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.”

Growing evidence shows that exposure to lead in the environment is associated with cardiovascular disease, including increased risk of hypertension. However, those studies have looked at lead concentrations in blood, not bone lead, a better indicator of cumulative lead exposure over time. In a new study, researchers at the Harvard School of Public Health (HSPH) and the University of Michigan School of Public Health found that bone lead was associated with a higher risk of death from all causes, particularly from cardiovascular disease. It is the first study to analyze the association between bone lead and mortality.

The study appears online on September 8, 2009, on the website of the journal Circulation and will appear in a later print edition. 

“The findings with bone lead are dramatic. It is the first time we have had a biomarker of cumulative exposure to lead and the strong findings suggest that, even in an era when current exposures are low, past exposures to lead represent an important predictor of cardiovascular death, with important public health implications worldwide,” said Marc Weisskopf, assistant professor of environmental and occupational epidemiology at HSPH and lead author of the study.

Air pollution was the main source of lead in the environment in recent years, though it has been decreasing since leaded gasoline was banned in the U.S. in the mid-1990s. Most of the lead circulating in the body is deposited in bone and remains there for years, unlike blood lead, which has a half life of about 30 days. Since adverse effects from lead on the cardiovascular system would be expected to show up over time, the researchers expected that bone lead would be a better marker of chronic toxicity.

The researchers, led by Weisskopf and senior author Howard Hu, professor of environmental health, epidemiology and internal medicine at the University of Michigan School of Public Health, analyzed data from 868 participants in the Department of Veterans Affairs Normative Aging Study, a study of aging in men that began in 1963. Blood lead and bone lead—analyzed using X-ray fluorescence—were measured for each of the participants. The results showed that the risk of death from cardiovascular disease was almost six times higher in men with the highest levels of bone lead compared to men with the lowest levels. The risk of death from all causes was 2.5 times higher in men with the highest levels of lead compared to those with the lowest levels. The results appeared independent of age, smoking, education, race, alcohol, physical activity, BMI, high density lipoprotein or total cholesterol levels, hypertension or diabetes.

There are a number of mechanisms, such as increased oxidative stress, by which lead exposure may result in cardiovascular mortality, say the authors. They also note that, in addition to high blood pressure, exposure to lead has been associated with widened pulse-pressure (an indicator of arterial stiffening) and heart disease.

Given that bone lead may be a better biomarker of cumulative lead exposure than blood lead, it may be the best predictor of chronic disease from exposure to lead in the environment. “In addition to spurring further public health measures to reduce exposure to lead and to begin monitoring for cumulative exposure, mechanistic and clinical research is needed to determine if opportunities exist to conduct targeted screening and treatment that can further reduce the burden of cardiovascular disease for the millions of adults who have had years of elevated lead exposure in the past,” said Hu.

Reference:    Harvard School of Public Health, Lead in bone associated with increased risk of death from cardiovascular disease in men, Boston, MA, September 9, 2009

The study described was initiated by the Israel Ministry of Health as an effort to respond to and deal with public concern about possible health disorders related to odorous emissions (composed of a great many of organic and inorganic chemicals) from the regional industrial park (IP) in the Negev, southern Israel. Previous ecological studies found that adverse health effects in the Negev Bedouin population were associated with residential proximity to the IP. The objective of the current study was to investigate a hypothesis concerning the link between the IP proximity and life prevalence (LP) of upper respiratory tract chronic diseases (URTCD) and asthma in children aged 0-14 years living in rural Negev, Israel, in small agricultural communities.  

The cross-sectional study was conducted in 7 localities simultaneously during 2002. The following indirect exposure indicators were used: (1) distance (less than 20 km/ more than 20 km) from the IP (‘distance’); (2) presence (yes/no) of the dominant wind direction being from the IP toward a child’s locality (‘wind direction’); and (3) the child’s mother having made odour complaints (yes/no) related to the IP (‘odour complaints’). A 20 km cut-off point was used for ‘distance’ dichotomization as derived from the maximum range of ‘odour complaints’. This gave 3 proximal and 4 distant localities, and division of these by the ‘wind direction’ gave one versus two localities. The study population consisted of 550 children born in the localities. Medical diagnoses were collected from local clinic records. The following were included in the interviewer-administered questionnaire for a child’s parents: (1) demography (the child’s birth date, gender, mother being married or not, parental origin and education, number of siblings); (2) the child’s birth history (pregnancy and delivery) and breast-feeding duration; (3) the child’s parental respiratory health; and (4) environmental factors (parental smoking and occupational hazardous exposure, domestic use of pesticides, domestic animals, outdoor odour related to the IP emissions). For statistical analysis, Pearson’s chi(2), t-tests and multivariate logistic regressions were used, as well as adjusted odds ratios (OR) within a 95% confidence interval.  

The multivariate analysis showed that increased LP of URTCD in children of proximal localities was statistically significant when associated with odour complaints (OR = 3.76 [1.16, 12.23]). In proximal localities, LP of URTCD was higher (at borderline level statistical insignificance p = 0.06) than in distant localities (OR = 2.31 [0.96, 5.55]). The following factors were found to be related to the excess of the LP of URTCD: (1) father’s lower education (by distance: OR = 2.62 [1.23, 5.57]; by wind direction: OR = 4.07 [1.65, 10.03]); (2) in-vitro fertilization (by distance: OR = 3.03 [1.17, 7.87]; by wind direction: OR = 4.34 [1.48, 12.72]). In proximal localities, the increase in asthma LP was associated with: (1) wind direction (OR = 1.95 [1.01, 3.76]); (2) a child’s male gender (OR = 2.95 [1.48, 5.87]); and (3) a child’s mother’s having had an acute infectious disease during pregnancy (OR = 4.84 [1.33, 17.63]).  

An increased LP of chronic respiratory morbidity among children living in small agricultural localities in the Negev was found to be associated with indirect measurements of exposure (distance, wind direction and odour complaints) to IP emissions. These results, in conjunction with previously reported findings in the Negev Bedouin population, indicate a need for environmental protection measures, and monitoring of air pollution and the health of the rural population. 

Reference: Karakis I, Kordysh E, Lahav T, Bolotin A, Glazer Y, Vardi H, Belmaker I, Sarov B., Life prevalence of upper respiratory tract diseases and asthma among children residing in rural area near a regional industrial park: cross-sectional study, School of Public Health, University of Haifa, Haifa, Israel. Rural Remote Health. 2009 Jul-Sep;9(3):1092 

The same mechanism that helps you detect bad-tasting and potentially poisonous foods may also play a role in protecting your airway from harmful substances, according to a study by scientists at the University of Iowa Roy J. and Lucille A. Carver College of Medicine. The findings could help explain why injured lungs are susceptible to further damage.  

The study, published online July 23 in Science Express, shows that receptors for bitter compounds that are found in taste buds on the tongue also are found in hair-like protrusions on airway cells. In addition, the scientists showed that, unlike taste cells on the tongue, these airway cells do not need help from the nervous system to translate detection of bitter taste into an action that expels the harmful substance. 

The hair-like protrusions, called motile cilia, were already known to beat in a wave-like motion to sweep away mucus, bacteria and other foreign particles from the lungs. 

The study is the first to show that motile cilia on airway cells not only have this “clearing” function, but also use the receptors to play a sensory role. The researchers also found that when the receptors detect bitter compounds, the cilia beat faster, suggesting that the sensing and the motion capabilities of these cellular structures are linked. 

“On the tongue, bitter substances trigger taste cells to stimulate neurons, which then evoke a response — the perception of a bitter taste. In contrast, the airway cells appear to use a different mechanism that does not require nerves,” said Alok Shah, a UI graduate student and co-first author of the study. “In the airways, bitter substances both activate the receptors and elicit a response — the increased beating of the cilia — designed to eliminate the offending material.”

Shah and co-first author Yehuda Ben-Shahar, Ph.D., an assistant professor of biology at Washington University who was a postdoctoral fellow at the UI when the study was conducted, worked in the lab of senior study author Michael Welsh, M.D. (photo, upper left), UI professor of internal medicine and molecular physiology and biophysics, who holds the Roy J. Carver Chair of Internal Medicine and Physiology and Biophysics. Welsh also is a Howard Hughes Medical Institute investigator. 

“These findings suggest that we have evolved sophisticated mechanisms to guard ourselves from harmful environmental stimuli,” Ben-Shahar said. “Our work also suggests that losing cilia in the lungs, due to smoking or disease, would result in a reduced general ability to detect harmful inhaled chemicals, increasing the likelihood of further damaging an injured lung.”

In addition to Ben-Shahar, Shah and Welsh, the UI team included Thomas Moninger, assistant director of the UI Central Microscopy Research Facility, and Joel Kline, M.D., UI professor of internal medicine. 

The study was funded by grants from the National Institutes of Health. 

Reference:   University of Iowa, Airway cells use ‘tasting’ mechanism to detect and clear harmful substances, July 24, 2009