Breakthrough study on Multiple Chemical Sensitivity shows MCS is an epidemic caused by toxic chemicals; peer-reviewed paper is published in prestigious toxicology reference work.

A major paper on multiple chemical sensitivity by Professor Martin L. Pall is to be published October 23, 2009 as chapter XX in a prestigious reference work for professional toxicologists, “General and Applied Toxicology, 3rd Edition” (John 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 susceptibility 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.

—

Martin 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 Website is: www.thetenthparadigm.org

Related Articles:

• Environmental Medicine: Dr. Martin Pall about Chemical Sensitivity
• Martin Pall about genetic evidence and Multiple Chemical Sensitivity
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• Multiple Chemical Sensitivity at General and Applied Toxicology 3rd Edition

Eva Caballé “Eva’s No Fun Blogspot“ from Spain reports:

Few days ago I discovered that my blog had some visitors from this Japanese website, a blog done by Prof. Masumi Yamamuro of Tokyo University. When I read this post, I discovered that it was my article “The Naked Truth about MCS” in Japanese and they mentioned that it had been translated by Citizens Against Chemicals Pollution (CACP) and I decided to write them. Takeshi Yasuma, from Citizens Against Chemicals Pollution (CACP), explained me that he found my article at The Canary Report and he immediately translated it into Japanese with the subtitle “Cry of Spanish MCS Patient’s Heart”, because he was very impressed by it. He published the Japanese version of my article in Citizens Against Chemicals Pollution website last August and also in the September issue of their monthly newsletter.

I also asked him about MCS situation in Japan, and now, with his permission, I post the part of his email where he explained it and I also reprint CACP’s mission.

Takeshi Yasuma wrote:

There is good news.

On October 1, 2009, the Medical Information System Development Center (MEDIS-DC), a subsidiary organization of Ministry of Health, Labor and Welfare (MHLW) published the revised list of ICD-10 Japanese Standard Disease Code Master in which MCS is categorized in T65.9: Toxic effect of other and unspecified substances / Toxic effect of unspecified substance.

It has been now clearly recognized in Japan that MCS is NOT a mental disease but a physical disease.

This decision is welcomed by MCS patients and their supporters and they expect the possible coverage of MCS by health insurance, but so far it remains uncertain whether or how it will change.

Patients and their supporters will take actions for calling on Japanese government to give urgent supports for MCS patients including coverage of MCS by health insurance, strengthening medical services, financial support for livelihood and provision of safer houses.

On October 31 at Tokyo, we will hold a MCS symposium celebrating the recognition and calling on Japanese government to take further measures for MCS.

CACP’s Mission:

To provide information to the public and take action necessary for protecting human health and environment from harmful chemicals based on Precautionary Principle and Environmental Justice.

Main Activities:

• To issue monthly newsletter [PICO].
• To issue weekly mail service.
• To provide information at our website.
• To publish books and booklets related to environmental health.
• To propose our policies to the Japanese Government and local governments.
• To hold seminars for citizens on protecting human health and environment.

I want to thank to Takeshi Yasuma for translating my article, for letting me publish all this information about MCS in Japan and also for asking me to write a message to MCS patients and their supporters to be presented at the MCS symposium. It will be an honour to me!

Author: Eva Caballé, Eva’s No Fun Blogspot

Thank you very much Eva! Big Hug, Silvia

NOTES:

• Original post in Spanish and English by Eva Caballé at No Fun Blogspot
• Post translated into German by Silvia K. Müller and published at CSN Blog
• Post translated into Japanese by Takeshi Yasuma and published at Citizens Against Chemicals Pollution website (October 7, 2009).
• Post linked at The Canary Report (October 8, 2009).

New study shows that Arctic has potential to alter Earth’s climate 

In a new study in the journal Ecological Monographs, ecologists estimate that Arctic lands and oceans are responsible for up to 25 percent of the global net sink of atmospheric carbon dioxide. Under current predictions of global warming, this Arctic sink could be diminished or reversed, potentially accelerating predicted rates of climate change. 

In their review paper, David McGuire of the U.S. Geological Survey and the University of Alaska at Fairbanks and his colleagues show that the Arctic has been a carbon sink since the end of the last Ice Age, which over time has accounted for between zero and 25 percent, or up to about 800 million metric tons, of the global carbon sink. On average, says McGuire, the Arctic accounts for 10-15 percent of the Earth’s carbon sink. But the rapid rate of climate change in the Arctic – about twice that of lower latitudes – could eliminate the sink and possibly make the Arctic a source of carbon dioxide. 

Carbon generally enters the oceans and land masses of the Arctic from the atmosphere and largely accumulates in permafrost, the frozen layer of soil underneath the land’s surface. Unlike active soils, permafrost does not decompose its carbon; thus, the carbon becomes trapped in the frozen soil. Cold conditions at the surface have also slowed the rate of organic matter decomposition, McGuire says, allowing Arctic carbon accumulation to exceed its release. 

But recent warming trends could change this balance. Warmer temperatures can accelerate the rate of surface decomposition, releasing more carbon into the atmosphere. More concerning, says McGuire, is that the permafrost has begun to thaw, exposing previously frozen soil to decomposition and erosion. These changes could reverse the historical role of the Arctic as a sink for carbon. 

“In the short term, warming temperatures could expose more Arctic carbon to decomposition,” says McGuire. “And with permafrost melting, there will be more available carbon to decompose.” 

On the scale of a few decades, the thawing permafrost could also result in a more waterlogged Arctic, says McGuire, a situation that could encourage the activity of methane-producing organisms. Currently, the Arctic is a substantial source of methane to the atmosphere: as much as 50 million metric tons of methane is released per year, in comparison to the 400 million metric tons of carbon dioxide the Arctic sequesters yearly. But methane is a very potent greenhouse gas – about 23 times more effective at trapping heat than carbon dioxide on a 100-year time scale. If the release of Arctic methane accelerates, global warming could increase at much faster rates. 

“We don’t understand methane very well, and its releases to the atmosphere are more episodic than the exchanges of carbon dioxide with the atmosphere,” says McGuire. “It’s important to pay attention to methane dynamics because of methane’s substantial potential to accelerate global warming.” 

But uncertainties still abound about the response of the Arctic system to climate change. For example, the authors write, global warming may produce longer growing seasons that promote plant photosynthesis, which removes carbon dioxide from the atmosphere; however, increasingly dry conditions may might counteract and overcome this effect. Similarly, dry conditions can lead to increased fire prevalence, releasing even more carbon. 

McGuire contends that only specific regional studies can determine which areas are likely to experience changes in response to climate change. 

“If the response of the arctic carbon cycle to climate change results in substantial net releases of greenhouse gases, this could compromise mitigation efforts that we have in mind for controlling the carbon cycle,” he says. 

Reference: Ecological Society of America, Arctic land and seas account for up to 25 percent of world’s carbon sink, October 14, 2009

Picture: A. David McGuire

Surprisingly little is known about the effects of big-city air pollution on olfactory function and even less about its effects on the intranasal trigeminal system, which elicits sensations like burning, stinging, pungent, or fresh and contributes to the overall chemosensory experience. 

Using the Sniffin’ Sticks olfactory test battery and an established test for intranasal trigeminal perception, we compared the olfactory performance and trigeminal sensitivity of residents of Mexico City, a region with high air pollution, with the performance of a control population from the Mexican state of Tlaxcala, a geographically comparable but less polluted region. 

We compared the ability of 30 young adults from each location to detect a rose-like odor (2-phenyl ethanol), to discriminate between different odorants, and to identify several other common odorants. The control subjects from Tlaxcala detected 2-phenyl ethanol at significantly lower concentrations than the Mexico City subjects, they could discriminate between odorants significantly better, and they performed significantly better in the test of trigeminal sensitivity. 

We conclude that Mexico City air pollution impairs olfactory function and intranasal trigeminal sensitivity, even in otherwise healthy young adults. 

Reference:    Guarneros M, Hummel T, Martínez-Gómez M, Hudson R., Mexico City Air Pollution Adversely Affects Olfactory Function and Intranasal Trigeminal Sensitivity, Chem Senses. 2009 Oct 9.

According to new research from the Monell Center and the Mount Sinai School of Medicine, certain common herbicides and lipid-lowering fibrate drugs act in humans to block T1R3, a nutrient-sensing taste receptor also present in intestine and pancreas.

Commonly used in agriculture and medicine, these chemical compounds were not previously known to act on the T1R3 receptor.

The T1R3 receptor is a critical component of both the sweet taste receptor and the umami (amino acid) taste receptor. First identified on the tongue, emerging evidence indicates that T1R3 and related taste receptors also are located on hormone-producing cells in the intestine and pancreas.

These internal taste receptors detect nutrients in the gut and trigger the release of hormones involved in the regulation of glucose homeostasis and energy metabolism.

“Compounds that either activate or block T1R3 receptors could have significant metabolic effects, potentially influencing diseases such as obesity, type II diabetes and metabolic syndrome,” noted Monell geneticist and study leader Bedrich Mosinger, M.D., Ph.D.

In the study, published online in the Journal of Medicinal Chemistry, researchers tested the ability of two classes of chemical compounds to block the T1R3 receptor. The compounds “fibrates and phenoxy-herbicides“ were selected based on their strong structural similarity to lactisole, a sweet taste inhibitor that exerts its taste effects by blocking T1R3.

Fibrates are a class of drugs frequently used to treat lipid disorders such as high blood cholesterol and triglycerides. Phenoxy-herbicides are used in agriculture to control broad-leaf weeds; the best known, 2,4-D, is one of the most extensively used herbicides worldwide.

Using an in vitro preparation, the researchers found that both classes of compounds potently blocked activation of the human sweet taste receptor, acting at micromolar concentrations to inhibit binding of sugars to the T1R3 component of the receptor.

Additional testing revealed that the inhibitory effect of both fibrates and phenoxy-herbicides on the T1R3 receptor is specific to humans. That is, the ability of these compounds to block the receptor did not generalize across species to the rodent form of the receptor.

Mosinger commented on the implications of the findings and noted the importance of testing chemicals intended for human use on human tissues. “The metabolic consequences of short- and long-term exposures of humans to phenoxy-herbicides are unknown. This is because most safety tests were done using animals, which have T1R3 receptors that are insensitive to these compounds,” he said.

The ability of fibrate drugs to interact with T1R3 receptors also was previously unknown. The study findings suggest that these receptors might be an important pharmacological target of first-generation fibrates, such as clofibrate, which were believed to act on a different receptor to affect lipid metabolism. Newer fibrate drugs are more specific for the second receptor and interact less with the T1R3 receptor.

Mosinger points out that little is known about how T1R3 blockade affects hormone levels and metabolism. “Given the number of compounds used in agriculture, medicine and the food industry that may affect human T1R3 and related receptors, more work is needed to identify the health-related effects of exposure to these compounds,” he said.

Reference:   Monell Chemical Senses Center, Common herbicides and fibrates block nutrient-sensing receptor found in gut and pancreas, Philadelphia, October 09, 2009