MCS A-1 Etiology: Dantoft 2014
MCS A-1 Etiology: References
MCS 2 The Etiology of MCS
MCS 3 Definition and Concensus Criteria
MCS 3a Criteria Amendment Research Points (CAR)
MCS 3b CAR References
MCS 3c CAR Documentation
MCS 3d Etiology: CAR Case Example
MCS 3e Etiology: CAR Moral Responsibility
MCS 3f Criteria Amendment Q and A
a) Preface
I) Introduction
II) How You Can Help
III) Impossibly Good
a) Preface
Not just knowing - but apply - at each stage of learning to give up something - even if a way of life we have always known.
Care deeply.
I) Introduction
Population increase 1 billion in the next 15 years - taught it is okay to engage in a lifestyle of combustion fueled activity - releasing an ambient combustion aerosol (ACA) threatening all life on earth - a mass extinction of ocean species is expected (Rogers 2011) with coral reefs already dissolving, climate is changing, and the ACA is causing, promoting, or supporting many diseases including Multiple Chemical Sensitivity (Gillespie 2013, Deering-Rice 2011, Latremoliere 2009, Bessac 2008, Calderon-Garciduenas 2008, 2000, Veronesi 2005, 2001, Block 2004, Meggs 1997).
There is conclusive evidence for an amendment to the 1999 Concensus Criteria for MCS - the large increase in research understanding of the last 15 years supports a more thorough and precise definition and etiology as reflected in the announcement - MCS 3a Criteria Amendment Research Points - article to be titled: Multiple Chemical Sensitivity: Amendment to the 1999 Concensus Criteria.
II) How you can help
Those professionally qualified are asked to support as co-author concensus for the journal article announcing the amendment which consists of adding to Pt 4 the words: "although exposure to the ambient combustion aerosol supporting the underlying disease process is continuous."
All of us can help by inviting doctors and researchers to participate.
Here is how east to send information and invitations:
a) Simply e-mail or letter the links below to the doctor or researcher on your list.
b) or mail forums in addition to the links.
III) Impossibly Good
A slower paced, reduced consumption, non combustion lifestyle is needed or human beings will go extinct due to loss of environment and resources.
Impossibly Good City Design
Better Morality
Population Stabilization
Low Speed, Injury Proof, Zero Emission Vehicles
Walk to School, Work, and Shopping
Thermostats 50 Degrees or Less
Engage Only Unwasteful Products and Activities
References
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Block M.L. et al. The outdoor air pollution and brain health workshop. Neurotox 33:972-84 2012
Block M.L.and Calderon-Garciduenas L. Air pollution: mechanisms of neuroinflammation & CNS disease. Trends Neuro 32(9): 506-16 2009
Block M.L. et al. Nanometer size diesel exhaust particles are selectively toxic to dopaminergic neurons; the role of microglia, phagocytosis, and NADPH oxidase. FASEB 10.1096/fj.041945fje 2004
Calderon-Garciduenas L. et al. Urban air pollution: influence on olfactory function and pathology in exposed children and young adults. Exp Tox Pathol 62:91-102 2010
Calderon-Garciduenas L. et al. Long-term air pollution exposure is associated with neuroinflammation, an altered innate immune response, disruption of the blood brain barrier, ultrafine particulate deposition, and accumulation of amyloid beta-42 and alpha-synuclein in children and young Calderon-Garciduenas L. et al. Brain inflammation and Alzheimer's-like pathology in individuals exposed to severe air pollution. Tox Pathol 32: 650-58 2004
Calderon-Garciduenas L., Maronpot R.R. et al. DNA damage in nasal and brain tissues of canines exposed to air pollutants is associated with evidence of chronic brain inflammation and neurodegeneration. Tox Pathol 31: 524-38 2003
Calderon-Garciduenas L., Mora-Tiscareno A. et al. Respiratory damage in children exposed to urban pollution. Pediatr Pulmonal 36: 148-61 2003
Calderon-Garciduenas L. et al. Air pollution and brain damage. Tox Pathol Calderon-Garciduenas L. et al. Respiratory tract pathology and cytokine imbalance in clinically healthy children chronically and sequentially exposed to air pollutants. Med Hyp 55(5): 373-378 2000
Deering-Rice C. et al. Electrophilic components of diesel exhaust particles (DEP) activate transient receptor potential ankyrin-1 (TRPA1): a probable mechanism of acute pulmonary toxicity for DEP. Chem Res Tox 24;6:950-9 2011
Gillespie P. et al. Particulate matter neurotoxicity in culture is size dependant. Neurotox 36: 112-17 2013
Latremoliere A. & Woolf C. Central sensitization: a generator of pain hypersensitivity by central neural plasticity. J Pain 10;9:895-926 2009
Meggs W.J. Arch Env H 54(5) 309-11 1999
Meggs W.J. Hypothesis for induction and propagation of chemical sensitivity based on biopsy studies. Env H Perspect 105(2): 473-78 1997
Meggs W.J. et al. Nasal pathology and ultrastructure in patients with chronic airway inflammation (RADS and RUDS) following an irritant exposure. J Tox Clin Tox 34;4: 383 1996
Meggs W.J. Neurogenic Inflammation and sensitivity to environmental chemicals. EHP 101;3:234-38 1993
Meggs W.J. and Cleveland Jr. C.H. Rhinolaryngoscopic examination of patients with multiple chemical sensitivity syndrome. Arch Env H 48: 1-14 1993a
Rogers A.D. and LaffoleyD.d'A. International earth system expert workshop on ocean stresses and impacts. Oxford 18pp 2011. International Programme on the State of the Ocean.org
Veronesi B. et al. Effects of subchronic exposure to concentrated ambient particles VII Degeneration of dopaminergic neurons in APO E-1 mice. Inhal Tox 17; 4-5: 235-41 2005
Veronesi B. et al. Electrostatic charge activates inflammatory vanilloid (VR1) receptors. Neurotox 24: 463-73 2003
Veronesi B. et al. The surface charge of visible particulate matter predicts biological activation in human bronchial epithelial cells. Tox and Appl Pharm 178: 144-54 2002a
Veronesi B. et al. Particulate matter inflammation and receptor sensitivity are target cell specific. Inhal Tox 14(2): 159-83 2002b
Veronesi B. and Oortgiesen M. Neurogenic inflammation and particulate matter (PM) air pollutants. Neurotox 22: 795-810 2001
Veronesi B. et al. Vanilloid capsaicin receptors influence inflammatory sensitivity in response to particulate matter. Tox Appl Pharm 15;169(1): 66-76 2000
