http://www.americanchronicle.com/articles/viewArticle.asp?articleID=24334

Governors and Mayor Proclaim May as
Multiple Chemical Sensitivity Awareness and Education Month


Lourdes Salvador

April 16, 2007


Governor Bill Ritter of Colorado, Governor Ted Strickland
of Ohio, Mayor Josephus Eggelletion of Broward County
Florida, Governor Jim Gibbons of Nevada, and Governor
Christine Gregoire of Washington are among the first
governors and mayors to proclaim the month of May 2007
as Multiple Chemical Sensitivity Awareness and Education
Month.

Multiple Chemical Sensitivities (MCS) is also known as
Environmental Illness (EI), Toxic Injury (TI), Toxicant Induced Loss
of Tolerance (TILT), and several other names. Originally
identified in a 1989 multidisciplinary survey of 89 clinicians and
researchers, and modified in 1999, top consensus criteria
(Nethercott et al, 1993) for MCS define the condition as:

1. A chronic condition.

2. Symptoms recur reproducibly.

3. Symptoms recur in response to low levels of chemical
     exposure.

4. Symptoms occur when exposed to multiple unrelated
     chemicals.

5. Symptoms improve or resolve when trigger chemicals are
     removed.

6. Multiple organ systems are affected.


Products that MCS patients react to include ANY quantity of
exposures to pesticides, secondhand smoke, alcohol, fresh
paint, scented products and perfumes, candles, fragrances, food
preservatives, flavor enhancers, aerosols, tap water, cosmetics,
personal care products, new carpets, petroleum products,
formaldehyde, outdoor pollutants, newspaper ink, cleaning
compounds, printing and office products, and other synthetically
derived chemicals. Some also react to natural products that are
highly concentrated such as natural orange cleaners due to high
volatile organic compound and pesticide concentration.
Symptoms can range from minor annoyances to life-threatening
reactions.

Prevalence

The prevalence of MCS, based on self-reported symptoms by
sample populations provides an estimate of 16% of the
population who experience reactions to everyday chemicals
(Gibson, 2005; Meggs et al, 1996). MCS affects more women
than men. All education levels, income levels, and nationalities
are affected equally.

Etiology (Causation)

There is no clear consensus as to what causes the symptoms of
MCS.  One of the first studies on MCS focused on possible long
term potentiation in the hippocampus and neural sensitization as
a central mechanism (Pall, 2003).

Later studies examined the role of the inflammatory process and
found that brain inflammation was correlated with symptoms of
MCS (Pall, 2003). In 1999, Meggs proposed that MCS is
caused by low molecular weight chemicals that bind to
chemoreceptors on sensory nerve C-fibers leading to the
release of inflammatory mediators (Meggs, 1999). Many
observable and empirical, scientific facts can help identify MCS
including SPECT scans and chemical encephalopathy, vitamin
deficiencies, mineral deficiencies, excess amino acid
deficiency, and disturbed lipid and carbohydrate metabolism
(Rea et al, 2006; Ziem, 2001; Callendar et al, 1995; Heuser et
al, 1994).

McKeown-Eyssen et al (2004) studied 203 MCS sufferers and
162 controls and found that blood tests revealed that genetic
differences relating to the body's detoxification processes were
present more often in those with MCS than those without. Data
showed that five genetic polymorphisms have a statistically
significant role in determining MCS prevalence (
McKeown-Eyssen et al 2004).

Each of these genes encode proteins that metabolize chemicals
previously implicated in MCS, notably the organophosphorus
pesticides (PON1 and PON2 genes) and the organic solvents
(CYP2D, NAT1 and NAT2 genes) ( McKeown-Eyssen et al
2004). People with a ''high'' expression of two specific genes
(CYP2D6 and NAT2) were 18 times more likely to have MCS
than those without ( McKeown-Eyssen et al 2004). It was
concluded that "a genetic predisposition for MCS may involve
altered biotransformation of environmental chemicals" (
McKeown-Eyssen et al 2004). Haley found similar, confirmatory
results with the PON1 gene in studies of the Gulf War syndrome
veterans.

A new study by Schnakenberg et al (2007) confirmed the
genetic variation previously found by McKeown-Eyssen and
Haley. A total of 521 unrelated individuals participated in the
study. Genetic variants of four genes were analyzed: NAT2,
GSTM1, GSTT1, and GSTP1.

The researchers concluded that individuals who are NAT2 slow
acetylators and those with homozygously deleted GSTM1 and
GSTT1 genes are significantly more likely to develop chemical
sensitivity (Schnackenberg et al, 2007). According to the study,
the glutathione S-transferases act to inactivate chemicals, so
people without these GSTM1 and GSTT1 genes are less able to
metabolize environmental chemicals because "glutathione
S-transferases play an important role in the detoxification of
chemicals" (Schnackenberg et al, 2007). The deletion of another
gene, the GSTP1 gene, leaves individuals more susceptible to
developing these diseases, as lack of these genes means a
loss of protection from oxidative stress (Schnackenberg, et al,
2007).


The NO/ONOO- cycle is implicated by Pall as being a plausible
etiology for Multiple Chemical Sensitivities (MCS), Fibromyalgia
(FM), Chronic Fatigue Syndrome (CFS), Post-Traumatic Stress
Disorder (PTSD), and Gulf War Syndrome.

Peroxynitrite (ONOO-) is oxidized from nitric oxide. Excess
peroxynitrite depletes energy stores, which is perceived to
cause extreme fatigue (Pall, ND). Of more interest to those who
suffer from MCS is the fact that peroxynitrite breaks down the
blood brain barrier and excess levels allow greater access to the
brain (Pall, ND). This greatly increases the effects of chemicals
on the brain. Essentially a non-MCS person has a barrier that
protects the brain from damage from low-level chemical
exposure, however a person who suffers from MCS has little or
no barrier making the brain subject to increased damage and
reactivity with minute exposures most people do not react to.

The key effect of nitric oxide (NO) is that it inhibits cytochrome
P-450 activity and slows degradation of hydrophobic organic
chemicals (Pall, ND). This means that excess nitric oxide slows
down the body's natural detoxification processes leaving MCS
patients subject to the effects of chemical exposure longer than
non-sufferers. Between a reduced blood-brain barrier and
increased time to naturally detoxify the body MCS patients are
subject to permanent and long-term brain and nervous system
damage which includes toxic encephalopathy.

"The only etiologic mechanism proposed for each of these is a
vicious cycle mechanism involving elevated levels of nitric oxide
and its oxidant product, peroxynitrite. This cycle may be initiated
by a variety of diverse short-term stressors, including viral and
bacterial infections, physical trauma, severe psychological
stress, organic solvent exposure, and exposure to three classes
of pesticides, organophosphorus / carbamate pesticides,
organochlorine pesticides and pyrethroid pesticides).

Each of these short-term stressors are known to be able to
trigger responses that lead to increases in nitric oxide levels.
Indeed, other initiating short-term stressors, including a
protozoan infection, carbon monoxide exposure, thimerosal
exposure and ciguatoxin exposure are also known or thought to
act to increase nitric oxide levels, as well" (Pall, 2006).


Regardless of cause, victims of MCS suffer isolation and require
the support of family, friends, and medical providers. The month
of May is designated to raise awareness of the condition and
foster better understanding of its cause and prevention. With
reasonable accommodations, victims can experience increased
ability to work, attend school, shop, dine, go to church, and
socialize. Accommodations are often simple and involve things
such as opening windows, increasing ventilation, and
substituting safer products that increase the safety of both the
patient and others the general population.


References

Callender, TJ, et al. (1995).  Evaluation of chronic neurological
sequelae after acute pesticide exposure using SPECT brain
scans.  Journal Toxicology & Environmental Health. 41:275-284.


Caress, S., & Steinemann, A. (2003). A Review of a Two-Phase
Population Study of Multiple Chemical Sensitivity. Environmental
Medicine. 111, 1490 - 1497.

Davidoff, L. (1989). Multiple Chemical Sensitivities (MCS). The
Amicus Journal. Winter.

Ferrie, H. (October 2003). Multiple Chemical Sensitivity:
Government and Medical Science Finally Recognize Crippling
Effects of MCS. Vitality, Retrieved May 17, 2006, from
http://www.vitalitymagazine.com/node/112

Gibson, P. (2005). Understanding & Accommodating People
with Multiple Chemical Sensitivity in Everyday Living.
Independent Living Research Utilization.

Haley, RW, Billecke, S, & La Du, BN (1999). Association of low
PON1 type Q (type A) arylesterase activity with neurologic
symptom complexes in Gulf War veterans. Toxicology and
Applied Pharmacology 157(3):227-33.

Heuser, G, et al. (1994).  Neurospect findings in patients
exposed to neurotoxic chemicals.  Toxicology & Industrial
Health. 10:561-571.

McKeown-Eyssen, G, Baines, C, Cole, D, Riley, N, Tyndale, R,
Marshall, L, & Jazmaji, V (2004).  Case-control study of
genotypes in multiple chemical sensitivity: CYP2D6, NAT1,
NAT2, PON1, PON2 and MTHFR].  International Journal of
Epidemiology 33, 1-8.

Meggs WJ, Dunn KA, Bloch RM, Goodman PE, Davidoff AL
(1996). Prevalence and nature of allergy and chemical sensitivity
in the general population. Archives of Environmental Health.
Jul-Aug;51(4):275-82.

Meggs, WJ (1999).  Mechanisms of allergy and chemical
sensitivity.  Toxicology and Industrial Health.  15:3-4, 331-338.

Nethercott J.R., Davidoff L.L., Curbow B., et al. (1993) Multiple
Chemical Sensitivities Syndrome: Toward a Working Case
Definition. Arch Environ Health, 48:19-26

Pall, M. (ND). Multiple Chemical Sensitivity: The End of
Controversy. Washington State University School of Molecular
Biosciences, Retrieved May 18, 2006, from:
http://molecular.biosciences.wsu.edu/faculty/pall/pall_mcs.htm

Pall, M (2006). The NO/ONOO- Cycle as the Cause of
Fibromyalgia and Related Illnesses: Etiology, Explanation and
Effective Therapy. Washington State University School of
Molecular Biosciences.

Pall, M (2003).  Elevated nitric oxide/peroxynitrite theory of
multiple chemical sensitivity:  central role of
N-methyl-D-aspartate receptors in the sensitivity mechanism.
Environmental Health Perspectives.  111:12, 1461-1464.

Pall, M. (2001). Multiple Chemical Sensitivity - The End of
Controversy. Washington State University, School of Molecular
Biosciences, Retrieved May 17, 2006, from
http://molecular.biosciences.wsu.edu/faculty/pall/pall_mcs.htm

Schnackenberg,E. et al (2007). A cross-sectional study of
self-reported chemical-related sensitivity is association with
gene variations of drug-metabolizing enzymes. Environmental
Health.

Ziem, G (2001). Medical Evaluation and Treatment of Patients
with Chemical Injury and Sensitivity. National Institute of
Environmental Health Sciences.


Disclaimer

This is for informational purposes and is not intended to replace
the examination, diagnosis and treatment of a licensed
physician and no such claims are inferred. The author and
publisher will not be responsible for misuse of this information
and recommend consulting with a doctor qualified to diagnose
MCS if it is suspected.


About the Author

Lourdes Salvador is a writer and social advocate based in
Hawaii. She is the president of MCS America and a featured
monthly writer for MCS America News at www.mcs-america.org.
She is a passionate advocate for the homeless, working with the
local governor to open new shelters and provide services to the
homeless based on a presentation of her ideas to the governor.
That passion soon turned to advocacy and activism for victims of
multiple chemical sensitivity. For more information about
Lourdes and her advocacy work, please visit:
www.mcs-america.org, www.thetruthaboutmcs.blogspot.com,
and www.cafepress.com/mcsamerica.



Copyrighted © 2007 Lourdes Salvador