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

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.

The Federal Institute for Occupational Safety and Occupational Medicine has published an alphabetical and systematic Thesaurus “Safety and Health at Work”. The Thesaurus has been created in a long-standing cooperation between documentalists, librarians and scientists from the Federal Institute of Occupational Safety and Occupational Medicine.    

The disease MCS – Multiple Chemical Sensitivity (ICD-10 T78.4) is mentioned at the Thesaurus “Safety and Health at Work”, alphabetical Part, Status May 2009, as: 

Multiple Chemical Sensitivity (B02.19.00)     

At the systematic Part MCS – Multiple Chemical Sensitivity is found at the category B02:  

“Work related Disease and Occupational Disease/Disease”  

integrated in Part:  

• B02.19 Other Disease 
• B02.19.00 Multiple Chemical Sensitivity  

Chronic Fatigue Syndrome (CFS) is integrated analogue.  

MCS is not classified as a mental disease

To clear up occurring doubts, it is to point out that MCS – Multiple Chemical Sensitivity is not integrated into chapter B02.15: Mental diseases, Depression, Neurosis, Post traumatic Stress Disorder or psychosomatic diseases. 

Thesaurus “Safety and Health at Work”

The Thesaurus offers a quick overview on the broad group of themes “Safety and Health at Work”. It contains about 3 500 main keywords and is the joining of the keywords from the two previous Thesauri “Safety at Work” and “Occupational Medicine”. The Thesaurus is based on the practical work of the Library group, documentation at the content development and their research of technical literature. It is a tool for documentation.   

The Thesaurus is intended for all who search for literature about “Safety and Health at Work”. It is supportive for prearrangement of research inquiries at the data pool LITDOK and can be helpful for searching in topic related databases.  

Author: Silvia K. Müller, CSN – Chemical Sensitivity Network, July 23, 2009  

Reference:  Thesaurus „Sicherheit und Gesundheit bei der Arbeit“ Alphabetischer Teil, Systemischer Teil, Dortmund/Berlin/Dresden 2009. 

Use of medications among people with chronic fatigue syndrome and healthy persons: a population-based study of fatiguing illness in Georgia 

Chronic fatigue syndrome (CFS) is a debilitating condition of unknown etiology and no definitive pharmacotherapy. Patients are usually prescribed symptomatic treatment or self-medicate. We evaluated prescription and non-prescription drug use among persons with CFS in Georgia and compared it to that in non-fatigued Well controls and also to chronically Unwell individuals not fully meeting criteria for CFS.  

A population-based, case-control study. To identify persons with possible CFS-like illness and controls, we conducted a random-digit dialing telephone screening of 19,807 Georgia residents, followed by a detailed telephone interview of 5,630 to identify subjects with CFS-like illness, other chronically Unwell, and Well subjects. All those with CFS-like illness (n=469), a random sample of chronically Unwell subjects (n=505), and Well individuals (n=641) who were age-, sex-, race-, and geographically matched to those with CFS-like illness were invited for a clinical evaluation and 783 participated (48 % overall response rate).  

Clinical evaluation identified 113 persons with CFS, 264 Unwell subjects with insufficient symptoms for CFS (named ISF), and 124 Well controls; the remaining 280 subjects had exclusionary medical or psychiatric conditions, and 2 subjects could not be classified. Subjects were asked to bring all medications taken in the past 2 weeks to the clinic where a research nurse viewed and recorded the name and the dose of each medication.  

More than 90% of persons with CFS used at least one drug or supplement within the preceding two weeks. Among users, people with CFS used an average of 5.8 drugs or supplements, compared to 4.1 by ISF and 3.7 by Well controls. Persons with CFS were significantly more likely to use antidepressants, sedatives, muscle relaxants, and anti-acids than either Well controls or the ISF group. In addition, persons with CFS were significantly more likely to use pain-relievers, anti-histamines and cold/sinus medications than were Well controls.  

Researchers and medical care providers of patients with chronic fatigue syndrome should be aware of polypharmacy as a problem in such patients, and the related potential iatrogenic effects and drug interactions. 

Reference:  Boneva RS, Lin JM, Maloney EM, Jones JF, Reeves WC, Use of medications among people with chronic fatigue syndrome and healthy persons: a population-based study of fatiguing illness in Georgia, Health Qual Life Outcomes. 2009 Jul 20;7(1):67.

Researchers for the first time have linked air pollution exposure before birth with lower IQ scores in childhood, bolstering evidence that smog may harm the developing brain. 

The results are in a study of 249 children of New York City women who wore backpack air monitors for 48 hours during the last few months of pregnancy. They lived in mostly low-income neighborhoods in northern Manhattan and the South Bronx. They had varying levels of exposure to typical kinds of urban air pollution, mostly from car, bus and truck exhaust. 

At age 5, before starting school, the children were given IQ tests. Those exposed to the most pollution before birth scored on average four to five points lower than children with less exposure. 

That’s a big enough difference that it could affect children’s performance in school, said Frederica Perera, the study’s lead author and director of the Columbia Center for Children’s Environmental Health.      

Dr. Michael Msall, a University of Chicago pediatrician not involved in the research, said the study doesn’t mean that children living in congested cities “aren’t going to learn to read and write and spell.” 

But it does suggest that you don’t have to live right next door to a belching factory to face pollution health risks, and that there may be more dangers from typical urban air pollution than previously thought, he said. 

“We are learning more and more about low-dose exposure and how things we take for granted may not be a free ride,” he said.

While future research is needed to confirm the new results, the findings suggest exposure to air pollution before birth could have the same harmful effects on the developing brain as exposure to lead, said Patrick Breysse, an environmental health specialist at Johns Hopkins’ school of public health. 

And along with other environmental harms and disadvantages low-income children are exposed to, it could help explain why they often do worse academically than children from wealthier families, Breysse said.  

“It’s a profound observation,” he said. “This paper is going to open a lot of eyes.”

The study in the August edition of Pediatrics was released Monday. 

In earlier research, involving some of the same children and others, Perera linked prenatal exposure to air pollution with genetic abnormalities at birth that could increase risks for cancer; smaller newborn head size and reduced birth weight. Her research team also has linked it with developmental delays at age 3 and with children’s asthma. 

The researchers studied pollutants that can cross the placenta and are known scientifically as polycyclic aromatic hydrocarbons. Main sources include vehicle exhaust and factory emissions. Tobacco smoke is another source, but mothers in the study were nonsmokers. 

A total of 140 study children, 56 percent, were in the high exposure group. That means their mothers likely lived close to heavily congested streets, bus depots and other typical sources of city air pollution; the researchers are still examining data to confirm that, Perera said. The mothers were black or Dominican-American; the results likely apply to other groups, researchers said. 

The researchers took into account other factors that could influence IQ, including secondhand smoke exposure, the home learning environment and air pollution exposure after birth, and still found a strong influence from prenatal exposure, Perera said. 

Dr. Robert Geller, an Emory University pediatrician and toxicologist, said the study can’t completely rule out that pollution exposure during early childhood might have contributed. He also noted fewer mothers in the high exposure group had graduated from high school. While that might also have contributed to the high-dose children’s lower IQ scores, the study still provides compelling evidence implicating prenatal pollution exposure that should prompt additional studies, Geller said. 

The researchers said they plan to continuing monitoring and testing the children to learn whether school performance is affected and if there are any additional long-term effects. 

Reference:    Columbia Center for Children’s Environmental Health, Kids’ lower IQ scores linked to prenatal pollution, July 20, 2009