Press Release: Epidemic of Multiple Chemical Sensitivity, A Disease Caused by Toxic Chemical Exposure

[Guest guest]

Epidemic of Multiple

Chemical Sensitivity,

A Disease Caused by

Toxic Chemical Exposure

 

A major paper on multiple chemical sensitivity by Professor

L. Pall was published October 23, 2009 as chapter XX in a prestigious reference

work for professional toxicologists, “General and Applied Toxicology, 3rd

Edition†( Wiley & Sons). 

Multiple chemical sensitivity (MCS) is also known as chemical

sensitivity, chemical intolerance and toxicant-induced loss of tolerance, with

this last name emphasizing the role of chemicals in initiating cases of this

disease.  Pall’s  paper, entitled Multiple Chemical

Sensitivity: Toxicological Questions and Mechanisms, establishes five important

facts about  MCS:

 

1.  MCS is a stunningly

common disease, even more common than diabetes.  This has been shown in a

series of nine

epidemiological studies from the U.S. and one study each from Canada, Germany,

Sweden and Denmark.  In the U.S.,

approximately 3.5% of the population is affected by severe MCS, with much larger

numbers, at least 12% of the population, being moderately affected.  MCS is,

therefore, a very large

international disease epidemic with major implications in terms of public

health.

 

2.  MCS is caused by

toxic chemical exposure.  Cases of

MCS are initiated by exposure to seven classes of chemicals.  These include

three classes of

pesticides and the very large class of organic solvents and related

compounds.  In addition, published

studies implicate mercury, hydrogen sulfide and carbon monoxide as

initiators.  All seven of these

classes of chemicals have been shown in animal studies to produce a common

response in the body, excessive activity of a receptor in the body known as the

NMDA receptor.  Furthermore animal

studies have demonstrated that chemicals belonging to each of these seven

classes can have their toxic responses greatly lowered by using drugs that lower

this NMDA response.  Because

excessive NMDA activity is implicated in MCS from other studies, we now have a

compelling common response that explains how such diverse chemicals can produce

the disease that we call MCS. 

 

3.  The role of

chemicals acting as toxicants in MCS has been confirmed by genetic studies. 

Four such studies have shown that genes

that determine the rate of metabolism of chemicals otherwise implicated in MCS,

influence susceptibility to becoming ill with MCS.  These four studies have

been published

by three research groups in three countries, the U.S., Canada and Germany, have

collectively implicated six genes in determining susceptibility to MCS.  Each

of these six genes has a role in

determining the rate of metabolism of MCS-related chemicals.  The German

studies by Schnakenberg and

colleagues are particularly convincing on this because of the extremely high

level of statistical significance of their studies implicating four of these six

genes. There is only one interpretation for the role of these six genes in

determining susceptiblity to MCS. 

It is that chemicals act as toxicants in initiating cases of MCS and that

metabolizing these chemicals into forms that are either less or more active in

such initiation, influences therefore, the probability that a person will become

ill with MCS.  It is clear,

therefore, that MCS is a toxicological phenomenon, with cases being caused by

the toxic response to chemical exposure.

 

4.  We have, a detailed

and generally well supported mechanism for MCS.   This mechanism explains both

the

high level chemical sensitivity that is the most characteristic symptom of MCS,

as well as many other symptoms and signs of this disease, can be generated.  

This mechanism is centered on a

biochemical vicious cycle, known as the NO/ONOO- cycle, which interacts with

other mechanisms previously implicated in MCS, notably neural sensitization and

neurogenic inflammation.  These act

locally, in various tissues of the body, to generate local sensitivity in

regions of the brain and in peripheral tissues including lungs, upper

respiratory tract and regions of the skin and the GI tract.  Because of this

local nature, different

MCS patients differ from one another in their sensitivity symptoms, because the

tissues impacted differ from one patient to another.  In addition to the

evidence discussed

above, this general mechanism is supported by various physiological changes

found in MCS and in related illnesses, by studies of MCS animal models, by

objectively measurable responses of MCS patients to low level chemical exposure

and by therapeutic responses reported for MCS and related illnesses. 

 

5.  For over 20 years,

some have falsely argued that MCS is a psychogenic disease, being generated in

their view by some ill defined psychological mechanism.  However this view is

completely

incompatible with all of the evidence discussed earlier in this release. While

such incompatibility is more than sufficient reason to reject these psychogenic

claims, the MCS toxicology paper lists eight additional serious flaws in the

psychogenic arguments.  There is a

long history of false psychogenic claims in medicine, where such diseases as

asthma, autism, Parkinson’s disease, ulcers, multiple sclerosis, lupus,

interstitial cystitis, migraine and ulcerative colitis have been claimed to be

generated by a psychological mechanism. 

The 2005 Nobel prize in physiology and medicine was give to Drs. Robin

Warren and Barry Marshall for showing that ulcers are caused by a bacterial

infection, and are not of psychogenic origin.  It is clear, now, that MCS is

physiological disease initiated by toxic chemical exposure that has been falsely

claimed to be psychogenic.

 

 

L. Pall is Professor Emeritus of Biochemistry and Basic

Medical Science, at Washington State University

 

He is located on Pacific time in the U.S. and can be contacted

at:  503-232-3883 and at martin_pall@ wsu.edu.  His web site is:

thetenthparadigm. org