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

References:

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.
www.certifiedmoldstrategies.com

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:

mfwolfe@csuchico.edu

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.

Sincerely,

XXX


Download, Edit, and Send:

http://www.mcs-america.org/LetterAboutFabricSoftener.doc

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.

-LS

Reference:
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
http://www.ehponline.org/members/2007/9984/9984.pdf

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!

-LS

Reference
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.

Scientific Study Opinion: 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.

The last two patients may have been grossly mistreated. Both received a psychiatric diagnosis without a provocation test to rule out contributing physical causation of EMF sensitivity. It is possible that they both had had a co-occurring psychiatric disorder as well as EMF sensitivity, but the EMF sensitivity was not tested for in favor of a psych diagnoses based on perceived psychiatric problems, which may indeed have been EMF related.

A psychiatric diagnosis should not be given unless all other causes are ruled out and no physiological cause can be found. It is well known that exposures, such as EMF, can cause neurotransmitters to misfire, which can cause mental symptoms that may fully resolve when the exposures are eliminated. It is therefore conceivable that the two patients that Hocking did not perform a challenge test on were grossly mistreated and potentially misdiagnosed. Hocking acted to continue this possible misdiagnosis by not issuing an appropriate challenge test. This is discriminatory treatment between patients with no history of psychiatric disturbance and patients with psychiatric disturbance.

Hocking only tested via provocation when the patient reported strictly physical symptoms. This serves as a lesson to patients to stick with reporting physical symptoms, such as pain, numbness, tingling as opposed to visual problems or other potentially "mental" problems. In this way, the patient can assure proper testing to rule out misdiagnoses and return to health more quickly. It is unfortunate that practitioners and researchers, such as Hocking, often rule out an additional diagnosis and leave the patient to navigate on their own in order to obtain appropriate tests.

It is quite plausible that patient three did not have a mere fear of EMF. This is the unfortunate aspect of how insurance and cost limits testing at the expense of proper diagnosis. Patient 3 was unwilling to accept the psychiatric diagnosis according to Hocking. Most patients who fear something know they fear it. In such cases, a psychiatric diagnosis would resonate with them. How many conditions did we previously believe were psychiatric in origin that eventually were proven physical? History would show nearly all conditions were originally thought to be psychiatric and later found to have a biological or physical causation, such as asthma for example.

If a patient is reluctant to accept a diagnosis, perhaps the diagnosis is wrong and a provocation challenge is in order. If the provocation proves no sensitivity, then EMF would be ruled out on a scientific basis. Ruling it out by the mere presence of a pre-existing mental disorder is "junk science". It is quite plausible for a patient to be diabetic, EMF sensitive, suffer cancer, and also have a mental disorder. Having one condition does not preclude another disorder from occurring.

Patients should not have proper tests ruled out on the basis of a co-occurring mental disorder. To do so it to disserve the patient and avoid proper diagnosis of other conditions that can be treated so the patient improves. Psychotherapy in such cases may only help the person digress because it is not addressing the true cause of symptoms. The patient is likely to become depressed and anxious as the symptoms continue despite psychotherapy. Tricking a patient into believing they are not having the symptoms and should think positive to avoid them may also trick them into further harm of their health. When symptoms do arise, the EMF condition is likely to be far more advanced and may not be as treatable as it once was if tested for in the beginning. Practical EMF avoidance, not denial, is essential.

Because patient 3 and 4 had psychiatric symptoms, all their health conditions were believed to be mental. This may be a gross disservice to patients and society. It is highly encouraged that practitioners rule out all other causes with scientific based clinical tests before reaching a psychiatric diagnosis.

-LS

Reference

Hocking, B. A physicians approach to EMF sensitive patients. World Health Organization Seminar on EMF Hypersensitivity, Prague. Retrieved on August 11, 2007 from:
http://www.who.int/peh-emf/meetings/archive/en/hocking.pdf

Scientific Studies: 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!

Well meaning friends often believe that chronic illness is psychological and victims just need to get out and have fun. Or, they may believe that the victim would not be tired if they got in shape. Or worse, they think the illness is affecting the chronically ill person at a psychological level and believe that to be the reason why the ill person does want to go out more often. In reality, those with chronic illness are quite adept at pacing themselves to avoid exhaustion. What friends fail to realize is that exertion is exertion, regardless of work or play. Now science has stepped in to provide evidence of this.

Researchers in Japan noted that patients with chronic fatigue syndrome (CFS) report substantial symptom
worsening after exercise and took an interest in the specific time course of the worsening. They investigated the influence of exercise on the subjective symptoms and cognitive function of 9 female CFS patients and compared them with 9 healthy women. An exercise test was conducted and monitoring of vital signs, cognitive function, and psychological status was performed from one week prior to exercise until two weeks after exercise.

Physical symptoms in the CFS patients did get worse on the fifth day. However cognitive and psychological status remained constant. There was no cognitive or psychological benefit to the exercise, yet patients became more fatigued and suffered physical decline.

Regardless of pleasure or pain, exertion is exertion. Pleasurable exertion holds the same fatiguing capability for the chronically ill as unpleasurable exertion. And there are no psychological benefits to boot. The next time we recommend to a CFS patient to get out more, have fun, and exercise, it might be best to think twice and opt for a quite home movie that won't make the person sicker and more discouraged instead.

-LS

Reference
Yoshiuchi K, Cook DB, Ohashi K, Kumano H, Kuboki T, Yamamoto Y, Natelson BH. A real-time assessment of the effect of exercise in chronic fatigue syndrome. Physiol Behav. 2007 Jul 24.

Scientific Studies: 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!

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, for a period of 90 minutes each. Several respiratory cycle parameters were measured, including the pause after inspiration, the pause after expiration, and the midexpiratory airflow velocity. They found the emissions induced sensory irritation, pulmonary irritation, and airflow limitation, revealing mild inflammation of the lungs.

So, what's in these dryer sheets that is a respiratory irritant that may 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. Perhaps your child's asthma and your allergies have a cause after all. Could it be your clothes?

The researchers went on to place a dryer sheet in a room with the mice 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. Do we really want these dangerous products in our homes, on our bodies, and near our children?

The results of this study provide a toxicological basis to explain human complaints of adverse reactions to fabric softener emissions. It might be time to go apologize to your neighbor.

Fortunately, there are inexpensive alternatives you both can use to enjoy better health and appreciate soft, clean clothes. Most health food stores have safer products, but what you really need may be lurking in your kitchen or garage already.

White Distilled Vinegar
¼ to 1 cup at start of rinse cycle.
Deodorizes & softens clothes.
Removes soap scum.
Leaves no vinegar odor when dry.
Do not hang colors in direct sunlight as they may fade.

Glycerin
Mix 1 cup of glycerin per gallon of water and add ½ cup to rinse cycle.

Baking Soda
1 cup at the start of the wash cycle.

Tennis Ball or Tennis Shoe
Put a clean, old tennis ball/shoe in the dryer to soften & reduce static.

3% Hydrogen Peroxide Solution
Soak a washcloth in peroxide and put it in the dryer to reduce static.

It is possible to live a healthier, safer, life. These simple solutions cost pennies and have many other uses in the home. Our health should be our first priority!

-LS

Reference
Anderson RC, Anderson JH. Respiratory toxicity of fabric softener emissions. J Toxicol Environ Health A. 2000 May 26;60(2):121-36.

Mercury High in New Yorkers

by Alan Moses

Opinion

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.

It was noted that people of Asian decent had higher rates of blood mercury levels, as it may be possible that they have the genetic ability to eliminate this toxin at faster rates. Mercury is known to concentrate and adhere to fatty tissues and organs and is not always on the move to exit. Others may not be able to expel this toxin at a high enough rate to discharge the danger.

Mercury in all forms may be dangerous, however it is proving to be genetic susceptibility that determines whether one might be able to escape the full onslaught. If you are genetically unable to expel this toxin quickly enough, then you may suffer the consequences. This seems rather simplistic and yet we can better understand the effects of all toxins if we want to.

As with the dangers of smoking, drinking, prescription pill abuse, or just plain over use of any toxin, the dangers are there and some people will not react the same as others. We need to get off the all people are the same theory. Not all vaccines, scented products, medications, cleaning products, or even foods will cause the same results. This toxin or that, we all react differently. We may all have five fingers and toes but our biology, physiology, or neurology is not the same.

This study has, in fact, proven that genetics plays a role. We have to put things in perspective. Those of us of the so-called anti-vaccine crowd do realize that we may have gone too far. Some vaccinations could help, yet we know that just plain better nutrition and cleaner environments do eliminate the chances of most of the diseases involved.

We banned the use of lead almost thirty years ago. However, new warnings about this banned toxin are being newly expressed as it is being found in imported toys. We are finding that our own minimal regulations are not even the tip of the iceberg. The world economy has gone beyond any regulations that we may apply. Our food supply is becoming another questionable source of danger to our health.

Mercury is only one of the many toxins that can create havoc upon our bodies and our minds. The list of heavy metals is extensive, and if you add the tens of thousands of other chemicals that are out there, you have a serious toxic soup. Global warming and chronic illness go hand in hand; as the earth suffers so do we. Why is this so hard for us to understand?

I hope that we don't forget the science that we were taught. We are poisoning ourselves. We have overused the toxicants that make us sick. ALS, ADD, ASD and all of the other alphabets prove to us that simplicity is the answer and nothing else.

- Alan Moses
© 2007 Alan Moses
Reprinted with Permission

MCS in the Creative Community: Fall Is Here

 

MCS in the Creative Community

Fall Is Here

                                                               by the members of MCS America

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

tis hard for some and easy for others, how could this possibly be
let's work together to figure this out, and maybe we will see

floors freshly waxed, desks bleached, "protective" pesticides sprayed
particle board arrived, latex paint applied, mold remediation delayed

students enter, as mandated by law, eager on their first day
then allergies/asthma begin, attention wanders, behavior hardly okay

their young brains are fragile, apparent harm is in the "air"
what's a parent to do, besides walk away and despair

more mandates pass down, new vaccines forced without debate
every child's health taken, transferred to the hands of the state

noncompliance earning expulsion, no more privilege to go to school
personal choice stolen, growing up was never so cruel

no money in the budget to protect our kids from harm
public/private politics over health, time to activate the alarm!

what kid can concentrate, while triggers abound in school?
don't know about you, but home schooling is looking very COOL!

 

 

 

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.

The first section "diagnosis and epidemiology" contradicts itself by using "absence of specific biological tests" to downplay the existence of multiple chemical sensitivity (MCS), while at the same time stating lymphocyte depletion and immunological differences present in MCS are also present in somatization disorders and depression, both of which also have an "absence of specific biological tests" themselves. By the authors implication that MCS does not exist, neither does somatization disorder or depression! In many cases, somatization disorder and depression are not actual mental illnesses, but rather symptoms caused by toxic chemical injury or an undiagnosed underlying medical condition and hence may have a biological origin.

The second page continues the misinformation with discussion of "active and sham" substances used in provocation challenges. Here, Das-Munshi claims that MCS subjects reacted to the sham substances in a test which in her perception supports her claim to a psychological origin for MCS. She failed to mention the fact that the sham substances used in the study were indeed also chemical substances. Knowing the sham substances were chemicals, it is easy to see why a chemically sensitive subject would react to the sham substances. The fact that a reaction did indeed occur to these chemicals actually supports the subjects belief that the chemicals are the cause of the reactions. Hence, she failed to examine the study close enough to uncover this crucial detail.

Das-Munshi goes on to suggest that reactions to chemicals experienced by subjects may be Pavlovian learned responses, yet there are no supporting studies for this claim. Das-Munshi's claim also fails to pass the test of logic. If, for example, an individual was fired (US) and associated the bosses cologne (CS) with ill feelings (UR/CR) in Pavlovian conditioning, then why would that individual have reactions to multiple classes of chemicals with explicitly varying odors (CR?) that are completely unrelated to the bosses cologne? Also lacking in this theory is the requirement of repeated exposure to the conditioned stimulus for learning to occur. Even if we were to go as far as saying that a subject learned to fear chemicals in general from this experience, as Little Albert learned to fear all furry animals in a classical conditioning experiment, repetition is missing. The subject would have to know that chemicals are in the cologne that the majority of the population generally regards as safe. Then the subject would need to add shampoo, glass cleaner, fabric softener, newspaper, carpet, and more to their repertoire of chemical incitants.

Das-Munshi also makes the error of assuming that co-occurring depression in a portion of subjects is the cause of MCS. If this were true, then 100% of the subjects would have co-occurring depression. Since that is not the case, depression may be ruled out as an etiologic mechanism. Das-Munshi does not examine the possibility of reactionary depression, in which people become depressed from lifestyle, financial, and social limitations as a result of a chronic illness. Reactionary depression is much more likely a result of living within the limitations of MCS. This in no way suggests that MCS itself is caused by psychological mechanisms. And indeed, no illness has ever been proven to result from psychological causes with specific biological tests. Nearly every illness known to medicine was first thought to be psychological until the biological etiology was discovered.

Das-Munshi failed to review studies on diagnosed cases of MCS that met the case criteria established by 89 clinicians and researchers in 1989 and revised in 1999, so her results are bound to be skewed and not representative of the population who meet the case criteria for diagnosis with MCS. She may well be looking at studies that do not represent the MCS population at all, but rather subjects with other etiologies for their symptoms. It is crucial that studies on MCS first apply the diagnostic criteria to subjects or select diagnosed subjects, lest the data obtained from the study be grossly flawed.

Finally, Das-Munshi's review failed to consider the variety of physiological, biochemical, and genetic studies on MCS. She has not provided any explanation for the factors distinguishing the chemicals involved in MCS from those that have no role, and she completely ignored the prospects for objective biomarker tests for MCS that have been published by Kimata, Millqvist, Bell, and Fox, each of which is based on measurable physiological changes in response to low level chemical exposures of MCS patients (Millqvist et al, 1999; Millqvist et al, 2005; Bell et al 1996; Bell et al 1998; Joffres et al, 2005). Most importantly, she has ignored the genetic data of McKeown-Eyssen and the earlier work of Haley showing that the chemicals initiating MCS act as toxicants, not as odors generating some strictly olfactory response (McKeown-Eyssen, 2004; Haley, 1999). These specific studies provide significant implication of the toxicogenic roles of chemicals previously implicated in MCS (McKeown-Eyssen, 2004; Haley, 1999).

References

Bell IR, Schwartz GE, Baldwin CM, Hardin EE. (1996). Neural sensitization and physiological markers in multiple chemical sensitivity. Regul Toxicol Pharmacol 24:S39-S47.

Bell IR, Baldwin CM, Schwartz GE. (1998). Illness from low levels of environmental chemicals: relevance to chronic fatigue syndrome and fibromyalgia. Am J Med 105:74S-82S.

Das-Munshi J, Rubin GJ, Wessely S. Multiple chemical sensitivities: review. Curr Opin Otolaryngol Head Neck Surg. 2007 Aug;15(4):274-280.

Haley, RW Billecke, S, & La Du, BN (1999). Association of low PON1 type Q (type A) arylesterase activity with neurologic symptom complexes in Gulf War veterans. Toxicology and Applied Pharmacology 157(3):227-33.

Joffres MR, Sampalli T, Fox RA. (2005). Physiologic and symptomatic responses to low-level substances in individuals with and without chemical sensitivities: a randomized controlled blinded pilot booth study. Environ Health Perspect 113:1178-1183.

Kimata H. (2004). Effect of exposure to volatile organic compounds on plasma levels of neuropeptides, nerve growth factor and histamine in patients with self-reported multiple chemical sensitivity. In J Hyg Environ Health 207:159-163.

McKeown-Eyssen, G, Baines, C, Cole, D, Riley, N, Tyndale, R, Marshall, L, & Jazmaji, V (2004). Case-control studies of genotypes in multiple chemical sensitivity: CYP2D, NAT1, NAT2, PON1, PON2 and MTHFR. International Journal of Epidemiology 33, 1-8.

Millqvist E, Bengtsson U, Lowhagen O. (1999). Provocations with perfume in the eyes induce airway symptoms in patients with sensory hyperreactivity. Allergy 54:495-499.

Millqvist E, Ternesten-Hasseus E, Stahl A, Bende M. (2005). Changes in levels of nerve growth factor in nasal secretions after capsaicin inhalation in patients with airway symptoms from scents and chemicals. Environ Health Perspect 113:849-852.

Curr Opin Otolaryngol Head Neck Surg. 2007 Aug;15(4):274-80.

Multiple chemical sensitivities: review.

Das-Munshi J, Rubin GJ, Wessely S.

Section of Epidemiology, Department of Health Services and Population Research, Institute of Psychiatry, King's College London, London, United Kingdom. spsljdm@iop.kcl.ac.uk

PURPOSE OF REVIEW: There have been a number of recent studies examining behavioural and social factors in the potential cause of Multiple Chemical Sensitivities, or Idiopathic Environmental Intolerance. The current review will draw together recent research and suggest directions for future investigation.

RECENT FINDINGS: Recent studies have implicated a number of different perspectives which may be helpful in understanding the cause of chemical sensitivities. A multifactorial model incorporating behavioural, physiological and sociological approaches may be useful. Cultural and historical factors, alongside individual expectations and beliefs, as well as maladaptive learning and conditioning processes, may be important in the specific cause of chemical sensitivities. Iatrogenesis, through the promise of unproven 'therapies', may perpetuate reported symptoms further. Although there are many recent experiments implicating potential behavioural or psychological causes for Multiple Chemical Sensitivities, there remains a paucity of treatment trials for this condition.

SUMMARY: Good-quality treatment trials examining psychological/behavioural approaches in the management of Multiple Chemical Sensitivities are urgently needed.

PMID: 17620903 [PubMed - in process]

Inside MCS America

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:
http://www.cafepress.com/mcsamerica.124654801

The same design is available on a woman's plus size scoop neck t-shirt for $29.99. This one makes a much bolder statement to the world!
http://www.cafepress.com/mcsamerica.124654492

Or, tell it like it is with a license plate frame for $14.99.
http://www.cafepress.com/mcsamerica.124654741

Community News

Community News

Radio Show:  Pushing Limits Friday, August 17th, 2007
http://kpfa.org/archives/index.php?arch=21806
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 

 

Our Assumptions About What Causes Chronic Diseases Could Be Wrong
Discoveries about how chemicals and environmental toxins interact with our DNA and make us susceptible to disease could revolutionize our concept of illness.
http://www.alternet.org/story/58482/

Chemical Company to End Use of Mercury
http://www.forbes.com/feeds/ap/2007/08/09/ap4006045.html

Staffers Say Renovation Made Them Ill
http://www.washingtonpost.com/wp-dyn/content/article/2007/08/08/AR2007080802093.html

See What You're Spewing As You Speed Along
http://www.sciencedaily.com/releases/2007/08/070805194322.htm

Cures or avoidance of Autism, ADD and many other physical and Neurological Disorders are at hand
http://www.americanchronicle.com/articles/viewArticle.asp?articleID=34488

Toxic Substances Quick Chemical Screening
http://pubs.acs.org/cen/news/85/i33/8533news5.html

Omega-3 again linked to calmer ADHD kids
http://www.nutraingredients-usa.com/news/ng.asp?n=78872&m=2NIU809&c=lnwjvmouqnsxszf

The Consumer : Cleanliness may not always be healthy
http://showbizandstyle.inquirer.net/lifestyle/lifestyle/view_article.php?article_id=81408

FEMA Finally Ends Use of Toxic Trailers
http://www.newsinferno.com/archives/1697

Omega-3 again linked to calmer ADHD kids
http://www.nutraingredients.com/news/printNewsBis.asp?id=78872

A Call to Reduce Toxic Chemicals
http://www.njbiz.com/article.asp?aID=71558

Toxic Sponge
http://www.sciencefriday.com/news/080707/aerogel0807071.html

 

Featured Research Studies

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.

Maes M, Mihaylova I, Kubera M, Bosmans E.

MCare4U Outpatient Clinics, Belgium.  Neuro Endocrinol Lett. 2007 Jul 11;28(4).

Chronic fatigue syndrome (CFS) is a medically unexplained disorder, characterized by profound fatigue, infectious, rheumatological and neuropsychiatric symptoms. There is, however, some evidence that CFS is accompanied by signs of increased oxidative stress and inflammation in the peripheral blood. This paper examines the role of the inducible enzymes cyclo-oxygenase (COX-2) and inducible NO synthase (iNOS) in the pathophysiology of CFS. Toward this end we examined the production of COX-2 and iNOS by peripheral blood lymphocytes (PBMC) in 18 CFS patients and 18 normal volunteers and examined the relationships between those inflammatory markers and the severity of illness as measured by means of the FibroFatigue scale and the production of the transcription factor nuclear factor kappa beta (NFkappabeta). We found that the production of COX-2 and iNOS was significantly higher in CFS patients than in normal controls. There were significant and positive intercorrelations between COX-2, iNOS and NFkappabeta and between COX-2 and iNOS, on the one hand, and the severity of illness, on the other. The production of COX-2 and iNOS by PBMCs was significantly related to aches and pain, muscular tension, fatigue, concentration difficulties, failing memory, sadness and a subjective experience of infection. The results suggest that a) an intracellular inflammatory response in the white blood cells plays an important role in the pathophysiology of CFS; b) the inflammatory response in CFS is driven by the transcription factor NFkappabeta; c) symptoms, such as fatigue, pain, cognitive defects and the subjective feeling of infection, indicates the presence of a genuine inflammatory response in CFS patients; and d) CFS patients may be treated with substances that inhibit the production of COX-2 and iNOS.

PMID: 17693978 [PubMed - as supplied by publisher]

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Not in the mind of neurasthenic lazybones but in the cell nucleus: patients with chronic fatigue syndrome have increased production of nuclear factor kappa beta.

Maes M, Mihaylova I, Bosmans E.  Neuro Endocrinol Lett. 2007 Jul 11;28(4)

MCare4U Outpatient Clinics, Belgium. crc.mh@telenet.be.

There is now some evidence that chronic fatigue syndrome is accompanied by an activation of the inflammatory response system and by increased oxidative and nitrosative stress. Nuclear factor kappa beta (NFkappabeta) is the major upstream, intracellular mechanism which regulates inflammatory and oxidative stress mediators. In order to examine the role of NFkappabeta in the pathophysiology of CFS, this study examines the production of NFkappabeta p50 in unstimulated, 10 ng/mL TNF-alpha (tumor necrosis factor alpha) and 50 ng/mL PMA (phorbolmyristate acetate) stimulated peripheral blood lymphocytes of 18 unmedicated patients with CFS and 18 age-sex matched controls. The unstimulated (F=19.4, df=1/34, p=0.0002), TNF-alpha-(F=14.0, df=1/34, p=0.0009) and PMA-(F=7.9, df=1/34, p=0.008) stimulated production of NFkappabeta were significantly higher in CFS patients than in controls. There were significant and positive correlations between the production of NFkappabeta and the severity of illness as measured with the FibroFatigue scale and with symptoms, such as aches and pain, muscular tension, fatigue, irritability, sadness, and the subjective feeling of infection. The results show that an intracellular inflammatory response in the white blood cells plays an important role in the pathophysiogy of CFS and that previous findings on increased oxidative stress and inflammation in CFS may be attributed to an increased production of NFkappabeta. The results suggest that the symptoms of CFS, such as fatigue, muscular tension, depressive symptoms and the feeling of infection reflect a genuine inflammatory response in those patients. It is suggested that CFS patients should be treated with antioxidants, which inhibit the production of NFkappabeta, such as curcumin, N-Acetyl-Cysteine, quercitin, silimarin, lipoic acid and omega-3 fatty acids

PMID: 17693979 [PubMed - as supplied by publisher]

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Environmental Exposure Assessment, Pollution Sources, and Exposure Agents: A Primer for Pediatric Nursing Professionals

Derek G. Shendell, D.Env, MPH; Ann Pike-Paris, MS, RN.  Pediatr Nurs. 2007;33(2):179-182. ©2007 Jannetti Publications, Inc.

Abstract

Children´s environmental health is a growing, interdisciplinary field of diverse professionals and community members working together in policy advocacy, research, health, and environmental interventions and treatment services. Understanding exposure assessment is central to improving children´s health across age, gender, indicators of socioeconomic status, and racial/ethnic groups. In general, children are more susceptible and vulnerable to adverse acute and chronic effects due to acute and chronic exposures to environmental toxicants since they eat more food, drink more fluids, and breathe in more air per unit of body weight than adults; their behaviors and rapid developmental changes also contribute to their risks. By enhancing knowledge and awareness of the basic concepts of human exposure assessment and key details of sources of environmental pollution, pediatric nursing professionals can enhance their practices — clinical and patient education skills — and thus improve daily work in their communities through the promotion of exposure reduction or prevention measures.

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Modulation of Human Glutathione S-Transferases by Polyphenon E Intervention

H.-H. Sherry Chow, Iman A. Hakim, Donna R. Vining, James A. Crowell, Margaret E. Tome, James Ranger-Moore, Catherine A. Cordova, Dalia M. Mikhael, Margaret M. Briehl and David S. Alberts.  Cancer Epidemiology Biomarkers & Prevention 16, 1662-1666, August 1, 2007. doi: 10.1158/1055-9965.EPI-06-0830.

There is now some evidence that chronic fatigue syndrome is accompanied by an activation of the inflammatory response system and by increased oxidative and nitrosative stress. Nuclear factor kappa beta (NFkappabeta) is the major upstream, intracellular mechanism which regulates inflammatory and oxidative stress mediators. In order to examine the role of NFkappabeta in the pathophysiology of CFS, this study examines the production of NFkappabeta p50 in unstimulated, 10 ng/mL TNF-alpha (tumor necrosis factor alpha) and 50 ng/mL PMA (phorbolmyristate acetate) stimulated peripheral blood lymphocytes of 18 unmedicated patients with CFS and 18 age-sex matched controls. The unstimulated (F=19.4, df=1/34, p=0.0002), TNF-alpha-(F=14.0, df=1/34, p=0.0009) and PMA-(F=7.9, df=1/34, p=0.008) stimulated production of NFkappabeta were significantly higher in CFS patients than in controls. There were significant and positive correlations between the production of NFkappabeta and the severity of illness as measured with the FibroFatigue scale and with symptoms, such as aches and pain, muscular tension, fatigue, irritability, sadness, and the subjective feeling of infection. The results show that an intracellular inflammatory response in the white blood cells plays an important role in the pathophysiogy of CFS and that previous findings on increased oxidative stress and inflammation in CFS may be attributed to an increased production of NFkappabeta. The results suggest that the symptoms of CFS, such as fatigue, muscular tension, depressive symptoms and the feeling of infection reflect a genuine inflammatory response in those patients. It is suggested that CFS patients should be treated with antioxidants, which inhibit the production of NFkappabeta, such as curcumin, N-Acetyl-Cysteine, quercitin, silimarin, lipoic acid and omega-3 fatty acids.

PMID: 17693979 [PubMed - as supplied by publisher]

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Excess dampness and mold growth in homes: an evidence-based review of the aeroirritant effect and its potential causes.

Hope AP, Simon RA.  Allergy Asthma Proc. 2007 May-Jun;28(3):262-70

Exposure to fungi produces respiratory disease in humans through both allergic and nonallergic mechanisms. Occupants of homes with excess dampness and mold growth often present to allergists with complaints of aeroirritant symptoms. This review describes the major epidemiological and biological studies evaluating the association of indoor dampness and mold growth with upper respiratory tract symptoms. The preponderance of epidemiological data supports a link between exposure to dampness and excess mold growth and the development of aeroirritant symptoms. In addition, biological and clinical studies evaluating potential causal substances for the aeroirritant effect, notably volatile organic compounds (VOCs), are examined in detail. These studies support the role of VOCs in contributing to the aeroirritant symptoms of occupants of damp and mold-contaminated homes.

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