A List of Case-specific Forms of Chemical Sensitivity and a Proposed Mechanism for MCS

Provided is an outline of
the 2002 proposed mecha-
nism for MCS. A pivotal
feature was added to the
diagram, in 2004. It, too,
is discussed herein. The
outline follows a listing of
the case-specific forms of
chemical sensitivity. Nine
web links are also included
in this post.
Identified & Defined Forms of Chemical Sensitivity
The forms of chemical sensitivity listed below are those
which have already been identified and defined by main-
stream medical science. The list automatically illustrates
that nontoxic\ambient levels of chemicals are not univers-
ally harmless. The list, therefore, illustrates the need for
a plurality of people to avoid pertinent chemical exposures.
The Merit in Making the List Known
The list serves to counter that which anti-MCS literature
serves to provoke. Needless to say, anti-MCS literature
serves to:
1] provoke the powers-that-be into depriving chemically
sensitive persons of reasonable accomodation;
2] provoke the powers-that-be into depriving severely
impaired chemically sensitive persons of disability com-
pensation;
3] persuade marketers into declining to provide consumer
product lines free of those chemical-bearing agents which
are known to trigger adverse reactions such as asthma.
When you illustrate that there are forms of chemical sensi-
tiity that have already been found to exist, you illustrate the
need of an entire class of people to avoid ambient levels
of the chemical-bearing agents known to harm them. You
don't have to wait for the universal recognition of MCS,
in order make this illustration. The recognition of irritant-
induced asthma alone, along with its subset condition,
Reactive Airways Dysfunction Syndrome, was all that
was needed to accomplish this.
Even if MCS comes to be declared a non-reality, there
will still exist the ethical requirement to consider the needs
of those who suffer from the case-specific forms of chem-
ical sensitivity. Matters involving formaldehyde-releasing
agents, the organophosphate\carbamate class of pesticide,
perfume ingredients, additives, & reasonable accomoda-
tion will still have to be addressed. Here is the list, con-
structed in two parts:
Generalized\Systemic and Localized Forms
Irritant-induced Asthma
Irritant Rhinitis\Rhinosinusitis
Halothane-induced Hepatitis
Photoallergic Contact Dermatitis
Benzene-induced Aplastic Anemia
Airborne Irritant Contact Dermatitis
Formaldehyde-induced Anaphylaxis
(chlorhexidine-induced & other forms)
Reactive Airways Dysfunction Syndrome
Irritant-associated Vocal Cord Dysfunction
(symptoms include shortness of breath)
Acute Generalized Exanthematous Pustulosi
Chemical Worker's Lung
(a type of Hypersensitivity Pneumonitis)
Occup. Asthma due to low-weight molecular agents
Occ. Urticaria (due to low-weight molec. agents),
as well as systemic forms of urticaria
Chemical-specific Forms
Pine Resin/Rosin Allergy Albietic Acid Sensitivity
Peruvian Lily Allergy (Tuliposide A Sensitivity)
Red Cedar Allergy (Plicatic Acid Sensitivity)
Methyltetrahydrophthalic Anhydride Allergy
IgE-mediated Triethanolamine Sensitivity
Phthalic Anhydride Hypersensitivity
(Acetylated) Salicylate Sensitivity
Cyanuric Chloride Sensitivity
Ethylene Diamine Sensitivity
Acetaminophen Sensitivity
Glutaraldehyde Sensitivity
Chlorhexidine Sensitivity
Methacrylate Sensitivity
Sulfite Hypersensitivity
Isocyanate Sensitivity
Chromate Sensitivity
Paraben Sensitivity
... etc., etc., etc.
Note 1: The list of chemical-specific forms is long. None
the less, the subset provided should suffice in
proving a point.
Note 2: Sick Building Syndrome was not listed because
it is not exclusively caused by ambient chemical
exposure. It can also be caused by viral and
mold exposure.
Note 3: Reactive Upper-Airways Dysfunction Syndrome
doesn't appear in the list, being that Irritant Rhinitis
was listed. None the less, RUDS is the subset of
irritant-induced rhinosinusitis or rhinitis that works
on the upper-respiratory tract the same way that
RADS works on the lower respiratory tract.
Note 4: Small Airways Disease was not listed, either. Yet,
it was found to exist in some of the WTC clean-
-up crew members who became ill during
or after the clean-up.
See: CT helps find cause of puzzling cough
in WTC Rescue workers. It is found at:
http://www.medicalnewstoday.com/medicalnews.php?newsid=17093
Note 5: There are a multiplicity of contact sensitivity con-
ditions that were not posted. They were omitted,
in order to avoid the appearance of redundancy.
Note 6: The diagnostic title, Reactive Intestinal Dysfunction
Syndrome (RIDS), has been proposed. See:
Reactive intestinal dysfunction syndrome caused
by chemical exposure - RIDS. It is found at:
http://www.findarticles.com/p/articles/mi_m0907/is_n5_v53/ai_21230719
The Most Recently Proposed Mechanism for MCS
The 21st Century proposed mechanism for MCS identifies
two general categories of chemical sensitivity. They are
Central Chemical Sensitivity and Peripheral Chemical
Sensitivity. The outline goes as follows:
Central Chemical Sensitivity
This type of chemical sensitivity involves the central nervous
system, and it's triggering point is proposed to be found in
chemoreceptor activation (action potential.)
Specific chemoreceptors, upon their activation, elevate
nitric oxide levels in the body. The nitric oxide then reacts
with superoxide, producing peroxynitrite.
While the nitric oxide is engaged in producing peroxynitrite,
it is simultaneously engaged in an additional function. That
function is "retrograde signaling."
Nitric oxide's role in retrograde signaling is proposed to be
that of sending an electrical signal to the presynapse cells,
thereby stimulating the release of two types of neurotrans-
mitters. The neurotransmitters involved are glutamate and
aspartate.
Those types of neurotransmitters then stimulate receptors in
the post synaptic cells, known as N-methyl-d-aspartate
receptors. Abbreviated "NMDA receptors", they react
by producing nitric oxide from their own sites, thereby
maintaining the inordinately high level of nitric oxide al-
ready present. Nitric oxide's ample presence proceeds
to maintain the inordinately high levels of peroxynitrite.
While the NMDA receptors are maintaining an elevated
nitric oxide level, peroxynitrite is engaged in causing the
cells that contain those receptors to be depleted of their
energy pools. That which is being depleted is adenosine
triphosphate (ATP), the carrier of energy in all living or-
ganisms. Peroxynitrite inhibits mitochondrial function, and
therefore, the production of ATP.
When cells containing NMDA receptors become deprived
of their energy pool's replenishment, the NMDA receptors
become hypersensitive to stimulation. And while the cells
containing NMDA receptors are being deprived of energy
replenishment, peroxynitrite is engaged in yet another pro-
cess; that of breaking down the blood brain barrier. This
enables increased chemical access to the brain.
Meanwhile, nitric oxide performs yet another function;
that of inhibiting cytochrome P450 activity. Therefore,
nitric oxide is proposed to inhibit the process by which
chemicals get metabolized and become harmless. The
result is heightened sensitivity to chemical exposure.
The aforementioned scenario was proposed by Dr. Martin
L. Pall, of the School of Molecular Biosciences of Wash-
ington State. And the aforementioned scenario is called
"a vicious cycle mechanism." A paper written by Dr. Pall
which describes this vicious cycle can be accessed by
clicking on the following web address:
http://ehp.niehs.nih.gov/members/2003/5935/5935.html
Vanilloid Receptor TRPV1
Recently added to this proposed mechanism is the first
member of the Vanilloid Receptor family, TRPV1. The
involvement of TRPV1 in MCS is the subject of a paper
written by Dr. Pall and a Dr. Julius Anderson, M.D., Ph.D.,
of West Hartford, Vermont. It is titled, The Vanilloid
Receptor as the Putative Target of Diverse Chemicals in
Multple Chemical Sensitivity. The bibliographical citation
for it is Arch Environ Health. 2004 Jul;59(7):363-75. (I
could not find it posted anywhere on the Internet, except
for the abstract of it at the ncbi website. And that was
only a paragraph or two in length.)
The vanilloid receptor is implicated as a major target for
a number of chemicals which can activate it. Therefore,
vanilloid receptor activation is proposed to be the point
where the vicious cycle begins. The vanilloid receptor
paper also addresses the phenomenon of masking, a
phenomenon duly noted in Central Chemical Sensitivity.
Masking is the phenomenon where a chemical exposure
scenario gets muted at the outset by the overshadowing
effect of a previous and different one. That same chemi-
cal exposure would have resulted in a notable adverse
reaction if it were the first one of that day. That same
chemical exposure will result in an adverse reaction when
it becomes the first one, on some future day. The masking
effect muted the presence of that one chemical exposure
encounter for that particular day.
The authors of the vanilloid receptor paper propose that
masking occurs during a cyclic phase known as dephos-
phorylation. It is a phase triggered by Ca2+ calmodulin
phosphatease calcineurin. The hypothesis is that vanilloid
receptor activity is decreased during that phase; the "de-
sensitization" phase. Conversely, it is during the alternate
phase, the one known as phosphorylation, when vanilloid
receptor activity increases, and hypersensitivity reactions
resume. Therefore, the phosphorylation state determines
the activity or inactivity (desensitization) of the vanilloid
receptors.
In addition to the paper that Martin Pall co-authored, there
is an article on the vanilloid receptor that he individually
authored. Titled, Multiple Chemical Sensitivity: towards
the end of controversy. It was published in in the August-
September 2005 edition of Townsend Letter for Doctors
and Patients. It can be accessed by clicking on the fol-
lowing web address:
http://www.findarticles.com/p/articles/mi_m0ISW/is_265-266/ai_n15688810/pg_3
The article cannot be regarded as a substitute for the recent
paper on TRPV1. But, it does provide enough information
to enable a reader to become familiarized with the recently
added feature of Dr. Pall's proposed mechanism for MCS.
In fact, clicking on the following web addresses can help
familiarize a reader with the basic of elements of the bio-
science involved in Martin Pall's proposed mechanism:
Concerning Chemoreceptors, one can refer to:
http://en.wikipedia.org/wiki/Chemoreceptors
Concerning Action potential, one can refer to:
http://en.wikipedia.org/wiki/Action_potential#Underlying_mechanism
And concerning Synapses, one can refer to:
http://en.wikipedia.org/wiki/Synapse#Signaling_across_chemical_synapses
Now, the proposed mechanism of Dr. Pall is a hypothesis.
It is a hypothesis which involves intricate details and in-
tricate mapping. This means that the objective medical
findings of chemically sensitive patients continue to carry
the sole weight in proving that chemical sensitivity is a
physiological condition and not a psychiatric one. The
objective medical findings include instances of anaphy-
laxis triggered by nontoxic/ambient/therapeutic levels
of chemical-bearing agents. The findings include cases
where two entirely different forms of localized chemical
sensitivity were found co-existing in the same one patient.
Such co-existence hints of the authentic existence of MCS.
Peripheral Chemical Sensitivity
This general type of chemical sensitivity is proposed to in-
volve the peripheral tissues. Reactive Airways Dysfunction
Syndrome is placed in this category, as is Reactive Upper-
airways Dysfunction Syndrome. The contact sensitivity
conditions, such as Airborne Irritant Contact Dermatitis,
are also placed in this category.
This type of chemical sensitivity is proposed to involve
neurogenic inflammation. One can obtain more informa-
tion on this type of chemical sensitivity by clicking on
the following links:
Hypothesis for Induction and Propagation of Chemical
Sensitivity Based on Biopsy Studies.
http://ehp.niehs.nih.gov/members/1997/Suppl-2/meggs-full.html
Neurogenic Inflammation and Sensitivity to Environmental Chemicals.
http://ehp.niehs.nih.gov/members/1993/101-3/meggs-full.html
