SAN FRANCISCO – The U.S. Environmental Protection Agency has filed suit against San Leandro based VF Corporation for the alleged sale and distribution of unregistered pesticides through their retail company, The North Face.

The EPA maintains that The North Face made unsubstantiated public health claims regarding unregistered products, and their ability to control germs and pathogens — a violation of the Federal Insecticide, Fungicide, and Rodenticide Act. Products discovered online and evidence found at The North Face retail store in San Francisco led the Agency to issue a complaint against the VF Corporation.

“The EPA takes very seriously its responsibility to enforce against companies that sell products with unsubstantiated antimicrobial properties,” said Katherine Taylor, associate director of the Communities and Ecosystems Division in EPA’s Pacific Southwest region. “Unverified public health claims can lead people to believe they are protected from disease-causing organisms when, in fact, they may not be.”

At issue were more than 70 styles of footwear that incorporated an AgION silver treated footbed. The company sold the products making unsubstantiated claims that the footwear would prevent disease-causing bacteria. Specifically, The North Face made the following public health claims about the footwear on-line and on product packaging:

• “AgION antimicrobial silver agent inhibits the growth of disease-causing bacteria”
• “Prevents bacterial and fungal growth”
• Continuous release of antimicrobial agents

After being contacted by EPA, The North Face stopped making claims that their footwear protects against germs, removed claims from their website, and revised their product packaging.

Products that kill or repel bacteria or germs are considered pesticides, and must be registered with the EPA prior to distribution or sale. The Agency will not register a pesticide until it has been tested to show that it will not pose an unreasonable risk when used according to the directions. Consumers should be careful to look for the EPA registration number printed on product labels, and to follow the directions for proper use.

Reference: EPA, “The North Face” Clothing Parent Company Facing Nearly $1M in Federal Fines Following Unsubstantiated Product Claims, 09/22/2009

To clarify the effect of indoor air pollutants on nerve growth factor (NGF) production in lung, male C3H/HeN mice were exposed to filtered air (control) or toluene at levels of 0.9ppm, 9ppm, or 90ppm for 30min via nose-only inhalation on days 0, 1, 2, 7, 14, 21, 28, 35, 42, 49 and 56. As an allergic mouse model, some mice (n = 24) were immunized with ovalbumin. Lungs from each mouse were collected to determine NGF and related receptor expressions using real-time reverse transcription polymerase chain reaction (RT-PCR) analysis. NGF and TrkA mRNAs were increased in the lungs of the immunized mice following exposure to 9ppm toluene (n = 6, P < 0.05 vs. 0ppm). Remarkably increased NGF-positive bronchiolus and alveolar epithelium cells were observed in 9ppm toluene-exposed, immunized mice. To determine NGF mediating signaling, we also examined mRNA expression of neurotrophin receptor p75 (p75(NTR)) and oxidative stress marker, heme oxygenase (HO)-1 in the lung. There is no difference in the expressions of p75(NT) and HO-1 between toluene-exposed and control mice. The expression of CCL2 and CCL3 mRNAs was significantly elevated in 9ppm toluene-exposed, immunized mice. These findings suggest that the exposure with volatile organic compounds enhanced NGF expression and airway inflammation stronger in allergic individuals than in healthy individuals.

Reference: Fujimaki H, Tin-Tin-Win-Shwe, Yamamoto S, Nakajima D, Goto S., The expression of nerve growth factor in mice lung following low-level toluene exposure, National Institute for Environmental Studies, Tsukuba, Ibaraki, 305-8506 Japan, Toxicol Lett. 2009 Sep 15.

Studies show chemicals act as toxicants in causing cases of Multiple Chemical Sensitivity; genes that metabolize these chemicals into other forms influence, therefore, susceptibility to getting MCS.

Guest post at Canary Report by Martin L. Pall, Professor Emeritus of Biochemistry and Basic Medical Sciences, Washington State University and Research Director, the Tenth Paradigm Research Group.

Martin Pall: I have emailed the following as an open letter to the Denver Post in response to the article on multiple chemical sensitivity (MCS) that was published this weekend. I think the published article was generally a step forward in terms of public understanding of MCS. But the article left out a number of important things and this letter is an attempt to deal with some of those. I have asked them to consider publishing this as an Op-Ed piece, but wanted to make it available regardless of whether or not they opt to do so.

Thank you for writing this article on multiple chemical sensitivity (MCS), the term that is used in most of the scientific literature on this disease. There are vast numbers of people who have been afflicted in this epidemic of chemical sensitivity and I am sure that they are all thanking you. I also thank you for mentioning a bit of my work on this disease.

Some of your readers have already made quite a number of important points about MCS so I can focus here on just a few remaining issues. How do chemicals act in MCS? We know now that the seven classes of chemicals implicated in MCS all produce a common toxic response in the body, excessive activity of a receptor in the body called the NMDA receptor. So even though we have a vast array of such chemicals, we know how they can produce similar responses in people.

There is compelling genetic evidence that these chemicals act as toxic agents (toxicants) in the body. Four such studies have been published by three research groups in three countries. Collectively they implicate six genes as influencing susceptibility to MCS, such that people carrying some forms of each of these genes are more susceptible to becoming chemically sensitive than are people carrying other forms of the same genes. All of these genes control the activity of enzymes that metabolize these chemicals into other forms. Most of these studies show a high level of what is called statistical significance. In the Schnakenberg and colleagues studies, the chances of getting their results by chance are less than one in a million billion. So obviously, these are not chance results. What these studies show is that chemicals are acting as toxicants in causing cases of MCS and that genes that metabolize these chemicals into other forms influence, therefore, susceptibility to getting MCS. These studies, then, provide compelling evidence that cases of MCS are caused by toxic chemical exposure. Clearly they also show that MCS is a real disease, otherwise one would not be able to do such studies clearly linking the chance of becoming ill with MCS to the action of chemicals acting as toxicants.

Dr. Herman Staudenmayer has, for some 20 years claimed just the opposite. He claims that MCS is psychogenic, caused by psychological responses and according to him, is not a toxicological phenomenon. He has maintained this claim by ignoring contrary data wherever it occurs. He has ignored all of the evidence that chemicals implicated in MCS produce a common response in the body; he has ignored the roughly two dozen studies showing that MCS patients show objectively measurable responses to low level chemical exposures, responses that differ from those of normals. He has ignored all of the evidence implicating excessive NMDA activity in MCS; he has ignored the dozens of animal model studies on MCS; he has ignored over 50 studies that show that cases of MCS typically occur following chemical exposures; he has ignored the various other measurable physiological changes reported to occur in MCS. This has all been documented in my book “Explaining – Unexplained Illnesses” and in my article on the toxicology of MCS that is coming out next month in a prestigious reference work for professional toxicologists “General and Applied Toxicology, 3rd Edition”. It is also documented on the MCS web page of my web site: The Tenth Paradigm

Clearly you cannot do science by simply ignoring the existence of vast arrays of contrary data. However, Staudenmayer provides us with a couple of other tests of his views in his book, predictions that allow us to test his theory. He predicts that psychological factors are necessary and sufficient to account for the properties of MCS. This, of course, is contradicted by all of the evidence I referred to earlier. Therefore we should reject his hypothesis based on his own prediction. He provides a second prediction as well (the exact quotes from his book on these predictions are provided on my MCS web page). He predicts that the variation of susceptibility to MCS is not caused by variable responses to toxic chemicals. Clearly the genetic studies discussed above have shown that this is false and therefore, his hypothesis should be rejected for that reason, as well.

It is clear, from the above, that Staudenmayer’s construct was basically a house of cards. Now that it has collapsed, where does that leave us?

Firstly it leaves us with reversing the errors of the past. We need to start treating MCS sufferers as victims of unsafe chemical exposure. Many of them have previously been used, abused and discarded. If we live in a society where people are not disposable items we need to “do unto others as you would have others do unto you.”

We obviously need to start regulating chemical usage much more carefully, to avoid initiating new cases of MCS. It is imperative to develop tests for chemical activity in MCS, just as we have developed tests for chemical activity as carcinogens. Then we need to use these tests to effectively regulate the use of toxic chemicals.

We need to develop specific biomarker tests for MCS, tests that can be used to objectively confirm diagnoses initially based on subjective symptoms. I think we already have several very promising approaches to doing this in the scientific literature and a minimal amount of further study may be all that is needed to develop such tests.

We need to confirm that chemical avoidance is key to therapy and to develop other therapeutic approaches to work along with avoidance. The environmental medicine physicians and others have already made very important progress in this direction and I am optimistic that further progress can be made quickly. Such progress is relevant not only to the treatment of MCS patients but also to the treatment of clearly related diseases including chronic fatigue syndrome/mylagic encephalomyelitis and fibromyalgia. All of these diseases are caused by what I have called the NO/ONOO- cycle and the way to treat them, in my judgment, is to lower the activity of that vicious cycle mechanism.

Martin L. Pall

Professor Emeritus of Biochemistry and Basic Medical Sciences, Washington State University and Research Director, the Tenth Paradigm Research Group

Reprinted with permission from the author. Dr. Pall cautions the reader that he is a PhD, not an MD, and none of this should be viewed as medical advice.

• Original Article posted by Canary Report Thank you for the permission to reprint Susie!
• Link to Martin Pall’s website: The Tenth Paradigm
• Link to an extended excerpt from Palls book Explaining “Unexplained Illnesses.”

Study shows deterioration in brain function following breast cancer therapy has negative effects on quality of life

One of the most problematic side effects of cancer treatment, chemobrain – a range of symptoms including memory loss, inability to concentrate, difficulty thinking and other subtle cognitive changes following chemotherapy – seriously diminishes women’s quality of life and daily functioning. As a result, they have to adopt a range of coping strategies to manage their restricted social and professional lives.

Breast cancer survivors tell their story in a descriptive study (1) of the effects that cognitive impairment has on women’s work, social networks and dealings with the health care profession. Dr. Saskia Subramanian from the UCLA Center for Culture and Health in the US and her colleagues have just published their work online in Springer’s Journal of Cancer Survivorship.

An increasing number of women survive breast cancer, yet survival comes at a price. Mild cognitive impairment following chemotherapy, known as “chemobrain” or “chemofog” is one of the most commonly reported post-treatment symptoms by breast cancer survivors. Dr. Subramanian and colleagues’ work shows that this deterioration in brain function has devastating effects on breast cancer survivors’ quality of life.

Through a combination of focus groups and in-depth interviews among 74 women who had completed their course of cancer treatment at least a year earlier, the researchers gathered data on patients’ medical background, treatment experience, post-treatment symptoms, reactions from medical staff and from family and friends, self-management, strength of social networks and their perceptions of themselves.

The women described a variety of cognitive changes which they found both frustrating and upsetting. Some were less able to retain material or to digest new information and recognized that they were not functioning as they once did. Others faced reduced independence, becoming limited in their ability to manage certain responsibilities or get around. These changes made women feel scared, dependent and emotionally drained. For some, coping meant having to cut back on work and social activities. Others had more or less accepted the limitations put on their lives and resigned themselves to a diminished cognitive capacity.

The majority of women complained about the lack of acknowledgement from the medical community when they mentioned their chemobrain symptoms. Many women wished they had received some warning and only a few got answers from their physicians. Some women felt that chemobrain confused their families and friends, and young children in particular.

Chemobrain also affected women’s performance at work. Because they were less able to focus, duties became more difficult and often took longer. This affected their efficiency and reduced their chances of promotion or assignment to projects.

The authors conclude: “These data underscore the very serious ways in which chemobrain can affect the life experiences of cancer survivors – emotionally, psychologically and economically. A clear understanding of the cognitive impairments experienced by survivors will aid researchers in developing targeted therapies and interventions aimed at improving or mitigating these post-treatment side effects.”

Reference:   Boykoff N, Moieni M, Subramanian S (2009). Confronting chemobrain: an in-depth look at survivors’ reports of impact on work, social networks, and health care response. Journal of Cancer Survivorship; DOI: 10.1007/s11764-009-0098-x

In the air, it is a serious pollutant. In the body, it plays a role in heart rate, blood flow, nerve signals and immune function. 

Nitric oxide, a gas well known to scientists for its myriad functions, has proven challenging to measure accurately outside the laboratory. A team of Princeton and Rice University researchers has demonstrated a new method of identifying the gas using lasers and sensors that are inexpensive, compact and highly sensitive. Such a portable device, suitable for large-scale deployment, could be of great value to atmospheric science, pollution control, biology and medicine. 

Nitric oxide is so potent that a few molecules of it per billion, or even trillion, molecules of air promote smog, acid rain and depletion of the ozone layer. Similarly tiny amounts in a patient’s breath could help diagnose asthma and other disorders. 

The researchers believe their device could find uses ranging from the study and control of car and truck emissions to monitoring human exposure to pollutants in urban and industrial environments. For medical uses the device is particularly attractive because the results are not corrupted by water vapor, which is present in breath samples. Testing for nitric oxide in a patient’s breath, for example, could reveal chronic obstructive pulmonary disease and inflammation. 

“The sensor we’ve developed is much more accurate and sensitive than existing systems, yet is far more compact and portable,” said Gerard Wysocki, assistant professor of electrical engineering at Princeton.

Wysocki is a co-leader of a team that developed the system and conducted preliminary tests during the 2008 Olympic Games in Beijing. The team included Rice researchers Frank Tittel and 1996 Nobel laureate Robert Curl, both pioneers in the field of molecular detection using lasers, as well as RafaÅ‚ Lewicki and James Doty III, also of Rice. The team published its results in the Aug. 4 issue of the Proceedings of the National Academy of Sciences. 

With improvements made after the Beijing test, the system could be made into a portable, shoe-box-sized device ideally suited for mass deployment in large-scale unattended sensor networks for global, real-time, continuous monitoring of nitric oxide and other gases present in trace amounts. 

Existing systems to detect nitric oxide and other trace gases have a variety of drawbacks. Some, such as carbon monoxide sensors for homes, are compact and inexpensive, but not very sensitive. These sensors can at best detect gases at parts-per-million concentrations — they can’t handle the parts-per-billion level, let alone the parts-per-trillion level that some applications require. High-end systems, such as mass spectrometers and gas chromatographs, are much more sensitive, but are slow, bulky, complicated and expensive — and impractical for use outside of a lab. 

Of intermediate sensitivity are optical systems that pass a laser beam through a gas sample and detect whether some of the laser light is absorbed by the gas sample. A weakness of this method is that the amount of absorption is very small compared to the overall amount of laser light, so the signal is hard to detect. Further, conventional optical sensors tend to be bulky, use large amounts of the sample, and require frequent operator intervention. 

The new system developed by Princeton and Rice researchers uses optical sensing as well, but produces a much stronger signal. In their setup, the researchers passed the laser light through polarizing filters that block all light unless nitric oxide is present. Roughly speaking, the more nitric oxide, the more light makes it through the filters, Wysocki said. “There’s no background signal to worry about.” 

Nitric oxide detectors have used similar methods before, but until now have been hampered by their reliance on large laser sources designed for laboratory use, he said. The new system, in contrast, uses a quantum cascade laser, a state-of-the-art device ideally suited for this sensing technique. This makes it possible to reliably detect the gas at a concentration of a few parts-per-billion. The device is so precise it can distinguish between different isotopes of nitrogen and oxygen in the nitric oxide molecules. 

“It’s remarkable we have that kind of sensitivity,” said Curl, who laid the groundwork for the detection technique in a paper he co-wrote with Tittel nearly 30 years ago. 

“A portable sensor that can continuously measure nitric oxide with such high sensitivity is a real breakthrough,” said Tittel.

Unlike other systems that need several liters of the sample gas, the new sensor needs only a few milliliters of it, inside a container just about 16 inches long and a half inch in diameter. This frugality is particularly important in delicate biological applications such as cell-culture studies, said Wysocki. Also important, the new system can run much longer without intervention — several hours compared to just a few minutes for even the best existing ones — which will allow for long-term unattended operation. 

Princeton researchers are working on various enhancements to the technology, further shrinking the size of the device and exploring an even more sensitive method of analysis called coherent detection. “This technique could help us achieve parts-per-trillion sensitivity,” Wysocki said. 

Reference: Princeton University, Portable and precise gas sensor could monitor pollution and detect disease, September 18, 2009

Picture: Frank Wojciechowski, Princeton University