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.

Neurobehavioral and pulmonary impairment in 105 adults with indoor exposure to molds compared to 100 exposed to chemicals 

Patients exposed at home to molds and mycotoxins and those exposed to chemicals (CE) have many similar symptoms of eye, nose, and throat irritation and poor memory, concentration, and other neurobehavioral dysfunctions. Aim of a study was to compare the neurobehavioral and pulmonary impairments associated with indoor exposures to mold and to chemicals. 

105 consecutive adults exposed to molds (ME) indoors at home and 100 patients exposed to other chemicals were compared to 202 community referents without mold or chemical exposure. To assess brain functions, the scientists measured 26 neurobehavioral functions. Medical and exposure histories, mood states score, and symptoms frequencies were obtained. Vital capacity and flows were measured by spirometry. Groups were compared by analysis of variance (ANOVA) after adjusting for age, educational attainment, and sex, by calculating predicted values (observed/predicted x 100 = % predicted). And p < .05 indicated statistical significance for total abnormalities, and test scores that were outside the confidence limits of the mean of the percentage predicted. 

People exposed to mold had a total of 6.1 abnormalities and those exposed to chemicals had 7.1 compared to 1.2 abnormalities in referents. Compared to referents, the exposed groups had balance decreased, longer reaction times, and blink reflex latentcies lengthened. Also, colour discrimination errors were increased and visual field performances and grip strengths were reduced. The cognitive and memory performance measures were abnormal in both exposed groups. Culture Fair scores, digit symbol substitution, immediate and delayed verbal recall, picture completion, and information were reduced. Times for peg-placement and trail making A and B were increased. 

One difference was that chemically exposed patients had excess fingertip number writing errors, but the mold-exposed did not. Mood State scores and symptom frequencies were greater in both exposed groups than in referents. Vital capacities were reduced in both groups. Neurobehavioral and pulmonary impairments associated with exposures to indoor molds and mycotoxins were not different from those with various chemical exposures. 

Reference: Kilburn KH, Neurobehavioral and pulmonary impairment in 105 adults with indoor exposure to molds compared to 100 exposed to chemicals, University of Southern California, Keck School of Medicine (ret.), Pasadena, CA, USA., Toxicol Ind Health. 2009 Sep 30.

To examine the effects of solvent exposure on hearing function, through an audiological test battery, in a population not occupationally exposed to high levels of noise. 

One hundred ten workers from a coating factory were studied. Jobs at the factory were divided into three different levels of solvent exposure. Hearing status was assessed with a test battery including pure-tone hearing thresholds (0.5-8 kHz), high-frequency hearing thresholds (12 and 16 kHz), and dichotic listening measured through dichotic digits test. Multiple linear regression models were created to explore possible association between solvent exposure and each of the hearing outcomes. 

Significant associations between solvent exposure and the three hearing outcomes were found. Covariates such as age, gender, race, and ethnicity were also significantly associated with the studied hearing outcomes. 

Occupational exposure to solvents may induce both peripheral and central auditory dysfunction. The dichotic digits test seems as a sensible tool to detect central auditory dysfunction associated with solvent exposure. Hearing loss prevention programs may use this tool to monitor hearing in solvent-exposed workers. 

Reference:   Fuente A, Slade MD, Taylor T, Morata TC, Keith RW, Sparer J, Rabinowitz PM., Peripheral and Central Auditory Dysfunction Induced by Occupational Exposure to Organic Solvents, J Occup Environ Med. 2009 Sep 25 

From the Escuela de Fonoaudiologia [School of Speech and Hearing Sciences] (Dr Fuente), Medical Faculty, Universidad de Chile, Santiago, Chile; Occupational and Environmental Medicine Program (Mr Slade, Dr Taylor, Ms Sparer, and Dr Rabinowitz), Yale University School of Medicine, New Haven, Conn; Division of Applied Research and Technology (Dr Morata), National Institute for Occupational Safety and Health; and Division of Audiology (Dr Keith), University of Cincinnati, Cincinnati, Ohio.

Plumes of harmful air pollutants can be transported across oceans and continents — from Asia to the United States and from the United States to Europe — and have a negative impact on air quality far from their original sources, says a new report by the National Research Council.  Although degraded air quality is nearly always dominated by local emissions, the influence of non-domestic pollution sources may grow as emissions from developing countries increase and become relatively more important as a result of tightening environmental protection standards in industrialized countries.  

“Air pollution does not recognize national borders; the atmosphere connects distant regions of our planet,” said Charles Kolb, chair of the committee that wrote the report and president and chief executive officer of Aerodyne Research Inc.  “Emissions within any one country can affect human and ecosystem health in countries far downwind.  While it is difficult to quantify these influences, in some cases the impacts are significant from regulatory and public health perspectives.” 

The report examines four types of air pollutants: ozone; particulate matter such as dust, sulfates, or soot; mercury; and persistent organic pollutants such as DDT.  The committee found evidence, including satellite observations, that these four types of pollutants can be transported aloft across the Northern Hemisphere, delivering significant concentrations to downwind continents.  Ultimately, most pollutants’ impacts depend on how they filter down to the surface.  

Current limitations in modeling and observational capabilities make it difficult to determine how global sources of pollution affect air quality and ecosystems in downwind locations and distinguish the domestic and foreign components of observed pollutants.  Yet, some pollutant plumes observed in the U.S. can be attributed unambiguously to sources in Asia based on meteorological and chemical analyses, the committee said.  For example, one study found that a polluted airmass detected at Mt. Bachelor Observatory in central Oregon took approximately eight days to travel from East Asia.  

The health impacts of long-range transport vary by pollutant.  For ozone and particulate matter — which cause respiratory problems and other health effects — the main concern is direct inhalation.  While the amount of ozone and particulate matter transported on international scales is generally quite small compared with domestic sources, neither of these pollutants has a known “threshold,” or concentration below which exposure poses no risk for health impacts.  Therefore, even small incremental increases in atmospheric concentrations can have negative impacts, the committee said.  For instance, modeling studies have estimated that about 500 premature cardiopulmonary deaths could be avoided annually in North America by reducing ozone precursor emissions by 20 percent in the other major industrial regions of the Northern Hemisphere. 

For mercury and persistent organic pollutants, the main health concern is that their transport and deposition leads to gradual accumulation on land and in watersheds, creating an increase in human exposure via the food chain.  For example, people may consume mercury by eating fish.  There is also concern about eventual re-release of “legacy” emissions that have been stored in soils, forests, snowpacks, and other environmental reservoirs. 

In addition, the committee said that projected climate change will lead to a warmer climate and shifts in atmospheric circulation, likely affecting the patterns of emission, transport, transformation, and deposition for all types of pollution.  However, predicting the net impacts of the potential changes is extremely difficult with present knowledge. 

In the coming decades, man-made emissions are expected to rise in East Asia, the report says.  These increases could potentially be mitigated by increasingly stringent pollution control efforts and international cooperation in developing and deploying pollution control technology. 

To enhance understanding of long-range transport of pollution and its impacts, the committee recommended a variety of research initiatives, such as advancing “fingerprinting” techniques to better identify source-specific pollutant characteristics, and examining how emissions from ships and aircraft affect atmospheric composition and complicate the detection of pollution from land-based sources.  The committee emphasized developing an integrated “pollution source-attribution” system that improves capabilities in emissions measurements and estimates; atmospheric chemical and meteorological modeling; long-term, ground-based observations; satellite remote sensing; and process-focused field studies.  

Moreover, the committee stressed that the United States, as both a source and receptor of long-range pollution, has an interest in remaining actively engaged in air pollutants that travel abroad, including support of more extensive international cooperation in research, assessment, and emissions control efforts. 

The report was sponsored by the U.S. Environmental Protection Agency, National Oceanic and Atmospheric Administration, NASA, and National Science Foundation.  The National Academy of Sciences, National Academy of Engineering, Institute of Medicine, and National Research Council make up the National Academies.  They are independent, nonprofit institutions that provide science, technology, and health policy advice under an 1863 congressional charter.  Committee members, who serve pro bono as volunteers, are chosen by the Academies for each study based on their expertise and experience and must satisfy the Academies’ conflict-of-interest standards.  The resulting consensus reports undergo external peer review before completion.  For more information, visit National Academies  A committee roster follows. 

Reference: National Academy of Sciences, Air Pollutants From Abroad a Growing Concern, Says New Report, Washington, September 29. 2009

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.”