SPC 1 Introduction: South Pole CAR (SPC) - A Character Test

[michael edward badolato jr]

SPC 1 Introduction: South Pole CAR (SPC) - A Character Test

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 Consensus Criteria

MCS 3a Criteria Amendment Research Points (CAR)

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

MCS 3b CAR References

SPC 1 Introduction: South Pole CAR (SPC) - A Character Test

Please choose the Incorrect Statement

SPC 1a) South Pole CAR may be an Antarctic character test - evidence proving ambient combustion aerosol (ACA) role in disease is overwhelming. The question is willingness to acknowledge and correct moral and environmental indiscretion.

 

SPC 1b) In the vast majority of cases airway damage - often subclinical - changes in the innate inflammatory immune system (Hogg 2009, Abbas 2007) - including tight junction defects, exposed sensory nerves, and leukocytic infiltrates - is prerequisite to systemic inflammatory events (Hiraiwa 2013, Hogg 2009, Calderon-Garciduenas 2008, 2003, 2001, Veronesi 2001, Meggs 1997).

SPC 1c) Once the airway is damaged - resulting systemic inflammatory events - including cardiopulmonary and CNS - are largely predictable - physiological fact of expected consequences (Block 2012, Deluca 2010, Hogg 2009, Calderon-Garciduenas 2008, Veronesi 2001, Meggs 1997).
The airway damage - changes in the innate inflammatory immune system - a combination of excessive exposure to toxics and genetic factors - is followed by expression of systemic oxidative stress - further influenced by genetics, individual lifestyle, and environment (Block 2012, Calderon-Garciduenas 2008).

SPC 1d) A healthy airway is defensive and protective - presenting a physical barrier and detox enzyme activity (Hiraiwa 2013, Hogg 2009, Calderon-Garciduenas 2008, 2003, 2001, Baulig 2009, 2003a, Veronesi 2001, Bonvallot 2001, 2000, Gerde 2001, 1997 Meggs 1997).

Exposed sensory nerves and alveolar macrophages in a damaged airway release excessive inflammatory mediators with resulting increase of circulating leukocytes and acute phase proteins (Hiraiwa 2014, 2013, Hogg 2009, Goto 2004, Mukae 2001, Veronesi 2001, Meggs 1997)

suppressed plasma detox activity (Deluca 2010, Liptrott 2009, Oslund 2008, Chun 2002, Sterner-Kock 1999, Tinel 1999, Tanabe 1996, Tapner 1996, Nadin 1995, Stadler 1994, Khatsenko 1993)

a fatty acid profile of lipid peroxidation (Deluca 2010, Terlecky 2006) -

and proatherogenic condition of systemic oxidative stress.

SPC 1e)

The principle receptor on exposed sensory nerves concerning MCS - critical to the release of inflammatory mediators and central sensitization  is TRPA1. (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).

SPC 1f) Unsafe environment is the major culprit including the ambient combustion aerosol (ACA) - which though not always the primary cause of disease initiating airway breakdown - will support existing disease process by acting upon exposed sensory nerve receptors, immune and epithelial cells in damaged airway epithelium increasing inflammatory mediator release (Hiraiwa 2014, 2013, Hogg 2009, Calderon-Garciduenas 2008, 2003, 2001 Goto 2004, Mukae 2001, Veronesi 2001, Meggs 1997)

providing input for central sensitization (Latremoliere 2009) and direct penetration of ACA UFPM (ultra fine particulate matter less than .1 micron) and PM 2.5 via neural and other systemic pathways (Block 2012, Calderon-Garciduenas 2010, 2008, Genter 2009, Matsui 2009, Elder 2006, Lewis 2005) - disease condition is one of permanent gaps in the epithelium - lacking physical barrier and detox enzyme activity ahead of potential nerve contact and deeper penetration (Block 2012, Calderon-Garciduenas 2010, 2008, Baulig 2009, 2003a, Genter 2009, Matsui 2009, Elder 2006, Lewis 2005, Bonvallot 2001, 2000, Gerde 2001, 1997).

SPC 1g) The ACA is an every breath exposure to chemicals and metals adsorbed on particles (PM) having lengthy residence time in tissue with a continual 2 phase release - initial rapid and extended gradual desorption - reflecting the bonding energies of vapor components condensed on carbonaceous particle cores upon emission from the source (Gerde 2001, 1991, Burtscher 1986, Adamson 1982, Natusch 1978).

SPC 1h) UFPM have an exponentially greater surface to mass ratio - capacity to deliver large amounts of adsorbed chemicals and metals - along with the prolonged residence time of embedded particles (Araujo 2009, Phalen 2009, Schmid 2009, Kreyling 2006, 2004, Donaldson 2003, 1996, Gerde 2001).

SPC 1i) These are characteristics that set the ACA including the UFPM component apart: continuous cumulative exposure, toxic chemical and metal load adsorbed on particles, prolonged residence time in tissue, and a deceiving rum dumb because of relentless saturation by ACA components. Every breath is chemicals and metals condensed and concentrated on vector driven UFPM (Baulig 2009, 2003a, Bonvallot 2001, 2000, Gerde 2001, Boland 2000, 1999, Baeza-Squiban 1999, Bayram 1998, Kumagai 1997, Thomas 1997).

SPC 1j) Changing the carpet or shampoo doesn't get it done - and there is no pill, potion, or protocal adequate for smoking cigarettes, marijuana, exhaust, or woodsmoke 24/7/365 - horizontal cone dispersal - tailpipe and chimney everywhere - 95% of the problem - especially for those who have cleaned up their personal environment.

SPC 1k) Its grim the dishonesty to sell combustion fuel vehicles and protect an industry - breathing exhaust since birth and conditioned to never walk always drive - an irrational intransigence - taking pride in this achievement - resistant to any correction of a disastrous lifestyle. UFPM (ultra fine particulate matter) are the most penetrating and destructive (Gillespie 2013, Pedata 2010, Araujo 2009, Phalen 2009, Schmid 2009, Valavanidis 2008, Calderon-Garciduenas 2008, deHaar 2006, Kreyling 2006, 2004, Donaldson 2003, Oberdorster 1996) - least removed by the catalytic converter which decreases larger particles and claims great weight reduction - misleading because the exhaust is lethal due to continued UFPM and gas phase emissions.

SPC 1L) It is best to overlook ACA PM in pollution caused disease (PCD) including cardiopulmonary, neurodegenerative, gastrointestinal, cancer, MCS, ME/CFS, and other forms of EI proven by thousands of credible research articles - because high speed combustion fuel vehicles are preferred - definition of reality obtained from vehicle manufacturer, oil company, or woodstove certification - diesel, gasoline, and woodburning are safe - a guiding light to acceptable behavior.

We are glad to maintain the deception of modern woodstove design - reducing weight of emission and smoky odor - instead releasing a relatively non descript brew of low oxygen chamber toxics including potent gas phase hydroxyl radicals ( Lee 2001) and deeply penetrating UFPM and PM 2.5 - so successful an illusion that many MCS and asthma people don't recognize the woodsmoke signature and attribute worsening of symptoms as due to the cold air.

Everyone has done an excellent job in communicating the danger of ACA PM, PCD, and global environmental implications. Support of drug development and futile emission control strategies has brought success in perpetuating high speed, combustion fuel vehicles including allowing diesel engines in pickup trucks and SUVs under a false pretense of improved emissions (Gillespie 2013, Pedata 2010, Araujo 2009, Phalen 2009, Schmid 2009, Valavanidis 2008, Calderon-Garciduenas 2008, deHaar 2006, Kreyling 2006, 2004, Donaldson 2003, 1996, Oberdorster 1996) diesel exhaust in every corner - from church on Sunday to the remotest places - guaranteeing career opportunities in a continued epidemic of PCD - expanded research and pharmaceutical therapies.
There is no need for lifestyle change - healthful walking to school, work, and shopping - electric and fuel cell for necessary transportation - addressing the plight of millions in traffic jams - unwalkable design - a nightmare of ACA emissions - global environmental destruction - and a boggling population growth rate: 4.4 billion 1960/2015 - 3 to 7.4 billion in just 55 years  (Worldometers 2015, World Almanac 2012: World and US Population - International Database, International Program Center, Population Division, US Census Bureau, US Department of Commerce; World Factbook, Central Intelligence Agency).