methylnaphthalene
2 ethers including MTBE, ETBE
12 aliphatic aldehydes including formaldehyde, acetaldehyde, propanal
3 olefinic aldehydes including crotonaldehyde, acrolein, methacrolein
2 aliphatic ketones including acetone, butanone
1 aromatic aldehyde: benzaldehyde; 4 aromatic ketones; 3 dicarbonyls
6 n-alkanoic acids; 2 alkanedioic acids; 2 aromatic acids; 3 other compounds
C1-30 organic compounds from medium duty diesel trucks
23 n-alkanes including n-butane, n-pentane, n-heptane
22 branched alkenes including isopentane; 9 n-alkenes including ethene, propene
2 branched alkenes; 1 diolefin: 1,3 butadiene; 1 alkyne: ethyne; 1 unsaturated cycloalkene
19 saturated cycloalkanes including cyclopentane, methylcyclopentane, cyclohexane, methylcyclohexane
38 aromatic hydrocarbons including benzene, toluene, ethylbenzene, m- and p-xylene, n-propylbenzene, p-ethyltoluene, m-ethyltoluene, 1,3,5,-trimethylbenzene,1,2,4,-trimethylbenzene, naphthalene, 2-methylnaphthalene, 1-methylnaphthalene, C2-naphthalenes, C3-naphthalenes, C4-naphthalenes
2 tricyclic terpenes; 1 diasterane; 4 hopanes; 4 steranes
12 aliphatic aldehydes including formaldehyde, acetaldehyde, propanal
3 olefinic aldehydes; 2 aliphatic ketones including acetone, butanone
3 aromatic aldehydes including benzaldehyde, acetophenone, 2,5-dimethylbenzaldehyde
3 docarbonyls; 11 n-alkanoic acids; 2 alkenedioic acids
2 aromatic acids; 4 other compounds; 1 unresolved complex mixture
C1-C29 organic compounds from fireplace combustion of wood
18 n-alkanes including methane, ethane, propane, n-butane, n-heptane
3 branched alkanes; 1 cycloalkane; 1 cycloalkene
9 n-alkenes including ethene, propene; 5 branched alkenes
1 alkyne: ethyne (acetylene); 2 diolefins includng 1,3-butadiene
41 aromatic hydrocarbons including benzene, toluene, naphthalene, phenanthrene
9 phenols and substituted phenols including phenol, o-cresol, m-and p-cresol, dimethylphenols, o-benzenediol
11 guaiacol and substituted guaiacols; 3 syringol and substituted syringols
7 aliphatic aldehydes including formaldehyde, acetaldehyde, propanal, hexanal, heptanal
2 aliphatic ketones including acetone, butanone
3 olefinic aldehydes including acrolein, crotonaldehyde, methacrolein
4 aromatic carbonyls; 4 dicarbonyls; 12 n-alkanoic acids
2 n-alkenoic acids; 9 resin acids; 2 sugars; 4 PAH ketones; 5 other compounds
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