Friday, August 31, 2007

Life, the environment and our ecosystem

J Inorg Biochem. 2007 Jul 16; [Epub ahead of print]Click here to read Links

Life, the environment and our ecosystem.

Inorganic Chemistry Laboratory, University of Oxford, South Parks Road, Oxford OX1 3QR, UK.

This article is dedicated to Ed Stiefel who not only contributed with distinction to the development of biological inorganic chemistry with a special interest in molybdenum and its chemistry but had begun the long task of increasing our awareness of the difficulties mankind faces arising from damage to the environment. Here, I take up this theme in an effort to illustrate the nature of today's problems by putting them in the perspective of the whole of evolution of our ecosystem. The central theme is that evolution of organisms has always had to come to terms with the systematic development of the environment. In the past, environmental changes have been slow so that adaptation through genetic adjustment has had time to follow. In the last two hundred years change has become fast and the adaptive process rests not with genes but with mankind's physical-chemical control.

PMID: 17709144 [PubMed - as supplied by publisher]

Influence of chemosensory pain-expectancy on olfactory event-related potentials

1: Neuroimage. 2007 Aug 7; [Epub ahead of print]Click here to read

Influence of chemosensory pain-expectancy on olfactory event-related potentials.

Department of Clinical and Health Psychology, Utrecht University, P.O. Box 80.140, 3508 TC Utrecht, The Netherlands.

Health symptoms attributed to environmental odor exposure are not well understood. Cognitive factors seem to play a significant role in odor-related illness. In the present study, we investigated whether such influences are predominantly interpretational (i.e. best understood as interpretations of perceived odors), or also perceptual (i.e. affect perceptions of the characteristics of the odor). To investigate the neuronal activation behind such processes olfactory ERPs were recorded. The experiment consisted of two conditions: one where participants expected just several administrations of one odor (labelled as the "non-painful" condition), and one where they also expected, in between the odor administrations, to feel irritation in the nose (labelled as the "painful" condition). Participants received painless H(2)S stimuli during both conditions. To reinforce pain-expectancy, a CO(2) pulse was given occasionally during the "painful" condition. Crucial comparisons were made between reactions to H(2)S, under the two expectancy conditions. Detection sensitivity (reflected by amplitudes and latencies of the early N1 peak) and stimulus salience (reflected by amplitudes and latencies of the late "cognitive" positivity) were examined. Peak amplitudes were unaffected by expectancy condition. However, a significant main effect of expectancy on the N1 latency was found, which suggests that expecting a painful stimulus reduces the time to detect a harmless odor. In conclusion, expectancies seem to alter early aspects of odor perception.

PMID: 17728154 [PubMed - as supplied by publisher]

The biochemical origin of pain: The origin of all pain is inflammation and the inflammatory response. Part 2 of 3 - Inflammatory profile of pain syndromes

Med Hypotheses. 2007 Aug 27; [Epub ahead of print]Click here to read

The biochemical origin of pain: The origin of all pain is inflammation and the inflammatory response. Part 2 of 3 - Inflammatory profile of pain syndromes.

Division of Inflammation and Pain Research, L.A Pain Clinic, 4019 W. Rosecrans Avenue, Los Angeles, CA 90250, United States.

Every pain syndrome has an inflammatory profile consisting of the inflammatory mediators that are present in the pain syndrome. The inflammatory profile may have variations from one person to another and may have variations in the same person at different times. The key to treatment of Pain Syndromes is an understanding of their inflammatory profile. Pain syndromes may be treated medically or surgically. The goal should be inhibition or suppression of production of the inflammatory mediators and inhibition, suppression or modulation of neuronal afferent and efferent (motor) transmission. A successful outcome is one that results in less inflammation and thus less pain. We hereby briefly describe the inflammatory profile for several pain syndromes including arthritis, back pain, neck pain, fibromyalgia, interstitial cystitis, migraine, neuropathic pain, complex regional pain syndrome/reflex sympathetic dystrophy (CRPS/RSD), bursitis, shoulder pain and vulvodynia. These profiles are derived from basic science and clinical research performed in the past by numerous investigators and serve as a Foundation to be built upon by other researchers and will be updated in the future by new technologies such as magnetic resonance spectroscopy. Our unifying theory or law of pain states: the origin of all pain is inflammation and the inflammatory response. The biochemical mediators of inflammation include cytokines, neuropeptides, growth factors and neurotransmitters. Irrespective of the type of pain whether it is acute or chronic pain, peripheral or central pain, nociceptive or neuropathic pain, the underlying origin is inflammation and the inflammatory response. Activation of pain receptors, transmission and modulation of pain signals, neuro plasticity and central sensitization are all one continuum of inflammation and the inflammatory response. Irrespective of the characteristic of the pain, whether it is sharp, dull, aching, burning, stabbing, numbing or tingling, all pain arise from inflammation and the inflammatory response. We are proposing a re-classification and treatment of pain syndromes based upon their inflammatory profile.

PMID: 17728071 [PubMed - as supplied by publisher]

A prospective study of thimerosal-containing Rho(D)-immune globulin administration as a risk factor for autistic disorders

J Matern Fetal Neonatal Med. 2007 May;20(5):385-90.Click here to read Links

A prospective study of thimerosal-containing Rho(D)-immune globulin administration as a risk factor for autistic disorders.

The Institute of Chronic Illnesses, Silver Spring, MD, USA.

BACKGROUND: This study evaluated the relationship between prenatal mercury exposure from thimerosal (49.55% mercury by weight)-containing Rho(D)-immune globulins (TCRs) and autism spectrum disorders (ASDs). METHODS: The Institutional Review Board of the Institute for Chronic Illnesses approved the present study. A total of 53 consecutive non-Jewish Caucasian patients with ASDs (Diagnostic and statistical manual of mental disorders, fourth ed. - DSM IV) born between 1987 and 2001 who presented to the Genetic Centers of America for outpatient genetic/developmental evaluations were prospectively collected from June 1, 2005 through March 31, 2006. Imaging and laboratory testing were conducted on each patient to rule out other causal factors for their ASDs. As race-matched controls, the frequency of Rh negativity was determined from 926 non-Jewish Caucasian pregnant women who had presented for outpatient prenatal genetics care to the Genetic Centers of America between 1980 and 1989. RESULTS: Children with ASDs (28.30%) were significantly more likely (odds ratio 2.35, 95% confidence interval 1.17-4.52, p < 0.01) to have Rh-negative mothers than controls (14.36%). Each ASD patient's mother was determined to have been administered a TCR during her pregnancy. CONCLUSION: The results provide insights into the potential role prenatal mercury exposure may play in some children with ASDs.

PMID: 17674242 [PubMed - indexed for MEDLINE]

Double-blind, multicenter trial comparing acetyl l-carnitine with placebo in the treatment of fibromyalgia patients

Clin Exp Rheumatol. 2007 Mar-Apr;25(2):182-8. Links

Double-blind, multicenter trial comparing acetyl l-carnitine with placebo in the treatment of fibromyalgia patients.

Rheumatology Unit, University of Verona, Italy.

OBJECTIVE: Fibromyalgia (FMS) is a chronic syndrome characterized by widespread pain, troubled sleep, disturbed mood, and fatigue. Several analgesic strategies have been evaluated but the results are moderate and inconsistent. Antidepressant agents are now considered the treatment of choice in most patients. It has been recently suggested that FMS may be associated with metabolic alterations including a deficit of carnitine. In this multicenter randomized clinical trial we evaluated the efficacy of acetyl L-carnitine (LAC) in patients with overt FMS. METHODS: One hundred and two patients meeting the American College of Rheumatology criteria for FMS were randomized into the study. The treatment consisted of 2 capsules/day of 500 mg LAC or placebo plus one intramuscular (i.m.) injection of either 500 mg LAC or placebo for 2 weeks. During the following 8 weeks the patients took 3 capsules daily containing either 500 mg LAC or placebo. The patients were seen during treatment after 2 (visit 3), 6 (visit 4) and 10 weeks (visit 5). The patients were also visited 4 weeks after treatment discontinuation (follow-up visit). Outcome measures included the number of positive tender points, the sum of pain threshold (kg/cm2 or "total myalgic score"), the Short Form 36 (SF36), a 100 mm visual analog scale (VAS) for self-perceived stiffness, fatigue, tiredness on awakening, sleep, work status, depression, and muscular-skeletal pain, and the Hamilton depression scale. RESULTS: The "total myalgic score" and the number of positive tender points declined significantly and equally in both groups until the 6th week of treatment. At the 10th week both parameters remained unchanged in the placebo group but they continued to improve in the LAC group with a statistically significant between-group difference. Most VAS scores significantly improved in both groups. A statistically significant between-group difference was observed for depression and musculo-skeletal pain. Significantly larger improvements in SF36 questionnaire were observed in LAC than in placebo group for most parameters. Treatment was well-tolerated. CONCLUSION: Although this experience deserves further studies, these results indicate that LAC may be of benefit in patients with FMS, providing improvement in pain as well as the general and mental health of these patients.

PMID: 17543140 [PubMed - indexed for MEDLINE]

Serum PCB levels and congener profiles among US construction workers

Serum PCB levels and congener profiles among US construction workers
Robert F Herrick , John D Meeker , Russ Hauser , Larisa Altshul and George A Weymouth

Environmental Health 2007, 6:25     doi:10.1186/1476-069X-6-25

Published   31 August 2007

Abstract (provisional)

The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.


The presence of PCB in caulking (sealant) material found in masonry buildings has been well-documented in several countries. A recent investigation of 24 buildings in the greater Boston area found that 8 buildings had high PCB levels in caulking materials used around window frames and in joints between masonry blocks. Workers removing caulking material have been shown to have elevated serum PCB levels.


This project compared serum PCB levels among male workers who installed and/or removed PCB-containing caulking material from buildings in the greater Boston area with reference serum PCB levels from 358 men from the same area. Serum PCB levels were measured in the same laboratory by liquid-liquid extraction, column chromatography clean-up and dual capillary column GC/microECD analysis.


When the congener profiles were compared between the reference population and the construction workers, the serum levels of the more volatile, lighter PCBs (di-, tri-and tetrachloro, sum of IUPAC# 6-74) were substantially higher among the construction workers. One of the youngest workers had the lowest total serum PCB levels (sum of 57 congeners) of all 6 workers, but the contribution of more volatile (less chlorinated) PCB congeners (#16, 26 ,28 ,33 ,74 ,66, and 60) was markedly higher than in other 5 workers and reference men. Only this worker was working on a job that involved removing PCB caulking at the time of the blood sampling.


While the results of this pilot study are based upon small numbers (6 construction workers who handled PCB caulking), the serum PCB levels among the construction workers exceed the referents. Comparison of the congener profiles suggests that there are substantial differences between the construction workers and the general population samples. These differences, and the similarities of profiles among the construction workers strongly suggest that occupational contact with caulking material can be a major source of PCB exposure for construction workers.

Free Full Text:

Evaluation of a new mobile system for protecting immune-suppressed patients against airborne contamination

Evaluation of a new mobile system for protecting immune-suppressed patients against airborne contamination

Jean-Louis Poirot MDa, Jean-Pierre Gangneux MDb, Alain Fischer MD, PhDc, Mireille Malbernard RNc, Svetlana Challier MDd, Nicolas Laudinet BSce and Vance Bergeron PhDf, Corresponding Author Contact Information, E-mail The Corresponding Author
aHôpital Saint-Antoine, Laboratoire de Parasitologie-Mycologie, Paris, France
bCentre Hospitalier Universitaire de Rennes, Laboratoire de Parasitologie-Mycologie, Rennes, France
cHôpital Necker, Service d'Immuno-Hématologie Pédiatrique, Paris, France
dLaboratoire de Microbiologie, Paris, France
eirInSpace SAS, Montigny-le-Bretonneux, France
fEcole Normale Supérieure de Lyon, Laboratoire de Physique CNRS UMR 5672, Lyon, France

Available online 29 August 2007.


Invasive aspergillosis is one of the most lethal airborne dangers for immune-suppressed subjects. Providing patient protection from such airborne threats requires costly and high-maintenance facilities. We herein evaluate a new self-contained mobile unit as an alternative for creating a patient protective environment.


Airborne contamination levels were monitored for different simulated scenarios and under actual clinical conditions. Functional tests were used to challenge the unit under adverse conditions, and a preliminary clinical study with patients and staff present was performed at 2 different French hospitals.


Functional tests demonstrated that the unit can rapidly decontaminate air in the protected zone created by the unit and in the surrounding room. In addition, the protected zone is not sensitive to large disturbances that occur in the room. The clinical study included 4 patients with 150 accumulated days of testing. The protected zone created by the unit systematically provided an environment with undetectable airborne fungal levels (ie, <1 CFU/m3) regardless of the levels in the room or corridor (P < .01).


These tests show that the unit can be used to create a mobile protective environment for immune-suppressed patients in a standard hospital setting.

No conflict of interest exists for any of the authors.
Corresponding Author Contact InformationAddress correspondence to Vance Bergeron, PhD, Ecole Normale Supérieure de Lyon, Laboratoire de Physique CNRS UMR 5672, 46 allée d'Italie 69007 Lyon, France.

American Journal of Infection Control
Volume 35, Issue 7, September 2007, Pages 460-466

Gene expression profiling of di-n-butyl phthalate in normal human mammary epithelial cells.

J Environ Pathol Toxicol Oncol. 2007;26(1):51-61. Links

Gene expression profiling of di-n-butyl phthalate in normal human mammary epithelial cells.

Molecular Epidemiology Team, Toxicology and Molecular Biology Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, MS L-3014, Morgan-town, WV 26505, USA.

Studies show that female workers in the personal-care industry have an increased risk of developing cancer believed to be the result of increased exposure to toxic and/or carcinogenic chemicals found in cosmetics, hair dyes, and nail polish. One chemical found in multiple personal-care products, di-n-butyl phthalate (DBP), is a known endocrine disruptor and has been found in increased levels in women of childbearing age. The goal of this study was to elucidate mechanisms of phthalate toxicity in normal human cells to provide information concerning interindividual variation and gene-environment interactions. Normal human mammary epithelial cell strains were obtained from discarded tissues following reduction mammoplasty [Cooperative Human Tissue Network (sponsors: NCI/NDRI)]. Gene transcription in each cell strain was analyzed using high-density oligonucleotide DNA microarrays (U133A, Affymetrix) and changes in the expression of selected genes were verified by real-time polymerase chain reaction (PCR) (ABI). DNA microarrays were hybridized with total RNA that was collected after DBP treatment for 5 hr and 10 hr. RNA was harvested from the vehicle control (acetone) at 10 hr. Data Mining Tool software (Affymetrix) was used to separate genes in clusters based on their expression patterns over time. Only 57 genes were found to be altered in all four cell strains following exposure to DBP. These included genes involved in fertility (inhibin, placental growth factor), immune response (tumor necrosis factor induced protein), and antioxidant status (glutathione peroxidase). Data from this study will help clarify the role of DBP in reproductive toxicity, and yield biomarkers of exposure for future epidemiology studies.

PMID: 17725530 [PubMed - in process]

Yellow tea is more potent than other types of tea in suppressing liver toxicity

Phytother Res. 2007 Jul;21(7):668-70. Click here to read Links

Yellow tea is more potent than other types of tea in suppressing liver toxicity induced by carbon tetrachloride in rats.

Department of Biofunctional Chemistry, Faculty of Agriculture, Kobe University, Japan.

The present study compared the effects of six Chinese teas categorized by their production process: green, white, yellow, oolong, black and pu-erh teas, on carbon tetrachloride (CCl4)-induced liver injury. Wistar rats were given ad libitum the Chinese teas prepared according to the home-style methods for 1 week, and then intraperitoneally injected with CCl4 (1 mg/kg body weight) or olive oil as a vehicle. The yellow tea significantly ameliorated the increase in the activity of the alanine- and aspartate-aminotransferases in plasma. Thus, the drinking of yellow tea may contribute to protection against liver injury. Copyright 2007 John Wiley & Sons, Ltd.

PMID: 17444574 [PubMed - indexed for MEDLINE]

Thursday, August 30, 2007

The dichotomy of relative humidity on indoor air quality

Environ Int. 2007 Aug;33(6):850-7. Epub 2007 May 17.Click here to read Links

The dichotomy of relative humidity on indoor air quality.

Indoor Environment Group, National Research Centre for the Working Environment, Lersø Parkallé 105, DK-2100 Copenhagen Ø, Denmark.

Dry and irritated mucous membranes of the eyes and airways are common symptoms reported in office-like environments. Earlier studies suggested that indoor pollutants were responsible. We have re-evaluated, by review of the literature, how low relative humidity (RH) may influence the immediately perceived indoor air quality (IAQ), including odour, and cause irritation symptoms (i.e. longer-term perceived IAQ). "Relative humidity" were searched in major databases, and combined with: air quality, cabin air, dry eyes, formaldehyde, inflammation, mucous membranes, offices, ozone, pungency, sensory irritation, particles, precorneal tear film, sick building syndrome, stuffy air, and VOCs. The impact of RH on the immediately and longer-term perceived IAQ by VOCs, ozone, and particles is complex, because both the thermodynamic condition and the emission characteristics of building materials are influenced. Epidemiological, clinical, and human exposure studies indicate that low RH plays a role in the increase of reporting eye irritation symptoms and alteration of the precorneal tear film. These effects may be exacerbated during visual display unit work. The recommendation that IAQ should be "dry and cool" may be useful for evaluation of the immediately perceived IAQ in material emission testing, but should be considered cautiously about the development of irritation symptoms in eyes and upper airways during a workday. Studies indicate that RH about 40% is better for the eyes and upper airways than levels below 30%. The optimal RH may differ for the eyes and the airways regarding desiccation of the mucous membranes.

PMID: 17499853 [PubMed - indexed for MEDLINE]

Manipulated data in Shell's Benzene Historical Exposure Study

Int J Occup Environ Health. 2007 Apr-Jun;13(2):222-32. Links

Manipulated data in Shell's Benzene Historical Exposure Study.

Brown University, Department of Community Health, Providence, Rhode Island, USA.

In 1983, in the face of mounting evidence of excess leukemia among workers at Shell Oil's Wood River (IL) and Deer Park (TX) petroleum refineries, Shell initiated the Benzene Historical Exposure Study (BHES). Shell's prior research had implicated occupational exposure to benzene as the source of the excess leukemia. The BHES report submission, which ultimately found no link between exposure and the excess morbidity, coincided with OSHA's planned hearings over a new regulatory standard for benzene. Over the next two decades, Shell published several papers based on or expanding the BHES data, all of which concluded that the excess of leukemia was unrelated to benzene. A review of the raw data on which Shell and its consultants relied reveals that Shell manipulated and omitted data in order to reach conclusions that exculpated it from liability and helped delay stricter benzene regulation.

PMID: 17718180 [PubMed - in process]

MCS America News - September 2007 Issue

MCS America News
Volume 2 Issue 9
September 2007

Full PDF:

Article Previews on the Web wtih Links to Individual Articles:

What You Should Know About Mold
Molds are fungi that grow best in damp, humid, warm conditions and reproduce and spread by making tiny spores that are not visible to the naked eye and float through the air indoors and outdoors. It is estimated that there are tens of thousands, to even perhaps three hundred thousand or more species.

Community Spotlight:  Marti F. Wolfe, PhD
Tell us a little about yourself and your background.
My hometown is San Jose, California; I lived there most of my life until I ran away to graduate school.  I've always been a science nerd.  I had my first chemistry lesson when I was four and my brother was six.  My mother used stuff in the kitchen, water and alcohol, baking soda and vinegar, and taught us to write a balanced chemical equation.  I started college as chemistry major, but it didn't take long for me to be seduced by biology – and this is our time in the sun, no question about it – biologists rule!

Activists Corner:  Fabric Softeners

Dear XXX,
I am concerned about fabric softener product emissions harming the children and pets in our neighborhood.  Have you noticed how many of the children have asthma?  I am wondering if you are aware of that scientific studies have found dangerous chemicals in common fabric softeners?

Vehicle Emissions Damage DNA
We've all heard news reports questioning the safety of vehicular traffic.  We've all heard implications that runners and those with respiratory problems are at high risk from exposure to vehicle exhaust fumes.  However, the affects be worse than fumes and emission induced asthma.  Particles from vehicle emissions may actually cause oxidative stress-induced DNA damage.  Worse, the damage may not be easily remedied.

Chemicals Injure the Central Nervous System
Our world is full of neurotoxicants, many of which we are not aware of.  A neurotoxicant is a chemical substance that can cause adverse effects on the nervous system, such as confusion, fatigue, irritability, and behavioral changes.  Central nervous system toxicity may also lead to degenerative diseases of the brain, such toxic encephalopathy. 

Diagnosing EMF Sensitivity
Bruce Hocking, a specialist in occupational medicine, presented a seminar entitled EMF Hypersensitivity for the World Health Organization.  In his presentation, he defines and discusses diagnosing electromagnetic field (EMF) sensitivity.  He then discusses four case studies, two of whom he completes challenge tests and confirms a diagnosis of EMF sensitivity and two of whom he did not complete a challenge test on, as he decided those two patients did not have EMF sensitivity, but rather a psychiatric disorder based on their prior case histories of such.

Exercise Worsens Chronic Fatigue
Most people with chronic illnesses, such as chronic fatigue syndrome (CFS), fibromyalgia (FM), and multiple chemical sensitivities (MCS), have been offered well meaning advice, such as joining a club, getting some exercise, and getting out more.  These infuriating, but well meaning, suggestions often leave the chronically ill individual feeling misunderstood.  After all, would it be appropriate to tell an paraplegic to have fun by going dancing?  Of course not! 

Could It Be Your Clothes?
There are many dangerous things in the world.  But did you ever think that your fabric softener might be one of them?  Products we use to wash our clothing leave behind residues that we wear on our skin constantly  They should be safe.  But are they?  Is that pesky neighbor of yours who claims your clothes dryer emissions make her ill onto something?  Science shows she is!

Mercury High in New Yorkers
A new report has just been released three years after the fact. The New York City Health Department has just given the results of the city's Health and Nutrition Examination Survey of 2004. Higher than expected blood mercury levels have been reported, yet the science is not explained to us. There was a failure to notify the public that blood mercury levels may not be reliable measures of the complexity of the situation.

MCS In the Creative Community
fall is fast upon us, preparations for the new school year
parents help get everything ready for their children they hold so dear

some will head off to school, and not have an ounce of fear
while others only grudgingly go, and shed many a tear

Sal's Place
It is disheartening when a researcher publishes a review which examines or attempts to prove a viewpoint about a condition that is contrary to literature at large.  Das-Munshi J, Rubin GJ, and Wessely S (2007) of Kings College London, Institute of Psychiatry did just that in Multiple chemical sensitivities: review.  Das-Munshi's review looked mainly at psychological studies on MCS to support her viewpoint.  She completely failed to consider the biological studies in literature, which outweigh psychological studies approximately 2:1.  Her review was therefore incomplete, misleading, and inaccurate.

Inside MCSA
It was another busy month at MCSA with lots of new ideas.  One of the smaller things we did was to create a new bumper sticker based on a suggestion from a member.  It's a "little" reminder of perfume toxicity.
Bumper Stickers available for $4.50 at:

Community News
Radio Show:  Pushing Limits Friday, August 17th, 2007
Pushing Limits presents a program on the pathology and politics of Multiple Chemical Sensitivity (MCS), hosted by Jackie Barshak, an art historian living with MCS.
Guests: Dr. Grace Ziem, Albert Donnay,Cindi Norwitz, Dr. Ann McCampbell

Text:     N/A

Certified Mold Strategies, Ltd.
419-433-2383 Ohio    888-568-2383 Toll Free
419-433-9555 Fax
Leader in the Home Inspection and IAQ Industry 
"Strategies for Easier Breathing"

Book Sale
Text:     N/A
While they last! Brand new and off-gassed copies of
Defining Chemical Sensitivity
by Bonnye L. Matthews. valued at $39.95 each
will be sold as part of our MCS Awareness month fundraiser and celebration!

Featured Research Studies
Not in the mind but in the cell: increased production of cyclo-oxygenase-2 and inducible NO synthase in chronic fatigue syndrome.

Multiple Chemical Sensitivities America

Copyrighted © 2007  MCS America

What You Should Know About Mold

by Christiane Tourtet, B.A.

Molds are fungi that grow best in damp, humid, warm conditions and reproduce and spread by making tiny spores that are not visible to the naked eye and float through the air indoors and outdoors. It is estimated that there are tens of thousands, to even perhaps three hundred thousand or more species.

The spores of mold may survive in dry conditions as well. Molds may be found outdoors and indoors in virtually every environment all year round, especially when there is lot of moisture. They may be found in damp, shady places or areas where vegetation such as leaves, for instance, are decomposing.

Some common indoor molds are Aspergillus, Penicillium, Cladosporium, Alternaria. Indoor molds may also be found in showers and basements where humidity levels are high.

Areas that have unusually high mold counts are summer cottages, construction areas, flower shops, antique shops, saunas, mills, farms and green houses.

Molds may cause health problems, as they produce irritants, allergens, and mycotoxins. Touching or inhaling mold spores or mold may cause allergic reactions in sensitive individuals. Stuffy, runny nose, skin rash, red eyes, sneezing and wheezing are quite common. These reactions can be immediate or delayed. People who are allergic to mold and also asthmatic may develop asthma attacks upon exposure to molds and have severe reactions that may include shortness of breath and fever. People with obstructive lung disease may develop mold infections in their lungs. Even in people that are not allergic to molds, irritation of the eyes, nose, skin, throat and lungs may occur.

Symptoms, other than the irritant and allergic types, are not commonly reported as a result of inhaling mold, however there is ongoing research on mold and it's health effects. To get more information on mold, you may want to consult a health professional, or your local or state health department.

Sensitive persons should try to avoid cut grass, compost piles, or wooded areas, as these are most likely to have mold. Inside a home, keeping the humidity levels between 40% to 60% and ventilating cooking areas and showers may slow the growth of mold. If at all possible, between 30% to 50% humidity would be ideal. Relative humidity can be measured with a humidity or moisture meter, which is an inexpensive (approximately $10- $50), small instrument available at various hardware stores.

It is recommended to use an air conditioner or a dehumidifier during humid months, make sure that the home has adequate ventilation and exhaust fans, and, preferably, no carpet in the basement and bathrooms. It is also advisable to replace or remove previously soaked upholstery and carpets.

When spills or water leaks occur indoors, it is important to act quickly to dry areas within 24 - 48 hours to try to prevent the growth of mold. Usually, it is not necessary to identify the species of mold in a home and CDC does not recommend sampling routinely for mold. No matter what type of mold it is, it should be removed. If the moldy area that is to be cleaned up is less than 3 ft. by 3 ft. you most probably can handle the job yourself. Mold growth can be removed from hard surfaces with soap and water, commercial products, or a bleach solution of 1 gallon of water with no more than 1 cup of bleach. If you decide to clean up mold using bleach, never mix ammonia or other household cleaners with bleach as it may produce dangerous and toxic fumes. Make sure that you open doors and windows to provide fresh air, and wear protective eye wear, such as goggles that do not have ventilation holes, and avoid getting mold spores or mold in your eyes. Wear long and non-porous gloves that extend to the middle of the forearm when using water and a mild detergent.

If you are using chlorine bleach, a strong disinfectant, or a cleaning solution, you should wear gloves made from neoprene, natural rubber, nitrile, polyurethane (PCV). Avoid touching moldy items or mold with your bare hands and avoid breathing in mold spores or mold. You may want to wear an N-95 respirator, to limit your exposure to air born mold, which can be purchased at many hardware stores. They usually cost about $12 to $ 25. To be effective, the mask or respirator must fit properly, so it is important to carefully follow the instructions supplied with the mask or respirator. When used in an occupational setting, the Occupational Safety and Health Administration (OSHA) requires that respirators have fit testing.

If there is more than 10 square feet of mold growth, it is best to consult the EPA's Mold Remediation in Schools and Commercial Buildings. Even though it focuses on schools and commercial buildings, it is applicable for other buildings as well.

If you decide to hire a professional service provider or a contractor be sure that this person has experience in cleaning mold. Check references carefully and ask the contractor to follow the guidelines from government or professional organizations, such as the American Conference of Governmental Industrial Hygienists (ACGIH), or recommendations from EPA's Mold Remediation in Schools and Commercial Buildings.

If you suspect that the ventilation/air conditioning/heating (HVAC) system may be contaminated with mold, you should consult EPA's guide before you take further action. If you suspect or know that the HVAC system is contaminated with mold, do not run the system, as mold could be spread throughout the building. If contaminated water, or sewage caused the mold damage, it is advised to call a professional who has experience in fixing and cleaning buildings damaged by contaminated water, and if you are concerned about health effects, before starting cleaning up, consult with a health professional.

-Christiane Tourtet, B.A.

© 2007 Christiane Tourtet
Reprinted with Permission


CDC, Department of Health and Human Services, Centers for Disease Control and Prevention.

EPA, United States Environmental Protection Agency.

Pictures for this article provided by
Certified Mold Strategies, Ltd.

Author's Biography
Christiane Tourtet graduated with an Associate in Science and an Associate in Arts degrees, both with high honors, from Florida Junior College. Then she graduated with a Bachelor in Arts, from Jacksonville University, Jacksonville, Florida. She is a well-known, writer, photo-journalist, photographer, poetess, former teacher and college instructor, radio producer/air personality, publicity model, television voice over talent, and artist. Her biography has been included in numerous world wide publications, notably in Who's Who in America and Who's Who in the World. As a role model for Society, her biography has been published in the Millennium 54th Edition of Who's Who in America and chosen to be included in the White House Millennium Time Capsule.

Community Spotlight: An Interview with Marti F. Wolfe, PhD

Tell us a little about yourself and your background.

My hometown is San Jose, California; I lived there most of my life until I ran away to graduate school. I've always been a science nerd. I had my first chemistry lesson when I was four and my brother was six. My mother used stuff in the kitchen, water and alcohol, baking soda and vinegar, and taught us to write a balanced chemical equation. I started college as chemistry major, but it didn't take long for me to be seduced by biology – and this is our time in the sun, no question about it – biologists rule! I got a BS in Conservation from UC Berkeley, then an MS in Biological Science from San Jose State; in those years my concentration was organismal biology, ecology, and evolution. I became interested in toxicology when I was working in industry, so I went off to get a PhD in Pharmacology/Toxicology from Washington State University. The divide between the two major arms of biology is about the size of the Grand Canyon, so it's rather unusual for a person to change from one to the other. But I think it's been helpful to me – I can look at diseases from an evolutionary perspective, and ecosystems and cells share many features, just at different scales. The more ways you have to view a problem, the greater your chances of solving it.

How did you become interested in MCS?

First, I need to say that I don't view MCS as a unique disease, but rather a one member of the family of diseases and syndromes for which Claudia Miller coined the term "multisystem illnesses". The core group of MSIs are MCS, CFS, FM and PTSD, but there are other candidates and evidence for their inclusion is accumulating rapidly. MCS and I go back to the mid-80s, first when I was still working in the semi-conductor industry, and then when I was working for an industrial hygienist while I was in graduate school at San Jose State. I have a BS in Conservation from UC Berkeley, MS in Biological Science from San Jose State, PhD in Pharmacology/Toxicology from Washington State. That's when I first got into the MCS literature, which was really in its infancy then. I partly supported myself in graduate school by writing briefs for attorneys who handled worker's comp and toxic tort/chemical injury cases. My PhD dissertation work was on interspecies and age-dependent differences in toxic response to organophosphorus insecticides. I wasn't specifically working on MCS directly, but it just continued to pop up in my life; when I was working for another industrial hygienist in Seattle, when I was at the EPA, and at National Pesticide Information Center. CFS came into my life when my best friend Rini, also a toxicologist, developed it so she and I got into that literature while I was trying to help her out. I think even that early, Rini and I had some conversations about some correspondences between CFS and MCS. Then my daughter developed fibromyalgia, and I while I was in Corvallis I became friends with a psychiatrist whose specialty is PTSD. And about that time, the first GWS articles started coming out, so there were hints at mechanism there. I was intrigued by the underlying commonality and annoyed by the articles proposing a psychogenic mechanism. I just knew that eventually an organic cause would be found, but it was always peripheral to whatever I was doing, so I didn't do much more than glance the literature.

In 2003, I was diagnosed with interstitial cystitis and mastocytosis, so plunged into that literature and joined patient support organizations for both diseases and I was struck, and I mean just bowled over by the degree of co-morbidity with CFS, MCS, FM, and I thought "There it is again, I really have to look into it, try to figure something out", but felt out of my depth, and also I was really sick. And of course, by that time the literature had just mushroomed. But, if you are marooned on your sofa with fatigue, you have lots of time to read.
So in the spring of 2004 I was PubMed crawling and what pops up but

Pall, M. L. 2001. Common etiology of posttraumatic stress disorder, fibromyalgia, chronic fatigue syndrome and multiple chemical sensitivity via elevated nitric oxide/peroxynitrite. Med Hypotheses 57: 139-45.

People use 'jaw-dropping' as a metaphor, but my jaw really did drop! I was just dumbstruck! It was just an absolute eureka moment!!! I mean, here was this idea that had been nibbling at the edge of my consciousness for 10 years or so and there it was AND it was accompanied by a mechanism which I found extremely compelling. AND, I saw immediately that it had potential links to IC and masto. AND then I saw who wrote and I nearly fell out of my chair!!! Because Marty Pall was my biochemistry professor when I was in graduate school. It was just such a funny coincidence.

I didn't make any real contact with Marty for another year, but spring 2005 was my last semester of teaching, so I sort of invited myself to work for Marty. I did sort of a post-doc with him for two years, helped him with his book and so forth. And learned tons!

And, I continued to accumulate and read articles, which you have a lot of time for if all your mitochondria tell you Adios and leave you velcroed to the sofa. After I'd been working with Marty for about three months, I
started on his protocol, and it produced an almost miraculous effect. That awful fatigue that makes you feel like your bones have turned to lead just lifted. It was very dramatic, I've always been an energetic person, so fatigue made me feel like I was trapped in someone else's body and when the NO/ONOO- protocol banished my fatigue, I felt as though I'd gotten my life back.

Do you believe toxicology plays a role in MCS and what, in your opinion, is the most likely cause of MCS?

Of course toxicology plays a role! Toxicology is simply the study of the adverse effects of xenobiotics on organisms. I have heard folks state that MCS doesn't belong to toxicology because toxicology is confined to effects that have a discernable dose-response relationship. In fact, some of the old guys were still saying that when I was in grad school. Some dose-response relationships are just more complex, but as more sophisticated statistical tools become more widely available, toxicologists are getting braver about tackling those tougher relationships to. And MCS is definitely one of the more challenging ones, no denying that.

Institutionally, toxicologists haven't contributed much to the task of unraveling MCS's mysteries, but it isn't so much a rejection, or official resistance as we see in some of the other professional societies, it's more like benign neglect. I submitted a proposal for a Special Session on MCS at the 2008 Society of Toxicology meeting – SoT is the largest organization of professional toxicologists in the country with 6000 attendees at the 2007 meeting. We just have to raise the profile of MCS among toxicologists.

And causal mechanism is the area in which toxicologists potentially have the greatest contribution to make to MCS. Of all the MSIs, MCS is the thorniest one to tackle, because there are so many odd features that any mechanistic model must account for. All the mechanisms currently under consideration – oxidative stress, free radical damage, redox disruption, NO/ONOO- vicious cycle, can be thought of collectively as Oxygen Behaving Badly.

Oxygen is dangerous stuff, so the cell handles it with utmost care, passing it gingerly from enzyme to enzyme until it can be reacted with something that will hold onto it. Because if it gets loose from the cell's careful controls, it acquires a charge – this is sort of like handing a juvenile delinquent a gun – and goes on a rampage in the cell, raising hell with various cell structures, including the very ones evolved to make oxygen behave itself. When you look beneath the proposed mechanisms, neurogenic inflammation, neural switching, long-term potentiation, etc, the front-runners share in common an impaired ability in the cell's handling of oxygen.

One of the most vexing mysteries of MCS – and the one that may mislead people into thinking that MCS lies beyond the domain of toxicology – is that the dose-response relationship is so obscure. Another conundrum is the latency phenomenon, the lag-time between exposure and the appearance of symptoms. Latency can make it difficult to connect the disease to the exposure that launched it. And the fact that symptoms may persist even after all contact with the initiating exposure has ceased was another factor that challenged investigators looking for the etiological mechanism.

Marty Pall's NO/ONOO- vicious cycle model ties these observations together into a coherent explanation. There are other vicious cycles in medicine, and certainly the role of free radicals/redox disturbances in many diseases is well documented. The NO/ONOO- vicious cycle draws on both those bodies of knowledge and is both explanatory and predictive – that's the part that makes the model so compelling. The model predicts a therapy; in the last two years or so, MCS and other MSI victims on this therapy are enjoying an improvement in their health and a return to normal life. So this is a very exciting time to be working on the MCS and the other MSIs.

What do you feel is the biggest block to MCS being recognized as a biological illness?

I've described what I call the 'natural history of emerging diseases' in which a syndrome when first described is almost automatically ascribed to psychogenic causes, especially if all its victims are mostly women, so both the patients and the doctors who care for them become marginalized. Then someone, often someone working on a completely different disease, or on some aspect of basic cell physiology, discover a key to a mechanism, more experiments are done, which ideally lead to a clinical test that's conclusive, and at that point the syndrome 'graduates' to the status of a disease and work on treatment accelerates. The unique and biggest challenge of MCS is the huge body of resistance against its recognition – for most diseases maybe a few academic reputations are on the line, but not multi-billion dollar industries pouring money into opposing the recognition of the disease. It's a David-and-Goliath battle; it scares me if I let myself think too much about the odds. Another barrier is that no clinical specialty 'owns' MCS, and some professional organizations actively oppose it, such as the AAAAI. It has helped fibromyalgia emerge from the shadows of psychogenesis, for instance, that it belongs to rheumatology; interstitial cystitis was always understood to be a urological problem even before all urologists believe it was a real disease. This is one reason I'm trying to raise the profile of MCS among toxicologists – it is a chemically-induced disease, we should embrace it as our disease and start doing our share.

Another challenge is the lack of a specific biomarker or clinical test. When you can identify a factor that is present in all or almost all of your affected cohort and completely absent from your control population, you've got a biomarker you can take to the bank. But associated with that challenge is the frustrating fact that we have many assays, tests, potential biomarkers that are used in research, but that just aren't being made available to the clinician or other end-user. We discussed that problem at this year's meeting of the International Society of Environmental BioIndicators and decided it is so important that we need to devote an entire session to it at next years meeting.

Do you think that MCS should be renamed?

Ouch! You can really tie your synapses in knots thinking about this! There are many proposed names, with arguments for and against, as well as for and against retaining MCS. What makes the problem so gruesome is that almost all the names and arguments have merit from someone's quite valid point of view, so a universally acceptable name will continue to elude us, I fear. I think I'll stop there, because I'm on the case definition team, and our deliberations are embargoed for the time being.

Where do we go as a community of researchers and patients from here?

Well, of course we need more research funds, that's so obvious it hardly needs mentioning. But I think we hamstring ourselves if we think money will solve all our problems. What really solves problems is good thinking. Marty Pall didn't have a grant to work on the NOI/ONOO- vicious cycle model, he sat in his office for a couple of years using only his brain. Activists and advocates like you and Cynthia Wilson of CIIN didn't wait around for big grants, you rolled up your sleeves and got to work. And physicians who have stuck with MCS and other MSI patients often take a financial hit to do it. Money is great stuff, but it doesn't take the place of dedication and brains.

So for researchers, that means keeping your mind open to new ideas. If you come into this field as an outsider, as I did, you can discern a pattern in which investigators come to conferences and present the latest development on one part of the problem and they do that year after year, but no one steps back and says "How do all these fit together?" And I say that to clinicians, as well. Stay up with the literature, don't keep doing the same things. And PUBLISH. I've been discovering that there are physicians who have been helping MSI patients with protocols they've worked out themselves, based on their reading of the literature on oxidative stress, free radical damage in cell chemistry. We need to have some system that makes it easier for practitioners to share these experiences, something more flexible and nimble than the traditional refereed journal approach that takes a year to get an article into print,

Collectively, I think we need to make common cause with the organizations supporting the other MSIs, to exploit the strengths that come with the recognition that these diseases are all connected in a very fundamental way.

And lastly, I think your word community is key. If we are a community with a common cause, then we need more cooperation. Many of the resources we need to solve the problem of MCS are already within reach. What's needed now is creative thinking and sustained cooperative, coordinated effort.

Thank you so much for inviting me, Sal. I'm always happy to answer questions on the toxicology aspects of MCS:

Activist's Corner

Activist's Corner

Letter regarding fabric softeners:

Dear XXX,

I am concerned about fabric softener product emissions harming the children and pets in our neighborhood. Have you noticed how many of the children have asthma? I am wondering if you are aware of that scientific studies have found dangerous chemicals in common fabric softeners?

Anderson Laboratories, Inc., located in West Hartford, Vermont, conducted a study in 2000 to determine whether there is any biological basis for complaints that fabric softener emissions can cause acute adverse effects in certain individuals. Using mice, researchers exposed them to the emissions of five commercial fabric softener dryer sheets, one at a time and found the emissions induced sensory irritation, pulmonary irritation, and airflow limitation, revealing mild inflammation of the lungs.

What is in these dryer sheets are respiratory irritants that contribute to allergies, asthma, multiple chemical sensitivities, and other respiratory disorders. The researchers performed gas chromatography / mass spectroscopy analysis of the emissions of one dryer sheet and found isopropylbenzene, styrene, trimethylbenzene, phenol, and thymol, all well known respiratory irritants!

Dry laundry, much like that which we wear each day, was shown to emit sufficient chemical residue to cause sensory irritation. The researchers went on to place a dryer sheet in a room overnight to see if it would have any effect. Sure enough, that single sheet doubled the rate of sensory irritation that wearing dry clothing produced. Pet's and small children, due to their smaller size, are much more vulnerable to these chemical emissions than adults. The results of this study provide a toxicological basis to explain human complaints of adverse reactions to fabric softener emissions.

I have been having difficulty breathing when you wash too. Would you be willing to try some alternatives? I'd be happy to provide a sample for you to try free of charge. A few of my favorites are ¼ to 1 cup of white distilled vinegar at the start of the rinse cycle, 1 cup of glycerin per gallon of water added as ½ cup to rinse cycle, 1 cup of baking soda at the start of the wash cycle, a clean, old tennis ball/shoe in the dryer to soften clothes and reduce static, and a washcloth soaked in 3% hydrogen peroxide solution and placed in the dryer to reduce static.

I appreciate your willingness to help improve the air in our neighborhood! Please let me know if you have any other ideas.



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Scientific Studies: Vehicle Emissions Damage DNA

Scientific Studies: Vehicle Emissions Damage DNA

We've all heard news reports questioning the safety of vehicular traffic. We've all heard implications that runners and those with respiratory problems are at high risk from exposure to vehicle exhaust fumes. However, the affects be worse than fumes and emission induced asthma. Particles from vehicle emissions may actually cause oxidative stress-induced DNA damage. Worse, the damage may not be easily remedied.

Bräune et al (2007) investigated oxidative damage to DNA and related repair capacity. Researchers examined twenty-nine healthy nonsmoking adults with controlled exposure to urban air particles in a two-factored design, testing subjects with biking exercise and without, in either filtered air or air with exposure to particles from vehicle exhaust.

Exposure to exhaust fume particles significantly increased DNA strand breaks, with a further increase in DNA strand breaks with exercise, presumably due to increased air ventilation. In addition, the dose-response relationship was significant, however simultaneous exposure to ozone, nitrogen oxides, and carbon monoxide had no influence. DNA damage was noted as an important initial event in carcinogenesis.

The researchers concluded that particles from vehicle exhaust cause "systemic oxidative stress with damage to DNA" and further they found "no apparent compensatory up-regulation of DNA repair within 24 hours", indicating the damage was not easily remedied.

The data of the researchers also shows that most of the particulate emissions that caused systemic oxidative stress were from diesel vehicles at exposure levels commonly encountered in streets and dwellings near roads. Not addressed in this study is whether or not antioxidants could help to protect individuals from the oxidative stress that caused damage to the subjects DNA strands.


Bräune EV, Forchhammer L, Møller P, Simonsen J, Glasius M, Wåhlin P, Raaschou-Nielsen O, & Loft S. Exposure to Ultrafine Particles from Ambient Air and Oxidative Stress–Induced DNA Damage. Environmental Health Perspectives Volume 115, Number 8, August 2007

Scientific Studies: Chemicals Injure the CNS

Our world is full of neurotoxicants, many of which we are not aware of. A neurotoxicant is a chemical substance that can cause adverse effects on the nervous system, such as confusion, fatigue, irritability, and behavioral changes. Central nervous system toxicity may also lead to degenerative diseases of the brain, such toxic encephalopathy. Chemical neurotoxicants also affect how the nerves carry sensory information and motor impulses, which can lead to tingling, seizures, weakness, lack of coordination, and inappropriate pain sensations. Examples of chemical neurotoxicants include organic solvents, heavy metals, organophosphate pesticides, excitotoxins, mycotoxins, and hundreds of other common chemicals used daily by most people.

Researchers reviewed central nervous system (CNS) injuries, including neurotoxic insults, and revealed the outcome of such insults is largely determined by cellular interactions, inflammatory mediators, the intensity and duration of the insult, the extent of both the primary neuronal damage and glial reactivity, and the developmental stage of the brain.

One would think that neurotoxic insults would cause degeneration of the brain, however the researchers believe that depending on particular circumstances, the brain inflammatory response can promote neuroprotection, regeneration, or neurodegeneration. Once the inflammatory process begins, glial reactivity is regarded as the central phenomenon of brain inflammation and has been used as an early marker of neurotoxicity. The researchers used serum-free aggregating brain cell cultures to test the effects of conventional neurotoxicants. They found their approach to help uncover the complex interactions involved in brain inflammatory responses.

The real question is, should these known neurotoxicants be legally allowed for use, despite the apparent harm they cause? Many think chemicals have improved our lives. Those who have been injured by chemicals and those who suffer neurotoxicity would beg to differ. The argument that "it will never happen to me" is familiar to many whom it has happened to. The words were often once said by those whom it has happened to because no one is immune from neurotoxicity.

These commonly used pesticides, cleaners, vaccine preservatives, food additives, and molds are everywhere in our environment and our bodies. There are alternatives and it's time to use them and abandon dangerous chemicals that damage the central nervous system. Our kids deserve a fighting chance!


Monnet-Tschudi F, Zurich MG, Honegger P. Neurotoxicant-induced inflammatory response in three-dimensional brain cell cultures. Hum Exp Toxicol. 2007 Apr;26(4):339-46.

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