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Thursday, 29 July 2010

London Pride And Pong

Wikipedia, under the title “Great Smog” has an article on the 1952 Great London Smog which over a period of a few days led to the deaths of around 12,000 people and had major effects on an estimated 100,000 more. It is likely that a larger number had some sort of reactions and how many might have sustained damage leading to later medical issues is not known. The figure will be high.

A few days after it ended I was down in London for several days and although at meetings in Westminster luckily was lodged in Putney which had been much less affected. Despite a few days of wind and rain the smell and foulness still persisted and everything in Central London seemed to have a coating of filth.

Much of this was relatively visible being made up of soot and other particles. It was not simply traffic fumes. This was the era of coal fires and boilers and in the central areas of London there was still a good deal of real industry and manufacturing. Also, there were coal fired power stations by the river and coal fired shipping on it. Many of the trains crossing the river were steam hauled by coal locomotives.

Earlier this week I was in London by Westminster and in Covent Garden. The air quality was foul. In my opinion we were close to being back to 1952. But this was a summer event arising from anticyclone weather, heat and high humidity. Clearly there was a great deal of traffic.

By the Embankment Station is a place where coaches pick up and put down travellers and tourists. This reduces the road to one lane in either direction and the traffic is backed up all along the river.

But a good deal of the immediate heat and bad air in the streets was being vented from all the food places and other buildings by their ventilation and air conditioning systems and it wasn’t going away. Then there were the hordes of people, snaking lines of tourists, lots of shoppers and all the workers in a hurry.

In 1952 they would smell of sweat, labour and of the smog. In 2010 many left a long trail of “fragrance” and chemical pollution behind them. The 1952 smells might be washed away, but the 2010 varieties once encountered stick and last and last and cannot be shifted. When you go home they will attach to your fabrics, permeate your wardrobe and bring the smog and filth of Central London to every corner of your home.

If you ask about it to any official body you will be told to try to avoid them and they are no aware of any figures or scientific proof. If the manufacturers are asked they say they do not go inside the body and in any case should they enter the bloodstream but some miracle of their making they cannot possibly enter the vital organs or the brain.

In 1952 as so many Parliamentarians were affected and the corpses were counted something then was done in the Clean Air Act of 1956. Nothing is going to happen now because nobody is counting. In any case all the tourists will be going home.

Monday, 26 July 2010

Wrapping Up The Future

There is an old saying that if something it too good to be true then it is too good to be true. I suspect that we may be seeing a lot of this material in the near future whether we like it or not.

Just what the implications of this nanotechnology are when applied to food wrapping and the human body are unknown. When I look at some of the nasty rashes I have had from fancy dressings I am far from sure.


ScienceDaily (July 26, 2010)

New Antibacterial Material for Bandages, Food Packaging, Shoes

A new form of paper with the built-in ability to fight disease-causing bacteria could have applications that range from anti-bacterial bandages to food packaging that keeps food fresher longer to shoes that ward off foot odor.

A report about the new material, which consists of the thinnest possible sheets of carbon, appears in ACS Nano, a monthly journal

Chunhai Fan, Qing Huang, and colleagues explained that scientists in the United Kingdom first discovered the material, known as graphene, in 2004. Since then, the race has been on to find commercial and industrial uses for graphene.

Scientists have tried to use graphene in solar cells, computer chips, and sensors. Fan and Huang decided to see how graphene affects living cells.

So they made sheets of paper from graphene oxide, and then tried to grow bacteria and human cells on top. Bacteria were unable to grow on the paper, and it had little adverse effect on human cells.

"Given the superior antibacterial effect of graphene oxide and the fact that it can be mass-produced and easily processed to make freestanding and flexible paper with low-cost, we expect this new carbon nanomaterial may find important environmental and clinical applications," the reports states.


The patent is at:

‘Ere we go again?

Thursday, 22 July 2010

Diving In The Deep End

One of the serious difficulties for people with chemical issues or MCS is how or why they became sensitised in the first place. After many years enjoying regular swims for exercise and leisure I had to give up. My skin started reacting very badly and given my more serious chemical problems it became too great a risk. This was in a Health Club pool, rather less used and more controlled than the local public one.

I had talked to the pool manager about it and he told me that that the job had become more demanding and complex in recent years. It was clear that the levels of general contamination had increased greatly causing more chlorine to be pumped in to meet the safety levels demanded.

Not only did people have far more chemical products on their skin and costumes but many fewer seemed to be showering. They believed that using a deodorant spray was a better way of freshening up for the pool.

The article below is interesting in this context.


Science News, ScienceDaily, 21 July 2010

Recreational Pool Disinfectants Linked to Health Problems

Splashing around in a swimming pool on a hot summer day may not be as safe as you think. A recent University of Illinois study links the application of disinfectants in recreational pools to previously published adverse health outcomes such as asthma and bladder cancer.

Each year, 339 million visits take place at pools and water parks across the United States. Not only is swimming fun, but it's also the second most popular form of exercise in the country. Because of this, disinfection of recreational pools is critical to prevent outbreaks of infectious disease.

However, Michael Plewa, U of I professor of genetics, said negative outcomes can occur when disinfection byproducts form reactions with organic matter in pool water.
Pool water represents extreme cases of disinfection that differ from the disinfection of drinking water as pools are continuously exposed to disinfectants.

"All sources of water possess organic matter that comes from decaying leaves, microbes and other dead life forms," Plewa said. "In addition to organic matter and disinfectants, pool waters contain sweat, hair, skin, urine, and consumer products such as cosmetics and sunscreens from swimmers."

These consumer products are often nitrogen-rich, causing concern that they may contribute to the generation of nitrogenous disinfection byproducts, Plewa added. When mixed with disinfectants, these products may become chemically modified and converted into more toxic agents.

These disinfection byproducts can mutate genes, induce birth defects, accelerate the aging process, cause respiratory ailments, and even induce cancer after long-term exposures. In this study, collections from public pools and a control sample of tap water were evaluated to identify recreational water conditions that could be harmful to your health.

A systematic mammalian cell genotoxicity analysis was used to compare the water samples. Plewa said this sensitive DNA technology examined genomic damage in mammalian cells, allowing researchers to investigate damage at the level of each nucleus within each cell.

The study compared different disinfection methods and environmental conditions. Results proved that all disinfected pool samples exhibited more genomic DNA damage than the source tap water, Plewa said.

"Care should be taken in selecting disinfectants to treat recreational pool water," Plewa advised. "The data suggest that brominating agents should be avoided as disinfectants of recreational pool water. The best method to treat pool waters is a combination of UV treatment with chlorine as compared to chlorination alone."

Plewa recommends that organic carbon be removed prior to disinfection when the pool water is being recycled.

Also, swimmers can help reduce the genotoxicity of pool water by showering before entering the water. Pool owners should also remind patrons about the potential harm caused by urinating in a pool. These simple steps can greatly reduce the precursors of toxic disinfection byproducts, Plewa said.

This research was published in Environmental Science & Technology and supported by grants from the National Science Foundation. Researchers included Michael Plewa and Elizabeth Wagner of the U of I, Danae Liviac of The Universitat Autonoma de Barcelona, and William Mitch and Matthew Altonji of Yale University.


Thursday, 15 July 2010

Poisoning Another Generation

From Grownups dot co dot nz Fyrebird in August 2008 It sums it up very well.


Is Perfume A Brilliantly Marketed Toxin?

I'm passing this article on because I, like many others today, find the smell of perfumes & colognes unpleasant at best and debilitating at worst. Now after checking out the subject on the internet I understand why I have the reactions I do, the chemicals used in these items are toxic and breathing in the fumes from them can be compared to breathing in second hand smoke.

What's the difference between perfume and pollution? Absolutely nothing. Perfumes may be sold as luxury items that enhance our wellbeing and sexuality, but at heart they are composed of neurotoxic solvents not dissimilar from those favoured by glue sniffers and volatile chemicals usually more at home in garages and industrial factories.

As far back as 1986, the US National Academy of Sciences targeted fragrance ingredients as one of six categories of neurotoxic chemicals in need of thorough investigation. This placed perfume ingredients right up there with insecticides, heavy metals, solvents and food additives as primary causes of disease in humans. But government and industry have been slow to get their acts together.

Under EU legislation there are few restrictions and even fewer outright bans on the quantities or combinations of fragrance chemicals that may be used in cosmetics. A typical perfume contains a mixture of fragrance chemicals (often between 50 and 100) mostly derived from petroleum.

These include benzene derivatives, aldehydes and many other known toxins capable of causing cancer, birth defects, central nervous system (CNS) disorders and allergic and asthmatic reactions.

These substances can get into the body by inhalation or by being absorbed through the skin. When fragrance chemicals penetrate the skin they can be toxic to the liver and kidneys.

Still others accumulate in fatty tissue and leach slowly back into the system or are passed on to children via breast milk. Inhaled, they can cause sore throat, runny nose, sinus congestion, wheezing, shortness of breath, nausea, headache, dizziness, lethargy, mood swings and muscle pain.

Perfume chemicals not only affect users but also those around them, and there are now urgent calls for second-hand scent to be considered in much the same light as we consider second-hand smoke.

There are environmental concerns as well, since fragrances are volatile compounds, which add to both indoor and outdoor air pollution. Synthetic musk compounds, for example, are carcinogenic and potential endocrine disrupters.

They are also persistent in the environment and contaminate waterways and aquatic wildlife.

The turnover of the fine fragrance market in the UK was £350B last year. Currently, the US Food and Drug Administration is considering a petition submitted by US environmental group the Environmental Health Network to have a well known perfume declared 'misbranded'. The basis of the petition is that none of the perfume's ingredients have been adequately tested for safety.

The ingredients are fairly representative of those found in all modern perfumes. While most women perceive it as a romantic floral fragrance, the reality is quite different.

Of the perfumes 41 known ingredients, 33 have no relevant safety data.
Of the rest, data suggests they are toxic, irritant, sensitising (capable of causing allergic-like reactions), damaging to the CNS and carcinogenic.

Accordingly, the campaigners want the label of this (and all other perfumes) to caution: ‘Warning: the safety of this product has not been determined.’


Benzyl Acetate: Synthetic fragrance (floral, fruity). Irritating to eyes and respiratory passages. Carcinogen, linked to pancreatic cancer.

Benzenethanol: Synthetic fragrance (sweet, floral, rose). Irritating to skin, eyes and upper respiratory tract. CNS disruption. Carcinogenic. Also affects bone marrow (the tissues that produce blood cells). Exposure can lead to aplastic anaemia, excessive bleeding, and damage to the immune system (by changes in blood levels of antibodies and loss of white blood cells).

Diethyl Phthalate: Solvent; carrier; fixative. Irritating to eyes and skin. CNS disruption. Causes fetal abnormalities. Sperm damage. Oestrogen mimic. Carcinogen.

Eugenol: Synthetic fragrance (clove oil substitute). Irritant. Contact dermatitis. Also a common fungicide, pesticide and insecticide ingredient.

Ethyl linalool; linalool: Synthetic fragrance (bergamot, French lavender). Narcotic, CNS disruption. Commonly used in pesticides.

Galaxolide 50: Synthetic fragrance (artificial musk). Hormone disruptor. Irritant. Carcinogenic.

Cyclopentadecanolide: Synthetic fragrance (artificial musk). Hormone disruptor. Irritant. Carcinogenic.

Benzaldehyde, 4-Hydroxy-3-Methoxy: Synthetic fragrance (vanilla). Irritation to the mouth, throat, eyes, skin, lungs, and the gastrointestinal tract, causing nausea and abdominal pain. Kidney damage. CNS disruption.

Benzenemethanol: Solvent (carrier for other fragrance chemicals); synthetic fragrance (sweet, floral). Irritating to skin, eyes and upper respiratory tract. CNS disruption. Carcinogen.

Phenol, 2, 6-BIS(1,1-Dimethylehyl)-4-Methyl: Fragrance; antioxidant. Irritant. Potential carcinogen. Reproductive toxin. Also used as a pesticide.


As the old saying goes, where there’s muck, there’s money.

Sunday, 11 July 2010

Bathwater For Beginners

Would you put your baby, or yourself into this? An item from Science Daily last year that explains itself.


Science Daily (August 10, 2009), Science News

Baby Bathwater Contains Fragrance Allergens

A group of chemists from the University of Santiago de Compostela (USC) has developed a method to quantify the fragrance allergens found in baby bathwater. The researchers have analysed real samples and detected up to 15 allergen compounds in cosmetics and personal hygiene products.

A team of scientists from the Department of Analytical Chemistry, Nutrition and Bromatology at the USC has developed a method to detect and quantify the 15 most common fragrance allergens included in soap, gel, cologne and other personal hygiene products.

"Applying the method to eight real samples obtained from the daily baths of a series of babies aged between six months and two years old, we discovered the presence of all the compounds under study in at least one of the samples," co-author of the study published this month in Analytical and Bioanalytical Chemistry, MarĂ­a Llompart, explained to SINC.

The scientists found at least six of the 15 compounds in all the samples. In some cases, concentrations were "extremely high", exceeding 100ppm (parts per million = nanograms/millilitre). Some of the substances that appeared were benzyl salicylate, linalol, coumarin and hydroxycitronellal.

"The presence and levels of these chemical agents in bathwater should be cause for concern," Llompart said, "bearing in mind that babies spend up to 15 minutes or more a day playing in the bath and that they can absorb these and other chemicals not only through their skin, but also by inhalation and often ingestion, intentional or not."

New Method to Detect Fragrances

Allergens were able to be detected due to the high level of sensitivity of the method, which for the first time applies the Solid-Phase Micro Extraction (SPME) technique to determining the ingredients of cosmetics and child hygiene products. This technique makes it possible to concentrate and isolate chemical components from a sample by absorbing them into fibres with a certain coating.

The researchers have also employed gas chromatography to separate compounds and mass spectrometry to identify and measure the abundance of each of the fragrances.

European regulations stipulate that the presence of such substances should be indicated on the label of the product when levels exceed a certain limit (0.1 or 0.01%, depending on the type of compound), but some associations believe these limits are excessively tolerant, particularly where child hygiene and baby and child care products are concerned.


And it is getting worse by the year, much worse.

Thursday, 8 July 2010

MCS - Progress In Recognition

This item appeared in the mail box this morning from a contact with serious MCS problems. Dr. Pall’s work has been a major advance in recognition of the nature of the issues and of interest to us all. You will not find any research of this kind being done anywhere in the UK despite the increasing number of people with severe medical issues.


Dr. Pall’s theory of Multiple Chemical Sensitivity disease mechanism confirmed by Roman study of MCS patients.

July 5, 2010 – Prohealth dot com Library

The physiological mechanism for Multiple Chemical Sensitivity proposed by biochemist Martin L. Pall has been confirmed with the recent findings of an independent research group in Rome.

Multiple chemical sensitivity (MCS), also known as chemical sensitivity and toxicant-induced loss of tolerance (TILT), is:

• A disease initiated by toxic chemical exposure,

• Leading to toxic brain injury

• That produces high level sensitivity to the same set of chemicals that are implicated in initiation of the disease.

Sensitivity responses in other areas of the body are also often seen.

“Epidemiological studies show that MCS is a stunningly common disease, even more common than diabetes,” said Pall, professor emeritus of biochemistry and basic medical sciences at Washington State University.

“My review of the literature and other research I’ve conducted over the past eleven years shows the probable central mechanism of MCS is a biochemical vicious mechanism, known as the NO/ONOO- cycle.”

Pall’s work is widely published in books and articles, the most recent of which is a chapter in the authoritative international reference manual for professional toxicologists, General and Applied Toxicology, 3rd Edition, 2009.

The NO/ONOO- cycle

The NO/ONOO- cycle, pronounced no-oh-no, is named for the chemical structures of nitric oxide (NO) and peroxynitrite (ONOO-). This biochemical vicious cycle mechanism predicts that each of the elements linked together in the cycle are elevated in patients suffering from MCS and related diseases.

Most of the elements of the cycle have been shown to be elevated in such related diseases as chronic fatigue syndrome and fibromyalgia and also in animal models of MCS. However, several cycle elements have never been measured in MCS patients.

The recent study conducted by the research group in Rome (Chiara De Luca, et al.) is significant in regard to the NO/ONOO- cycle theory because it shows that three elements of the cycle are elevated in MCS patients.

[Their report - “Biological definition of multiple chemical sensitivity from redox state and cytokine profiling and not from polymorphisms of xenobiotic-metabolizing enzymes” was published online April 27 by the journal Toxicology and Applied Pharmacology.

Those elements are the inflammatory cytokines, nitric oxide, and oxidative stress. Each of these measurements provides important confirmation of the disease mechanism proposed by Pall.

• The inflammatory cytokines and nitric oxide elevation have never before been measured in MCS patients, although they have been shown to be elevated in animal models of MCS.

• Oxidative stress has been reported in two earlier studies of MCS patients, but the data provided in the De Luca et al. study are much more extensive than are the earlier data.

Consequently, these new data all provide important confirmation of the NO/ONOO- cycle as the central disease mechanism in MCS.

The NO/ONOO- cycle also is useful in understanding the role of toxic chemicals in MCS and the role of treatment. Each of the seven classes of chemicals implicated in MCS are thought to act indirectly to increase the activity of the NMDA receptors, which are glutamate receptors for controlling synaptic plasticity and memory function.

This activity, in turn, leads to rapid increases in intracellular calcium (Ca2+), nitric oxide and peroxynitrite (ONOO-), acting to greatly stimulate the NO/ONOO- cycle.

“Many of the agents used by environmental medicine physicians to treat MCS patients can be viewed as lowering different parts of the cycle, and thus are validated in part by this mechanism,” Pall said.

“Consequently, the NO/ONOO- cycle mechanism can be viewed as validating therapeutic approaches used in environmental medicine in the U.S., in Germany and some other areas of Europe and in some other countries.”


Martin L. Pall, PhD Professor Emeritus of Biochemistry and Basic Medical Sciences Washington State University(1*) 503-232-3883

Source: Martin L Pall/Washington State University, press release, Jul 5, 2010

Note: Asked if he would have more news for us, Dr. Pall replied "There will always be more."


Tuesday, 6 July 2010

How Long Will It Take?

BBC4 repeated the “Medical Mavericks” programme last night that dealt with researchers who arrived at conclusions by unorthodox methods including experimenting on themselves. Dr. Barry Marshall featured who with Dr. Robin Warren earned a Nobel Prize for establishing that the bacteria Helicobacter Pylori playing a major role in cases of gastritis that might become severe and lead on to stomach ulcers.

For a long time ulcers had been attributed to stress, spicy foods and lifestyle eating and had been treated in various expensive ways often including major surgery. I recall too many people who suffered badly from ulcers which were then considered a curse of modern living. Marshall’s work meant that ulcers could be treated far more simply and quickly with readily available antibiotics and bismuth. He and Warren were awarded the Nobel Prize in 2007.

Despite modern communications and the rapid transmission of knowledge it still took over twenty years for most of the medical establishment and practitioners to accept Marshall’s work and more importantly to act on it. Perhaps because it was cheap and quick and meant a great many products and a great many people were affected by it. Marshall was working in Western Australia with a small number of people in a community that were happy with independent thinkers.

If we look back across history we can see much longer periods before medical and other authorities accepted that major medical issues were caused or affected by things they did not allow for or expect. It often took someone who was on the fringe of the profession or even an outsider to make the critical breakthrough and often they received few thanks or recognition. Read the medical histories and those of industrial development for the many examples.

In my lifetime it took a long time before it was recognised that tobacco had adverse effects and consequences. The Prime Minister, Harold Macmillan (1957-1963) famously refused to allow the matter to be discussed in Cabinet on the grounds that smoking was no more dangerous than crossing the road. I wonder if he ever tried to cross The Strand or Oxford Street, or even Whitehall on a busy weekday?

His refusal might have had something to do with the duties on tobacco which yielded 17% then of tax revenues and the number of marginal constituencies with large tobacco factories in them. Never mind the number of members of his cabinet or party in the House of Commons with financial and other interests in the industry. Also despite the UK’s continuing problems with the Balance of Trade in which tobacco imports were a major item, but most of it came from the USA, and of course there was the Special Relationship to worry about.

I am clear in my mind that there is a substantial public health crisis in train and will soon emerge. It arises from the extent of chemical contamination of our daily lives and the impact on the human body. What I believe is one of the worst areas of this is the unregulated, irresponsible and extensive impact of the synthetic fragrance industry. It is going to hit, to hit hard and not just some time in the distant future.

One thing that will be certain will be the difficulty of gaining acceptance of the idea that severe air pollution can cause health problems. You might think you already know this. We accept that coal miners and quarry workers are at high risk. We accept that factory workshops need thorough ventilation. We accept that traffic emissions are a real problem. We accept that tobacco can cause many people severe health issues. We accept that millions of people were gassed to death in the Second World War.

But the media, the government and their related interests will never accept that pumping unlimited amounts of synthetic chemicals into our lungs can ever cause a problem so long as they are labelled as fragrances.

Saturday, 3 July 2010

Sniffing Can Damage Your Health

Another long article culled from Science Daily, but not so hard as the last one. Mostly because those who suffer from asthma and/or strong fragrance reactions and others will be able to work out exactly what it means. Given the rapid and huge expansion of putting fine particles into day to day consumer products it might bear out my forecasts of a public health disaster on its way.
From Science Daily of 1st July 2010

Ultrafine Particles in Air Pollution May Heighten Allergic Inflammation in Asthma

A new academic study led by UCLA scientists has found that even brief exposure to ultrafine pollution particles near a Los Angeles freeway is potent enough to boost the allergic inflammation that exacerbates asthma.

Published online in the American Journal of Physiology-Lung Cellular and Molecular Physiology in June, the study shows that the tiniest air pollutant particles, those measuring less than 180 nanometers, or about one-thousandth the width of a human hair, incited inflammation deep in the lungs.

The researchers used a "real-time" testing method in an animal model to isolate the effects of vehicular emission particles on the immune response in the lung.

Since these ultrafine particles are primarily derived from vehicular emissions and are found in highest concentrations on freeways, the results have particular significance for the study of the impact of traffic-related emissions on asthma flares in urban areas.

The findings also point to the importance of understanding the role air-pollution particles play in asthma flares in order to develop new approaches for asthma therapy.

"The immune processes involved in asthma, and current treatments, are traditionally thought to be dominated by a specific initial immune response, but our study shows that ultrafine pollution particles may play an important role in triggering additional pathways of inflammation that heighten the disease," said the study's principal investigator, Dr. Andre E. Nel, professor of medicine and chief of nanomedicine at the David Geffen School of Medicine at UCLA.

Pollution particles emitted by vehicles and other combustion sources are coated with a layer of organic chemicals that can be released into the lungs. These chemicals generate free oxygen radicals, which excite the immune system in the lung through a cell and tissue damaging process known as oxidation. Oxidation contributes to allergic inflammation in the lungs of people with asthma.

Although other studies have shown that larger air-pollution particles can cause an oxidative response in asthma, this is the first study to show that real-time breathing of collected ultrafine pollutant particles triggers the same reaction and may even be more damaging, due to the particles' tiny size, the researchers noted.

Because of their size and large surface area, ultrafine particles have the capacity to carry and deposit a rich load of active organic chemicals deep in the lung. The chemicals coming off the particles in the small airways in the lung promote oxidative stress at those sites.

In the study, researchers initially gave mice a surrogate allergen, similar to exposing humans to an allergen such as pollen. After further sensitization, half the mice received ultrafine pollutants, taken in real time near a freeway in downtown Los Angeles, while the other half breathed filtered air.

The study utilized sophisticated exposure technologies developed by Dr. Costas Sioutas, the Fred Champion Professor of Civil and Environmental Engineering at the University of Southern California and co-director of the Southern California Particle Center.

The multicampus team also included researchers from Michigan State University and the University of California, Irvine. The research at the Southern California Particle Center and the UCLA Asthma and Allergic Disease Center was funded by the U.S. Environmental Protection Agency and the National Institutes of Health.

Researchers found that exposure to air containing ultrafine particles for a few hours a day over five days significantly enhanced allergic airway inflammation, which correlated to the changes found in the immune system and genes expressed.

Scientists discovered that the most profound effects of the allergic inflammation were observed deep in the lung. "We found that even small exposure amounts to the ultrafine particles could boost the pro-inflammatory effects," said first author Ning Li, an assistant researcher in the UCLA Division of Nanomedicine.

The level of ultrafine particle exposure in the study was two to five times higher than levels commuters are subject to while traveling in their vehicles on Los Angeles freeways.

Researchers noted that the development of asthma may be more complicated than originally thought, with mounting evidence pointing to the involvement of additional pathways of immune activity associated with the effects of oxidative stress.

"A number of new therapies are now targeting the role of oxidative stress in asthma exacerbation," Nel said. "One possible strategy may be the use of antioxidants that may interfere with development of oxidative stress."

In addition to new considerations for asthma treatment, the study findings may also help epidemiologists further establish the link between surges of pollutants near freeways and asthma flares and to pinpoint the amount of ultrafine particle concentrations involved.

The next stage of research will help identify the chemical components responsible for boosting the effect of particulate pollutants on the allergic inflammation found in asthma and will explore the immunological mechanisms behind it at the molecular level.

Asthma, which affects 15 to 20 million people in the United States, is a chronic inflammatory disease of the small airways in the lung and can trigger acute episodes of airway tightening and wheezing.

Other study authors included Jack R. Harkema, Ryan P. Lewandowski, Meiying Wang, Lori A. Bramble, Glenn Gookin, and Zhi Ning.
No further comment.