The aim of  the following study was to ascertain whether MCS patients present brain single photon emission computed tomography (SPECT) and psychometric scale changes after a chemical challenge.

This procedure was performed with chemical products at non-toxic concentrations in 8 patients diagnosed with MCS and in their healthy controls. In comparison to controls, cases presented basal brain SPECT hypoperfusion in small cortical areas of the right parietal and both temporal and fronto-orbital lobes.

After chemical challenge, cases showed hypoperfusion in the olfactory, right and left hippocampus, right parahippocampus, right amygdala, right thalamus, right and left Rolandic and right temporal cortex regions(p</=0.01). By contrast, controls showed hyperperfusion in the cingulus, right parahippocampus, left thalamus and some cortex regions (p</=0.01). The clustered deactivation pattern in cases was stronger than in controls (p=0.012) and the clustered activation pattern in controls was higher than in cases (p=0.012).

In comparison to controls, cases presented poorer quality of life and neurocognitive function at baseline, and neurocognitive worsening after chemical exposure. Chemical exposure caused neurocognitive impairment, and SPECT brain dysfunction particularly in odor-processing areas, thereby suggesting a neurogenic origin of MCS.

Reference:  Orriols R, Costa R, Cuberas G, Jacas C, Castell J, Sunyer J., Brain dysfunction in multiple chemical sensitivity, Servei de Pneumologia, Hospital Universitari Vall d’ Hebron, Barcelona, Catalonia, Spain; CIBER Enfermedades Respiratorias (CIBERES), Spain, J Neurol Sci. 2009 Oct 2.

Toxic Sofas, toxic Furniture – Searching for a cause  

Sitting in new chairs or sofas has elicited dermatitis in numerous patients in Finland and in the U.K. since autumn 2006. The cause of the dermatitis seemed to be an allergen in the furniture materials.

The aim of the following study was to determine the cause of the dermatitis in patients with furniture-related dermatitis. 

Altogether 42 patients with furniture-related dermatitis were studied. First, 14 Finnish patients were patch tested with the standardized series and with the chair textile material. A thin-layer chromatogram (TLC) strip and an extract made from the same textile material were tested in seven Finnish patients. The test positive spot of the TLC and the content of a sachet found inside a sofa in the U.K. were analysed by using gas chromatography-mass spectrometry. All chemicals analysed were patch tested in 37 patients. 

A positive patch test reaction to the chair textile and to its extract was seen in all patients tested, one-third of whom had concurrent reactions to acrylates. Positive reactions to the same spot of the TLC strip were seen in five of seven patients and dimethyl fumarate was analysed from the spot as well as from the sachet contents. Dimethyl fumarate (0.01%) elicited positive reactions in all the patients. The other chemicals analysed did not elicit positive reactions, but one patient in the U.K. had a positive reaction to tributyl phosphate. 

Sensitization to dimethyl fumarate was seen in all the patients with furniture-related dermatitis. Concurrent sensitization or cross-reactions were common among the sensitized patients. 

Reference:   Lammintausta K, Zimerson E, Hasan T, Susitaival P, Winhoven S, Gruvberger B, Beck M, Williams JD, Bruze M.,  An epidemic of furniture-related dermatitis: searching for a cause., Department of Dermatology, Turku University Hospital, PO Box 52, 20521 Turku, Finland, Br J Dermatol. 2009 Jul 20.

Chemicals and Molds often associated with Sick Building Syndrome   

A study was performed to explore possible environmental risk factors, including indoor chemicals, mold, and dust mite allergens, which could cause sick building syndrome (SBS)-type symptoms in new houses. 

The study was conducted in 2004 and 2005 and the final study population consisted of 86 men and 84 women residing in Okayama, Japan. 

The indoor concentrations of indoor aldehydes, volatile organic compounds, airborne fungi, and dust mite allergens in their living rooms were measured and the longitudinal changes in two consecutive years were calculated. 

A standardized questionnaire was used concomitantly to gather information on frequency of SBS-type symptoms and lifestyle habits. About 10% of the subjects suffered from SBS in the both years. 

Crude analyses indicated tendencies for aldehyde levels to increase frequently and markedly in the newly diseased and ongoing SBS groups. Among the chemical factors and molds examined, increases in benzene and in Aspergillus contributed to the occurrence of SBS in the logistic regression model. 

Indoor chemicals were the main contributors to subjective symptoms associated with SBS. A preventive strategy designed to lower exposure to indoor chemicals may be able to counter the occurrence of SBS. 

Reference:  Takigawa T, Wang BL, Sakano N, Wang DH, Ogino K, Kishi R.,    A longitudinal study of environmental risk factors for subjective symptoms associated with sick building syndrome in new dwellings, Sci Total Environ. 2009 Sep 15;407(19):5223-8.

Studies show chemicals act as toxicants in causing cases of Multiple Chemical Sensitivity; genes that metabolize these chemicals into other forms influence, therefore, susceptibility to getting MCS.

Guest post at Canary Report by Martin L. Pall, Professor Emeritus of Biochemistry and Basic Medical Sciences, Washington State University and Research Director, the Tenth Paradigm Research Group.

Martin Pall: I have emailed the following as an open letter to the Denver Post in response to the article on multiple chemical sensitivity (MCS) that was published this weekend. I think the published article was generally a step forward in terms of public understanding of MCS. But the article left out a number of important things and this letter is an attempt to deal with some of those. I have asked them to consider publishing this as an Op-Ed piece, but wanted to make it available regardless of whether or not they opt to do so.

Thank you for writing this article on multiple chemical sensitivity (MCS), the term that is used in most of the scientific literature on this disease. There are vast numbers of people who have been afflicted in this epidemic of chemical sensitivity and I am sure that they are all thanking you. I also thank you for mentioning a bit of my work on this disease.

Some of your readers have already made quite a number of important points about MCS so I can focus here on just a few remaining issues. How do chemicals act in MCS? We know now that the seven classes of chemicals implicated in MCS all produce a common toxic response in the body, excessive activity of a receptor in the body called the NMDA receptor. So even though we have a vast array of such chemicals, we know how they can produce similar responses in people.

There is compelling genetic evidence that these chemicals act as toxic agents (toxicants) in the body. Four such studies have been published by three research groups in three countries. Collectively they implicate six genes as influencing susceptibility to MCS, such that people carrying some forms of each of these genes are more susceptible to becoming chemically sensitive than are people carrying other forms of the same genes. All of these genes control the activity of enzymes that metabolize these chemicals into other forms. Most of these studies show a high level of what is called statistical significance. In the Schnakenberg and colleagues studies, the chances of getting their results by chance are less than one in a million billion. So obviously, these are not chance results. What these studies show is that chemicals are acting as toxicants in causing cases of MCS and that genes that metabolize these chemicals into other forms influence, therefore, susceptibility to getting MCS. These studies, then, provide compelling evidence that cases of MCS are caused by toxic chemical exposure. Clearly they also show that MCS is a real disease, otherwise one would not be able to do such studies clearly linking the chance of becoming ill with MCS to the action of chemicals acting as toxicants.

Dr. Herman Staudenmayer has, for some 20 years claimed just the opposite. He claims that MCS is psychogenic, caused by psychological responses and according to him, is not a toxicological phenomenon. He has maintained this claim by ignoring contrary data wherever it occurs. He has ignored all of the evidence that chemicals implicated in MCS produce a common response in the body; he has ignored the roughly two dozen studies showing that MCS patients show objectively measurable responses to low level chemical exposures, responses that differ from those of normals. He has ignored all of the evidence implicating excessive NMDA activity in MCS; he has ignored the dozens of animal model studies on MCS; he has ignored over 50 studies that show that cases of MCS typically occur following chemical exposures; he has ignored the various other measurable physiological changes reported to occur in MCS. This has all been documented in my book “Explaining – Unexplained Illnesses” and in my article on the toxicology of MCS that is coming out next month in a prestigious reference work for professional toxicologists “General and Applied Toxicology, 3rd Edition”. It is also documented on the MCS web page of my web site: The Tenth Paradigm

Clearly you cannot do science by simply ignoring the existence of vast arrays of contrary data. However, Staudenmayer provides us with a couple of other tests of his views in his book, predictions that allow us to test his theory. He predicts that psychological factors are necessary and sufficient to account for the properties of MCS. This, of course, is contradicted by all of the evidence I referred to earlier. Therefore we should reject his hypothesis based on his own prediction. He provides a second prediction as well (the exact quotes from his book on these predictions are provided on my MCS web page). He predicts that the variation of susceptibility to MCS is not caused by variable responses to toxic chemicals. Clearly the genetic studies discussed above have shown that this is false and therefore, his hypothesis should be rejected for that reason, as well.

It is clear, from the above, that Staudenmayer’s construct was basically a house of cards. Now that it has collapsed, where does that leave us?

Firstly it leaves us with reversing the errors of the past. We need to start treating MCS sufferers as victims of unsafe chemical exposure. Many of them have previously been used, abused and discarded. If we live in a society where people are not disposable items we need to “do unto others as you would have others do unto you.”

We obviously need to start regulating chemical usage much more carefully, to avoid initiating new cases of MCS. It is imperative to develop tests for chemical activity in MCS, just as we have developed tests for chemical activity as carcinogens. Then we need to use these tests to effectively regulate the use of toxic chemicals.

We need to develop specific biomarker tests for MCS, tests that can be used to objectively confirm diagnoses initially based on subjective symptoms. I think we already have several very promising approaches to doing this in the scientific literature and a minimal amount of further study may be all that is needed to develop such tests.

We need to confirm that chemical avoidance is key to therapy and to develop other therapeutic approaches to work along with avoidance. The environmental medicine physicians and others have already made very important progress in this direction and I am optimistic that further progress can be made quickly. Such progress is relevant not only to the treatment of MCS patients but also to the treatment of clearly related diseases including chronic fatigue syndrome/mylagic encephalomyelitis and fibromyalgia. All of these diseases are caused by what I have called the NO/ONOO- cycle and the way to treat them, in my judgment, is to lower the activity of that vicious cycle mechanism.

Martin L. Pall

Professor Emeritus of Biochemistry and Basic Medical Sciences, Washington State University and Research Director, the Tenth Paradigm Research Group

Reprinted with permission from the author. Dr. Pall cautions the reader that he is a PhD, not an MD, and none of this should be viewed as medical advice.

• Original Article posted by Canary Report Thank you for the permission to reprint Susie!
• Link to Martin Pall’s website: The Tenth Paradigm
• Link to an extended excerpt from Palls book Explaining “Unexplained Illnesses.”

A recent paper on sauna therapy by Dr. Martin L. Pall argues for a novel mechanism for its mode of action (1). Pall argues that sauna therapy acts primarily by increasing the availability of a compound called tetrahydrobiopterin (BH4) in the body. BH4 is reported or thought to be depleted in a number of medical conditions that are also reported to respond positively to sauna therapy, including multiple chemical sensitivity, fibromyalgia, chronic fatigue syndrome, hypertension, vascular endothelial dysfunction and heart failure. This pattern of action can be explained, therefore, if sauna therapy increases the availability in the body of BH4.

Pall argues for two distinct mechanisms by which sauna therapy is expected to increase availability of BH4. Both of these act by increasing the synthesis of an enzyme, known as GTP cyclohydolase I, the rate limiting enzyme in the biosynthesis of BH4.

Sauna therapy is known to produce large increases in blood flow in the outer heated parts of the body and the consequent increase in vascular shear stress has been shown to induce large increases in GTP cyclohydrolase I activity and consequent increases in BH4.

A second such mechanism is mediated through the action of the heat shock protein, Hsp90, a protein known to be induced by modest tissue heating and a protein that is recruited into a complex of proteins containing GTP cyclohydrolase I. The Hsp90 protein lowers the proteolytic degradation of GTP cyclohydrolase I protein, leading to increased BH4 synthesis and this has been shown to lower, in turn, the partial uncoupling of the eNOS nitric oxide synthase. Increases in BH4 synthesis in response to both of these two mechanisms may be expected to feed BH4 to various tissues in the body including those not directly impacted by sauna therapy.

The health benefits of vigorous exercise may also be mediated, in part, via these same mechanisms.

A number of additional diseases are reported to involved BH4 depletion including Alzheimer’s, Parkinson’s, asthma, schizophrenia, bipolar disorder, pulmonary hypertension and type 2 diabetes so that each of these may respond to sauna therapy, as well.

It has been commonly assumed that the response of MCS cases to sauna therapy is mediated by a detoxification process known as depuration. There is some published evidence that some increase in detoxification does occur in response to sauna therapy. However the main influence of sauna therapy on MCS cases and certainly in these other medical conditions may well be through increased BH4 availability.

Reference: 1. Pall ML. 2009 Do sauna therapy and exercise act by raising the availability of tetrahydrobiopterin? Med Hypotheses. 2009 Jul 4.