Thursday, January 31, 2008

Developmental impacts of heavy metals and undernutrition.

Basic Clin Pharmacol Toxicol. 2008 Feb;102(2):212-7.Click here to read Links

Developmental impacts of heavy metals and undernutrition.

Division of Child and Adolescent Psychiatry, Columbia University, New York, NY, USA.

A recent Lancet series highlighted enormous loss to young children's developmental potential in developing countries, from exposure to sociocultural and health risks. The possibility that nutritional deficiencies might exacerbate the adverse impact of environmental exposures to developmental toxicants such as heavy metals and pesticides has not been explored. While both arsenic and manganese exposures have known neurotoxicity in adults, systematic investigation in young children has only recently begun. Five hundred and ninety 6- and 10-year-old Bangladeshi children participated in three overlapping studies. Well-water arsenic and manganese were measured from home wells; urine and blood samples were provided; and sociodemographic and household characteristics obtained. For new analyses, 'stunting' was defined as 2 or more standard deviations below the Centers for Disease Control and Prevention gender-specific height-for-age norms. Developmental assessments employed culturally adapted variants of the WISC-III (age 10) or WPPSI-III (age 6). In prior analyses, after adjusting for social factors, well-water arsenic and manganese were both significantly associated with poorer developmental scores at age 10; associations for water arsenic at 6 years were significant, but attenuated. Negative associations with metal exposures held up in newer analyses, and stunting was significantly associated with lower intellectual functioning in analyses considering either metal. There were no significant stunting-by-metal interactions. Developmental risks often co-occur. Millions in South Asia are exposed to naturally occurring arsenic and manganese through household wells. Stunting affects more than 25% of young children in developing countries. The combined neurocognitive loss from both risks, although rarely jointly studied, represents a substantial loss of global potential.

PMID: 18226076 [PubMed - in process]

Wednesday, January 30, 2008

Assessing developmental toxicant exposures via biomonitoring.

Basic Clin Pharmacol Toxicol. 2008 Feb;102(2):100-8.Click here to read

Assessing developmental toxicant exposures via biomonitoring.

Organic Analytical Toxicology Branch, National Center for Environmental Health, Centers for Disease Control and Prevention, Atlanta, GA 30341-3724, USA.

Most of the developmental effects that populations experience are believed to be linked with their exposure scenario and/or their susceptibility to these exposures. In environmental public health, most studies have focused on exposures to environmental chemicals but certainly other environmental factors and susceptibility factors must be considered. Our laboratory assesses exposure to environmental chemicals by measuring the chemical, its metabolite(s) or chemical adduct(s) in a biological matrix taken from members of the populations of interest (via biomonitoring). To help interpret data from the many uses of biomonitoring and for other purposes in public health, we have determined, and made public, data on the concentrations of environmental chemicals in the general population of the USA. Exposures at critical time periods of development to many of these chemicals have been linked with adverse developmental effects. In this paper, we examine this linkage using several chemicals as examples and providing biomonitoring information for these chemicals in the US population as a whole but also at various life stages.

PMID: 18226062 [PubMed - in process]

Mercury-induced cognitive impairment in metallothionein-1/2 null mice.

Neurotoxicol Teratol. 2007 Dec 15 [Epub ahead of print]Click here to read

Mercury-induced cognitive impairment in metallothionein-1/2 null mice.

Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, United States.

Metallothioneins are central for the metabolism and detoxification of transition metals. Exposure to mercury during early neurodevelopment is associated with neurocognitive impairment. Given the importance of metallothioneins in mercury detoxification, metallothioneins may be a protective factor against mercury-induced neurocognitive impairment. Deletion of the murine metallothionein-1 and metallothionein-2 genes causes choice accuracy impairments in the 8-arm radial maze. We hypothesize that deletions of metallothioneins genes will make metallothionein-null mice more vulnerable to mercury-induced cognitive impairment. We tested this hypothesis by exposing MT1/MT2-null and wild-type mice to developmental mercury (HgCl(2)) and evaluated the resultant effects on cognitive performance on the 8-arm radial maze. During the early phase of learning metallothionein-null mice were more susceptible to mercury-induced impairment compared to wildtype mice. Neurochemical analysis of the frontal cortex revealed that serotonin levels were higher in metallothionein-null mice compared to wild-type mice. This effect was independent of mercury exposure. However, dopamine levels in mercury-exposed metallothionein-null mice were lower compared to mercury-exposed wild-type mice. This work shows that deleting metallothioneins increase the vulnerability to developmental mercury-induced neurocognitive impairment. Metallothionein effects on monoamine transmitters may be related to this cognitive effect.

PMID: 18226494 [PubMed - as supplied by publisher]

Pesticide toxicity and the developing brain.

Basic Clin Pharmacol Toxicol. 2008 Feb;102(2):228-36.Click here to read

Pesticide toxicity and the developing brain.

Center for Children's Environmental Health Research, School of Public Health, University of California, Berkeley, CA 94704, USA.

Organochlorine pesticides are used in some countries for malaria control and organophosphate pesticides are widely used in agriculture and in homes. Previous literature documents children's exposure to these chemicals both in utero and during development. Animal studies suggest that many of these chemicals are neurodevelopmental toxicants even in moderate doses, but there are few studies in human beings. Associations of children's pesticide exposure with neurodevelopment from studies being conducted worldwide are summarized. In addition, we present the work of the CHAMACOS study, a longitudinal birth cohort study of Mexican-American children living in the Salinas Valley of California. In this study, we investigated the relationship of children's neurodevelopment with maternal dichlorodiphenyltrichloroethane and dichlorodiphenyldichloroethylene serum levels, as well as prenatal and child organophosphate urinary metabolite levels. We have examined the association with children's performance on the Brazelton Neonatal Assessment Scales and at 6, 12 and 24 months on the Bayley Scales of Infant Development (mental development and psychomotor development) and mothers report on the Child Behaviour Checklist. We observed a negative association of prenatal dichlorodiphenyltrichloroethane exposure and child mental development. We also observed adverse associations of prenatal but not postnatal organophosphate pesticide exposure with mental development and pervasive developmental disorder at 24 months.

PMID: 18226078 [PubMed - in process]

Tuesday, January 29, 2008

Impact of air fresheners and deodorizers on the indoor total volatile organic compounds

Kokuritsu Iyakuhin Shokuhin Eisei Kenkyusho Hokoku. 2007;(125):72-8.

[Impact of air fresheners and deodorizers on the indoor total volatile organic compounds]

[Article in Japanese]

Indoor air quality is a growing health concern because of the increased incidence of the building-related illness, such as sick-building syndrome and multiple chemical sensitivity/idiopathic environmental intolerance. In order to effectively reduce the unnecessary chemical exposure in the indoor environment, it would be important to quantitatively compare the emissions from many types of sources. Besides the chemical emissions from the building materials, daily use of household products may contribute at significant levels to the indoor volatile organic compounds (VOCs). In this study, we investigated the emission rate of VOCs and carbonyl compounds for 30 air fresheners and deodorizers by the standard small chamber test method (JIS A 1901). The total VOC (TVOC) emission rates of these household products ranged from the undetectable level (< 20 microg/unit/h) to 6,900 microg/unit/h. The mean TVOC emission rate of the air fresheners for indoor use (16 products) was 1,400 microg/unit/ h and that of the deodorizers for indoor use (6 products) was 58 microg/unit/h, indicating that the fragrances in the products account for the major part of the TVOC emissions. Based on the emission rates, the impacts on the indoor TVOC were estimated by the simple model with a volume of 17.4 m3 and a ventilation frequency of 0.5 times/h. The mean of the TVOC increment for the indoor air fresheners was 170 microg/m3, accounting for 40% of the current provisional target value, 400 microg/m3. These results suggest that daily use of household products can significantly influence the indoor air quality.

PMID: 18220049 [PubMed - in process]

Too Sick to Move

This is a scanned news article about MCS housing concerns and an individual with multiple chemical sensitivity living in Canada.

Too Sick to Move
Village Gleaner.  Winter 2008 edition

Monday, January 28, 2008

Featured Research Studies

Featured Research Studies
MCS America News, Volume 3, Issue 2, February 2008.

Int J Law Psychiatry. 2008 Jan 7 [Epub ahead of print]
The impact of judges' perceptions of credibility in     fibromyalgia claims.
Le Page JA, Iverson GL, Collins P.
University of British Columbia, Department of Psychiatry, Vancouver, B.C., Canada.
Fibromyalgia (FM) is a confusing and controversial diagnosis, characterized by widespread pain and tenderness at specific anatomical sites. The cause of this syndrome is unknown, and the course of the condition is difficult to predict. Without a known cause, predictable course, or effective treatment, it is not surprising that FM is a contentious diagnosis from a medical perspective, as well as a civil litigation and disability insurance industry perspective. The purpose of this study was to investigate judges' perceptions of credibility in litigated cases involving FM claims in the Canadian courts, and the relation between perceived credibility and awards granted. A systematic review was conducted of every trial-by-judge litigated FM claim in Canada (N=194 cases) up to 2003. The cases were examined in relation to credibility factors. The role and responsibility of the plaintiff was central in claims involving issues of misrepresentation, fraud, non-disclosure, failure to mitigate, and contributory negligence. The presence of these issues suggested a possible decrease or loss in the claim as a result of the plaintiff's conduct. In regards to the actions of defendants, the presence of investigative and surveillance information alone did not affect the awards granted. However, the credibility of that information had a large effect on the amount of award granted. Plaintiff credibility played a similar role, indicating that plaintiffs perceived as more credible were typically granted greater awards. An examination of medical expert credibility revealed that judges appear to perceive experts as more credible overall than plaintiffs, regardless of the expert's role in the case.
PMID: 18191454 [PubMed - as supplied by publisher]
Environmental Health Perspectives Volume 116, Number 1, January 2008
Air Pollution and Postneonatal Infant Mortality in the United States, 1999–2002
Tracey J. Woodruff,1* Lyndsey A. Darrow,2 and Jennifer D. Parker3
1Department of Obstetrics, Gynecology, and Reproductive Sciences, University of California, San Francisco, California, USA; 2Department of Epidemiology, Emory University, Atlanta, Georgia, USA; 3National Center for Health Statistics, Centers for Disease Control and Prevention, Hyattsville, Maryland, USA

Objective: Our goal was to evaluate the relationship between cause-specific postneonatal infant mortality and chronic early-life exposure to particulate matter and gaseous air pollutants across the United States.
Methods: We linked county-specific monitoring data for particles with aerodiameter of ≤ 2.5 µm (PM2.5) and ≤ 10 µm (PM10) , ozone, sulfur dioxide, and carbon monoxide to birth and death records for infants born from 1999 to 2002 in U.S. counties with > 250,000 residents. For each infant, we calculated the average concentration of each pollutant over the first 2 months of life. We used logistic generalized estimating equations to estimate odds ratios of postneonatal mortality for all causes, respiratory causes, sudden infant death syndrome (SIDS) , and all other causes for each pollutant, controlling for individual maternal factors (race, marital status, education, age, and primiparity) , percentage of county population below poverty, region, birth month, birth year, and other pollutants. This analysis includes about 3.5 million births, with 6,639 postneonatal infant deaths.
Results: After adjustment for demographic and other factors and for other pollutants, we found adjusted odds ratios of 1.16 [95% confidence interval (CI) , 1.06–1.27] for a 10-µg/m3 increase in PM10 for respiratory causes and 1.20 (95% CI, 1.09–1.32) for a 10-ppb increase in ozone and deaths from SIDS. We did not find relationships with other pollutants and for other causes of death (control category) .
Conclusions: This study supports particulate matter air pollution being a risk factor for respiratory-related postneonatal mortality and suggests that ozone may be associated with SIDS in the United States.
Environ Health Perspect 116:110–115 (2008) . doi:10.1289/ehp.10370 available via [Online 24 October 2007]
Semin Arthritis Rheum. 2008 Jan 11 [Epub ahead of print]
Central Sensitivity Syndromes: A New Paradigm and Group Nosology for Fibromyalgia and Overlapping Conditions, and the Related Issue of Disease versus Illness.
Yunus MB.
Professor of Medicine, Section of Rheumatology, The University of Illinois College of Medicine at Peoria, Peoria, Illinois.
OBJECTIVES: To discuss the current terminologies used for fibromyalgia syndrome (FMS) and related overlapping conditions, to examine if central sensitivity syndromes (CSS) is the appropriate nosology for these disorders, and to explore the issue of disease versus illness. METHODS: A literature search was performed through PubMed, Web of Science, and ScienceDirect using a number of keywords, eg, functional somatic syndromes, somatoform disorders, medically unexplained symptoms, organic and nonorganic, and diseases and illness. Relevant articles were then reviewed and representative ones cited. RESULTS: Terminologies currently used for CSS conditions predominantly represent a psychosocial construct and are inappropriate. On the other hand, CSS seems to be the logical nosology based on a biopsychosocial model. Such terms as "medically unexplained symptoms," "somatization," "somatization disorder," and "functional somatic syndromes" in the context of CSS should be abandoned. Given current scientific knowledge, the concept of disease-illness dualism has no rational basis and impedes proper patient-physician communication, resulting in poor patient care. The concept of CSS is likely to promote research, education, and proper patient management. CONCLUSION: CSS seems to be a useful paradigm and an appropriate terminology for FMS and related conditions. The disease-illness, as well as organic/non-organic dichotomy should be rejected.
PMID: 18191990 [PubMed - as supplied by publisher]
Copyrighted © 2008  MCS America

Community News

Community News
MCS America News, Volume 3, Issue 2, February 2008.

HPV vaccine 'expensive and deadly drug'
FEMA offers refunds for Katrina trailers
Chemical Additives - Are They Slowly Killing Our Children?
Health effects of diesel fumes
Baby products under scrutiny
UC policy report says chemical exposures cost state estimated $2.6 billion
Lawmakers question safety of chemical used to seal baby formulas
Protest against toxic dangers
CDC Opens Investigation into Unexplained Dermopathy, or "Morgellons Disease"
Study shows how ultrafine particles in air pollution may cause heart disease
Chemical exposures cost California an estimated $2.6 billion, research shows
Emissions are tiny but deadly
Post Traumatic Stress Has Tripled Among Combat-exposed Military Personnel
Toxic Chemicals in Cars
Copyrighted © 2008  MCS America


MCS America News, Volume 3, Issue 2, February 2008.
Chemically safe housing offered in Bend, Oregon
Seven-year old straw bale house.  Cement floors, in-floor heating.  Stucco walls, never painted.  No scents of any kind inside for last 3 /12 years.  Few, if any, before that.


Inside MCS America

Inside MCS America
MCS America News, Volume 3, Issue 2, February 2008.
MCS America launched a new service called MCS Safer Salvage and Share.  MCS Safer Salvage and Share is similar to Freecycle, except it's a free recycling program for safer reusable goods geared towards individuals with MCS, CFS, FM, and other related conditions correlated with the environment. 

The purpose of this program is to find and recycle needed "safe" or "safer" items.  All items are exchanged for free. Shipping cost are arranged between donor and recipient.  Participation is simple:

1. Select an appropriate subject line.  Acceptable phrases include:
     OFFER: air purifier
     TAKEN: air purifier
     WANTED: air purifier
     RECEIVED: air purifier
     List the location of the item and whether you will pay shipping, not pay, or it     
     is negotiable.
     Describe the item.
     List a way to contact you.

2.  Post again when your item is received (wanted posts) or taken (offer posts).
     TAKEN: air purifier
     RECEIVED: air purifier

3.  Rules
      Keep it free, no selling and no trading.
      Respond to individuals, not the group.
      Items may include gift certificates for food, shelter, medications, and other 
      basic needs.
      All posts are moderated.

4.  Disclaimer
This service is provided free of charge by volunteer efforts.  Offered items are not considered tax deductible donations.  MCS America does not and cannot guarantee the safety of items or members.  Post at your own risk.  Posting does not constitute endorsement by MCS America.  Neither MCS America nor Lourdes Salvador will be responsible for misuse of this information or any outcome. 
To join
Copyrighted © 2008  MCS America

Sal's Place

Sal's Place
MCS America News, Volume 3, Issue 2, February 2008.

This month I'd like to share on the lighter side.  Each year the Washington Post's Style Invitational asks readers to take any word from the dictionary, alter it by adding, subtracting, or changing one letter and supply a new definition.  We decided to do that with multiple chemical sensitivity (MCS) in mind.  Here are the results:

Chempagne (n)
A campaign against chemicals. 
A synthetic champagne.
Wealthcare (n)
What doctors personally think about when the go into the healthcare field.

Chemicab (n)
A taxicab filled with the drivers cologne and laundry fragrances.

Chemicam (n)
A camera that can sense volatile organic compounds and other chemicals in the air.

Chemican (n)
The trash can, where all chemicals belong.

Chemicap (n)
A hat worn to keep chemical residue in the air from getting on a person's hair.

Chemicar (n)
A vehicle that transports toxic waste.

Chemicaw (n)
A macaw with chemical sensitivity

Chemicat (n)
A feline/cat with chemical sensitivity
Toxicab (n)
A taxicab filled with the drivers cigarette smoke.  

Chempion (n)
A person who believes chemicals make the world a better place. 
Resticide (n)
A pesticide which is designed to put one to rest.
Chemicalm (adj)
A synthetic state produced by an anti-anxiety pharmaceutical drug.

Copyrighted © 2008  MCS America


Letters to the Editor

Letters to the Editor
MCS America News, Volume 3, Issue 2, February 2008.

Fragrances, fragrances everywhere!
How do we motivate people to understand that the use of scented products has become so pervasive that it poses a serious air pollution problem in our schools, our homes, at shopping malls and individual stores, and even in outdoor air?
Because the fragrance chemical industry is unregulated, users of fragranced products may believe that if you can buy them, they must have been approved by government agencies.  But the fragrance industry is unregulated and does not have to disclose what is in their products.
Copyrighted © 2008  MCS America

Scientific Studies: PBDE: The Cost of Safety

Scientific Studies:  PBDE:  The Cost of Safety
MCS America News, Volume 3, Issue 2, February 2008.

Most people are led to believe that flame retardants are good, that they protect us from harm by reducing the chance of fire.  However on deeper investigation, information published in the Lancet indicates there is more to fire retardants than meets the eye.  
There is a price living organisms pay for the fire safety flame retardants provide.  The precautionary principle warrants more investigation into the use of flame retardants, particularly polybrominated diphenyl ethers (PBDEs).   While the chance of a fire is slim, the chances of exposure to PBDEs is much greater.  
Copyrighted © 2008  MCS America

Scientific Studies: Kids and Environmental Hazards

Scientific Studies:  Kids and Environmental Hazards
MCS America News, Volume 3, Issue 2, February 2008.

Infants and children are more susceptible to environmental hazards than adults due to their smaller body size.  The same exposure is more concentrated in infants and children than it is in adults.
Certain time windows, known as the critical period of development, also render the fetus and infant more vulnerable to common and unavoidable environmental toxicants, especially those which disrupt development.
Copyrighted © 2008  MCS America

Scientific Review: Sick Buildings and Non-Allergic Rhinitis

Scientific Review:  Sick Buildings and Non-Allergic Rhinitis
MCS America News, Volume 3, Issue 2, February 2008.

Sick building syndrome is described by the Environmental Protection Agency as "a situations in which building occupants experience acute health and comfort effects that appear to be linked to time spent in a building, but no specific illness or cause can be identified."
Copyrighted © 2008  MCS America

Scientific Studies: Is MCS Cause by Diseased Teeth?

Scientific Studies:  Is MCS Cause by Diseased Teeth?
MCS America News, Volume 3, Issue 2, February 2008.

Diseased teeth have been implicated in many illnesses.  Dr. Price, a dentist, experimented with his patients in the early 1900's after suspecting that root canals were related to their degenerative diseases. 
Price remembered how bacterial cultures were taken from ill patients and injected into animals, producing the same disease in the animal.  Price experimented by removing the root canalled tooth from the patient and inserting under a rabbits skin.  In nearly all the cases in which Price did this, the patient recovered from their illness and the rabbit died of the same illness.  Price chose rabbits because they have weak immune systems.  He concluded that microbes hidden deep in tiny tubules of the root canalled tooth may spread and cause degenerative diseases.  
Copyrighted © 2008  MCS America

Scientific Studies: Diagnostic Markers for MCS

Scientific Studies:  Diagnostic Markers for MCS
MCS America News, Volume 3, Issue 2, February 2008.

Researchers at the Department of Public Health Sciences at the University of Toronto set out to find diagnostic markers, also known as biomarkers, for multiple chemical sensitivity (MCS).  MCS has an estimated American prevalence of 15%.  In the past, diagnostic makers have been elusive with no consistently abnormal tests that are shared by all subjects.
Physicians treating MCS often observe low mineral levels or changes in intra-erythrocytic minerals (IEMs) that may affect proper detoxification of xenobiotics (foreign chemical substances found in the body). 
Copyrighted © 2008  MCS America

Activist's Corner: Write the Presidential Candidates About MCS

Activist's Corner: Write the Presidential Candidates About MCS
MCS America News, Volume 3, Issue 2, February 2008.

Now is the time to begin educating the presidential candidates about multiple chemical sensitivity (MCS) and its devastating effects on the individual, the community and our nation!
MCS America has sent a letter to each of the presidential hopefuls and you can send one too. 
Either write your own letter, or use our pre-written letter to inform all the presidential hopefuls about the facts, figures, and findings of MCS.  Let them know we need funding, a committee to address MCS, and more research.  You may download a word file with the 13 pre-addressed, ready-to-print letters at:
Please input your own name and address on the bottom of each letter.  A sample appears on the following page.
Presidential Hopefuls
Hillary Rodham Clinton
4420 North Fairfax Drive
Arlington, VA 22203
John Cox
PO Box 5353
Buffalo Grove, IL 60089-5353
John Edwards
410 Market Street, Suite 400
Chapel Hill, NC 27516
Rudy Giuliani
295 Greenwich St, #371
New York, NY 10007
Mike Gravel
PO Box 948
Arlington, VA 22216-0948
Mike Huckabee
PO Box 2008
Little Rock, AR 72203
Duncan Hunter
9340 Fuerte Drive, Suite 302
La Mesa, CA 91941
Alan L. Keyes
PO Box 50597
Provo, UT 84605-0597
Dennis J. Kucinich
PO Box 110475
Cleveland, OH 44111
John McCain
PO Box 16118
Arlington, VA 22215
Barack Obama
PO Box 8102
Chicago, IL 60680
Ron E. Paul
3461 Washington Blvd., Suite 200
Arlington, VA 22201
W. Mitt Romney
PO Box 55899
Boston, MA 02205-5899
Sample Letter

City, State, Zip
Dear XXX;
As you campaign to be our next president, please consider an important health issue – multiple chemical sensitivity (MCS).  Sensitivity to chemicals has been researched by scientists for 60 years.  The Centers for Disease Control and Prevention (CDC) recently recognized chemical sensitivity as one symptom of Chronic Fatigue Syndrome (CFS), yet diagnostic tests and effective medical treatments for MCS have yet to be discovered.  For afflicted Americans, proper diagnosis of MCS through confirmatory diagnostic testing would mean better care, treatment, and outcome, all of which would improve many lives.

Here are a few documented and published facts about MCS:
· Several studies published between 1993 and 2005 suggest that at least 45 million men, women, and children in the US report various chemical sensitivities.  Seventy percent of these people have not been diagnosed properly by a health care provider.
· Brain scans show reduced blood flow to the brain when under chemical exposure.
· Numerous physiological abnormalities have been identified in MCS subjects, including brain inflammation, oxidative stress, excitotoxicity, cardiac and airway disease, auto-immune disorders, and many others.
· Mast cell activation and disorders of porphyrin metabolism have been linked to MCS.
· Genetic differences relating to detoxification processes are present more often in those with MCS than those without.
· Studies have shown that avoidance of inciting chemicals and proper environmental control is the most efficacious treatment known to date.  Ninety-five percent of patients report improvement upon practicing avoidance and 94% report improvement upon moving to a chemical free living space.
· *Citations may be found at:
MCS is already formally recognized by the governments of Germany, Canada, and Denmark.  Sweden recognizes electrical sensitivity.  Last year, more than one half of state governors proclaimed the month of May as MCS and/or Toxic Injury Awareness Month.  The Office of Disease Prevention and Health Promotion, U.S. Department of Health and Human Services, National Health Observance Calendar lists May as MCS Awareness Month. 
Funding is needed for programs that educate both health care professionals and the general public about MCS.  A committee is also needed to help coordinate health agency research, promote the exchange of information, hold federal agencies accountable, and give advocates a voice in policy decisions. Research offers the greatest prospect of returning people with MCS to healthy, productive lives. 
I will continue to monitor your campaign and actions.  As I consider how to cast my ballot, I hope I can count on your help in this important matter.
Your Name
Your Address
Your City, State Zip
Copyrighted © 2008  MCS America
Permission granted to use the letter as indicated.

Mission for Truth: Critical Thinking

Mission for Truth:  Critical Thinking
MCS America News, Volume 3, Issue 2, February 2008.
When researcher A says yes and researcher B says no, confusion abounds.    For those who are counting on scientific data, this can be very frustrating.  In a world where science is biased, facts are manipulated, doctors are mislead, industry acts to misinform, and few can be trusted, how do we find the truth? 
When it comes to controversial illnesses, such as multiple chemical sensitivity (MCS), fibromyalgia (FM), and chronic fatigue syndrome (CFS), patients, doctors, and researchers must employ critical thinking skills to sort through the bunk and get to the facts and the real truth.  
Copyrighted © 2008  MCS America

Multiple Chemical Sensitivity Beleaguered, Part 1

Multiple Chemical Sensitivity  Beleaguered, Part 1
MCS America News, Volume 3, Issue 2, February 2008.
Several studies published from 1993-2005 suggest that at least 45 million men, women, and children in the US report various symptoms of multiple chemical sensitivity (MCS).1-8  Seventy percent of these people have not been diagnosed properly by a health care provider.1-8   More severe cases often lead to permanent and total disability. 
The recurring question is "Why is MCS not yet acknowledged by many medical professionals in the community?"  It's not disregarded because it's not a real illness, or researchers lack scientific data.  It's not ignored for lack of the epidemic rate of affliction that currently exceeds the rate of autism.  It's not misunderstood for lack of treatment modalities.  Rather, multiple chemical sensitivity is intentionally cast aside for industry profits.
Copyrighted © 2008  MCS America

Saturday, January 26, 2008

Washington Governor Signs 2008 MCS Proclamation!

Washington Governor Signs 2008 MCS Proclamation!

Florida Governor Signs MCS Proclamation!

Florida Governor Signs 2008 MCS Proclamation!

Patulin influences the expression of Th1/Th2 cytokines by activated peripheral blood mononuclear cells and T cells through depletion of intracellular glutathione.

Environ Toxicol. 2008 Jan 23 [Epub ahead of print]Click here to read Links

Patulin influences the expression of Th1/Th2 cytokines by activated peripheral blood mononuclear cells and T cells through depletion of intracellular glutathione.

Department of Molecular Biology, University of Salzburg, Austria.

Patulin is a mold toxin secreted mainly by fungi of the Penicillium species. Exposure generally results from consumption of moldy fruits and fruit products. Since recent studies identified mold exposure as a risk factor for allergic diseases, we examined the effects of patulin on human peripheral blood mononuclear cells (PBMC) prepared from buffy coats of healthy donors. Cells were stimulated with CD3- and CD28-specific antibodies in the presence or absence of patulin. Effects of patulin on PBMCs were evaluated by proliferation, viability assays, and cytokine ELISAs. The presence of 50 ng/mL patulin strongly decreased the amounts of several cytokines in the supernatant of stimulated PBMCs. This decrease in cytokine secretion was not due to cytotoxic effects of patulin. Moreover, the extent of the reduction of cytokine amounts was cytokine specific, affecting some (IL-4, IL-13, IFNgamma, and IL-10), but not others (IL-8, IL-5). We show that all effects could be abolished by adding thiol containing compounds. A depletion of intracellular GSH could be measured after incubation of cells with patulin. Taken together, our data indicate that patulin modulates the functional activation of PBMCs with respect to proliferation and cytokine secretion patterns by depletion of intracellular GSH. The depletion of intracellular glutathione may influence the balance between Th1 and Th2 cells and have implications for allergic diseases. (c) 2008 Wiley Periodicals, Inc. Environ Toxicol, 2008.

PMID: 18214930 [PubMed - as supplied by publisher]

Effects of the insecticides malathion and diazinon on the early oogenesis in mice in vitro.

Environ Toxicol. 2008 Jan 23 [Epub ahead of print]Click here to read Links

Effects of the insecticides malathion and diazinon on the early oogenesis in mice in vitro.

Departamento de Ciencias de la Salud, Universidad Autónoma Metropolitana‐Iztapalapa, CP 09340, DF. México.

Malathion and diazinon are two of the most commonly used organophosphorous (OP) agrochemicals. Several studies show that these pesticides exert several effects on mammalian spermatogenesis. Nevertheless, there are no studies concerning their effects on oogenesis. The objective of this study was to evaluate the effects of these insecticides on the viability of in vitro cultured mouse oocytes during the early oogenesis and to get a further understanding of the molecular mechanisms by which OP insecticides act and affect germinal cells. Oocytes were cultured from fetal ovaries for 10 days, when most oocytes had reached the diplotene stage (germinal vesicle stage). Cultures were exposed to different concentrations of malathion or diazinon for 24 h, and the effect on oocyte viability was assessed. Gene expression in oocytes exposed to the insecticides was analyzed by generating cDNA libraries and performing differential screenings. Results show a significant decrease in oocytes survival after 24-h exposure to 250 muM malathion or 900 nM diazinon, and the effect of these insecticides on the regulation of genes encoding proteins involved in transcription (BP75), translation (ribosomal protein S5), and mitochondrial function (cytochrome oxidase subunits I and III), providing evidence for OP insecticides as toxicants for mammals oocytes during the early oogenesis. (c) 2008 Wiley Periodicals, Inc. Environ Toxicol, 2008.

PMID: 18214912 [PubMed - as supplied by publisher]

A model for energetics and bioaccumulation in marine mammals with applications to the right whale.

Ecol Appl. 2007 Dec;17(8):2233-50. Links

A model for energetics and bioaccumulation in marine mammals with applications to the right whale.

Biology Department, MS#34, Woods Hole Oceanographic Institution, Woods Hole, Massachusetts 02543, USA.

We present a dynamic energy budget (DEB) model for marine mammals, coupled with a pharmacokinetic model of a lipophilic persistent toxicant. Inputs to the model are energy availability and lipid-normalized toxicant concentration in the environment. The model predicts individual growth, reproduction, bioaccumulation, and transfer of energy and toxicant from mothers to their young. We estimated all model parameters for the right whale; with these parameters, reduction in energy availability increases the age at first parturition, increases intervals between reproductive events, reduces the organisms' ability to buffer seasonal fluctuations, and increases its susceptibility to temporal shifts in the seasonal peak of energy availability. Reduction in energy intake increases bioaccumulation and the amount of toxicant transferred from mother to each offspring. With high energy availability, the toxicant load of offspring decreases with birth order. Contrary to expectations, this ordering may be reversed with lower energy availability. Although demonstrated with parameters for the right whale, these relationships between energy intake and energetics and pharmacokinetics of organisms are likely to be much more general. Results specific to right whales include energy assimilation estimates for the North Atlantic and southern right whale, influences of history of energy availability on reproduction, and a relationship between ages at first parturition and calving intervals. Our model provides a platform for further analyses of both individual and population responses of marine mammals to pollution, and to changes in energy availability, including those likely to arise through climate change.

PMID: 18213965 [PubMed - in process]

Wednesday, January 23, 2008

Newspapers and Newspaper Ink Contain Agonists for the Ah Receptor.

Toxicol Sci. 2008 Jan 17 [Epub ahead of print]Click here to read Links

Newspapers and Newspaper Ink Contain Agonists for the Ah Receptor.

Department of Environmental Toxicology, University of California, Davis 95616.

Ligand dependent activation of the aryl-hydrocarbon receptor (AhR) pathway leads to a diverse array of biological and toxicological effects. The best studied ligands for the AhR include polycyclic and halogenated aromatic hydrocarbons, the most potent of which is 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). However, as new AhR ligands are identified and characterized, their structural and physiochemical diversity continues to expand. Our identification of AhR agonists in crude extracts from diverse materials raises questions as to the magnitude and extent of human exposure to AhR ligands through normal daily activities. We have found that solvent extracts of newspapers from countries around the world stimulate the AhR signaling pathway. AhR agonist activity was observed for DMSO, ethanol, and water extracts of printed newspaper, unprinted virgin paper, and black printing ink, where activation of luciferase reporter gene expression was transient, suggesting that the AhR active chemical(s) was metabolically labile. DMSO and ethanol extracts also stimulated AhR transformation and DNA binding, and also competed with [(3)H]TCDD for binding to the AhR. In addition, DMSO extracts of printed newspaper induced cytochrome P450-1A (CYP1A) associated 7-ethoxyresorufin-O-deethylase (EROD) activity in zebrafish embryos in vivo. While the responsible bioactive chemical(s) remain to be identified, our results demonstrate that newspapers and printing ink contain relatively potent metabolically labile agonists of the AhR. Given the large amount of recycling and re-processing of newspapers throughout the world, release of these easily extractable AhR agonists into the environment should be examined and their potential effects on aquatic organisms assessed. (244 words).

PMID: 18203687 [PubMed - as supplied by publisher]

Tuesday, January 22, 2008

A review of 241 subjects who were patch tested twice: could fragrance mix I cause active sensitization?

Br J Dermatol. 2008 Jan 17 [Epub ahead of print]Click here to read Links

A review of 241 subjects who were patch tested twice: could fragrance mix I cause active sensitization?

Department of Cutaneous Allergy, St John's Institute of Dermatology, St Thomas' Hospital, London SE1 7EH, U.K.

Background Active patch test sensitization is an uncommon phenomenon which may have undesirable consequences for those undergoing this gold-standard investigation for contact allergy. Objectives To perform a retrospective analysis of the results of 241 subjects who were patch tested twice in a monocentre evaluating approximately 1500 subjects per year. Methods Positivity to 11 common allergens in the recommended Baseline Series of contact allergens (European) was analysed: nickel sulphate; Myroxylon pereirae; fragrance mix I; para-phenylenediamine; colophonium; epoxy resin; neomycin; quaternium-15; thiuram mix; sesquiterpene lactone mix; and para-tert-butylphenol resin. Results Only fragrance mix I gave a statistically significant, increased rate of positivity on the second reading compared with the first (P = 0.011). This trend was maintained when separately analysing a subgroup of 42 subjects who had been repeat patch tested within 1 year; this analysis was done to minimize the potential confounding factor of increased usage of fragrances with a wide interval between both tests. To reduce the confounding effect of age on our data, we calculated expected frequencies of positivity to fragrance mix I based on previously published data from our centre. This showed a marked excess of observed cases over predicted ones, particularly in women in the age range 40-60 years. Conclusions We suspect that active sensitization to fragrance mix I may occur. Similar published analysis from another large group using standard methodology supports our data.

PMID: 18205877 [PubMed - as supplied by publisher]

Saturday, January 19, 2008

Ameliorating the developmental neurotoxicity of chlorpyrifos: a mechanisms-based approach in PC12 cells.

Environ Health Perspect. 2007 Sep;115(9):1306-13.Click here to read Links

Ameliorating the developmental neurotoxicity of chlorpyrifos: a mechanisms-based approach in PC12 cells.

Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA.

BACKGROUND: Organophosphate developmental neurotoxicity involves multiple mechanisms converging on neural cell replication and differentiation. OBJECTIVES: We evaluated mechanisms contributing to the adverse effects of chlorpyrifos (CPF) on DNA synthesis, cell number and size, and cell signaling mediated by adenylyl cyclase (AC) in PC12 cells, a neuronotypic cell line that recapitulates the essential features of developing mammalian neurons. RESULTS: In undifferentiated cells, cholinergic receptor antagonists had little or no protective effect against the antimitotic actions of CPF; however, when nerve growth factor was used to evoke differentiation, the antagonists showed partial protection against deficits in cell loss and alteration in cell size elicited by CPF, but were ineffective in preventing the deterioration of AC signaling. Nicotine, which stimulates nicotinic acetylcholine receptors but also possesses a mixture of prooxidant/antioxidant activity, had adverse effects by itself but also protected undifferentiated cells from the actions of CPF and had mixed additive/protective effects on cell number in differentiating cells. The antioxidant vitamin E also protected both undifferentiated and differentiating cells from many of the adverse effects of CPF but worsened the impact on AC signaling. Theophylline, which prevents the breakdown of cyclic AMP, was the only agent that restored AC signaling to normal or supranormal levels but did so at further cost to cell replication. CONCLUSIONS: Our results show definitive contributions of cholinergic hyperstimulation, oxidative stress, and interference with AC signaling in the developmental neurotoxicity of CPF and point to the potential use of this information to design treatments to ameliorate these adverse effects.

PMID: 17805420 [PubMed - indexed for MEDLINE]

Living with toxic poisioning.

 Aust Fam Physician. 2007 Dec;36(12):1053.Click here to read Links

Living with toxic poisoning.

In 1991 I was working as an administration officer at a school in North Queensland. I worked with two other women in a very small office and there were three other offices nearby, each with one person in them. The education department decided to put down new flooring around these offices, down the adjoining stairway and along the adjoining hallway. The new flooring was made up of coloured chips spread over the floor coated by a two part resin. At the time the flooring was being laid, the weather was very wet and humid. The two part coating would not set. It was soft to touch and smelt toxic. After complaints from office staff to the education department, the floor was patched up. This process happened about three times over a 3 year period.

PMID: 18075634 [PubMed - indexed for MEDLINE]


Wednesday, January 16, 2008

Increased release of histamine in patients with respiratory symptoms related to perfume.

 Clin Exp Allergy. 2007 Nov;37(11):1676-80. Epub 2007 Sep 17.Click here to read Links

Increased release of histamine in patients with respiratory symptoms related to perfume.

The Danish Research Centre for Chemical Sensitivities, Gentofte University Hospital, Gentofte, Denmark.

BACKGROUND: Environmental perfume exposure may cause respiratory symptoms. Individuals with asthma and perfume contact allergy report such symptoms more frequently than others. However, immunologic mechanisms have not been demonstrated and the symptoms are not associated with IgE-mediated allergy. The study aimed to investigate whether basophils from patients with respiratory symptoms related to perfume released more histamine in the presence of perfume as compared with healthy volunteers. METHODS: Histamine release was measured by the glass fibre method. Blood was obtained from healthy volunteers (n=20) and patients with respiratory symptoms related to perfume (n=17) attending a dermatological outpatient clinic for patch testing. The effect of an international brand perfume was investigated using the basophil histamine release test with perfume. Furthermore, basophils from a healthy non-atopic donor were incubated with participant's sera and histamine release induced by perfume was measured. RESULTS: In both groups incremental perfume concentrations showed a positive and significant (P<0.001) dose-response effect on the release of histamine. At the highest perfume concentration, the basophils released significantly (P<0.05) more histamine in patients as compared with healthy volunteers. No difference was found between the groups when sera were incubated with basophils from a healthy non-atopic donor. CONCLUSION: Perfume induces a dose-dependent non-IgE-mediated release of histamine from human peripheral blood basophils. Increased basophil reactivity to perfume was found in patients with respiratory symptoms related to perfume.

PMID: 17877753 [PubMed - indexed for MEDLINE]

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