Scientists Urge UN to Take Action on Chemicals in Consumer Products and Pesticides

A group of influential scientists have called for swift action by the UN to prevent harm from a wide variety of synthetic chemicals in consumer products and pesticides that play a role in increased incidences of reproductive diseases, cancer, obesity, and type-2 diabetes worldwide.

The scientists include authors of a recent report by the World Health Organization (WHO) and the United Nations Environment Program (UNEP), which underlines the urgent need for global action to address the dangers of hormone or endocrine disrupting chemicals (EDCs).

The scientists’ statement is part of a growing international effort to identify and control the harmful effects of chemicals that damage hormonal (endocrine) systems in humans and wildlife that is supported by more than 100 countries engaged in a process to develop a global plan for the safe management of chemicals.

“Exposure to EDCs during fetal development and puberty plays a role in the increased incidences of reproductive disease, endocrine-related cancers, behavioral and learning problems including ADHD, infections, asthma and perhaps obesity and diabetes in humans,” said William F. Young, Jr., MD, president of The Endocrine Society, the most active organization devoted to research on hormones and the clinical practice of endocrinology. The Society’s 2009 Scientific Statement on EDCs was the first in-depth scientific report to draw attention to the unique properties of these chemicals, and the Society and its members remain active in advancing endocrine science and the knowledge of how EDCs affect health.

EDCs are commonly found in food and food containers, plastic products, furniture, toys, carpeting, building materials, and cosmetics. EDCs include chemicals such as bisphenol A (water bottles, can linings), certain phthalates (various plastic products and cosmetics), and pesticides such as chlorpyrifos (used on a wide variety of food crops). They are often released from the products that contain them and enter the bodies of humans and wildlife through dust or through the food chain. Tests show the presence of dozens of chemicals with hormone disrupting properties in people, including developing children. Manufacturers of suspected EDCs include some of the world’s largest chemical manufacturers, such as Exxon Mobil, Dow, DuPont, BASF, Monsanto, Eastman Chemical, and others.

In their letter addressed to UNEP, WHO, Organization for Economic Cooperation and Development (OECD) and the Strategic Approach to International Chemicals Management (SAICM), the scientists recommended a number of key principles, supported by current scientific research, to guide upcoming efforts in this area.

A clear definition of EDCs. Endocrine disrupting chemicals are chemicals, or chemical mixtures, that interfere with normal hormone action.

Vulnerability of living organisms. Hormones and their signaling pathways are critical for normal functioning in all vertebrates and invertebrates.

EDCs effects occur at low doses. Many EDC effects occur at low doses even when high dose effects are not apparent.

EDCs can affect future generations and timing of exposure is key. The most sensitive period is during periods of development, from the fetal and post-natal periods, which can extend into infancy and childhood for some tissues.

Exposure to EDC mixtures may be different than exposure to single substances. Humans and animals are exposed to complex mixtures of hundreds of EDCs.

The Precautionary Principle is key. Decision-making should err on the side of precaution.
“EDCs present unacceptable risks to human health and the environment, and that is why more than 100 governments reached consensus agreement that action is needed,” said Olga Speranskaya, co-chair, IPEN. “In our letter, we outline the most important principles for actions on EDCs. We urge the international agencies to utilize these principles as the basis for moving forward as quickly as possible.”

A recent report from WHO and UNEP, State of the Science of Endocrine Disrupting Chemicals, 2012, said that recent increases in the incidence of endocrine-related diseases in people and wildlife cannot be explained by genetics alone and that EDCs are a “global threat that needs to be resolved.” A recent editorial in Environmental Health Perspectives, a leading, peer-reviewed journal, identified EDCs as a global problem requiring global solutions. And more than 100 countries participating in an international process for implementing a global safe chemicals management plan (SAICM) reached consensus agreement that EDCs are an emerging issue requiring capacity building and awareness-raising and the translation of research results into control actions.

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New breath test for lung cancer uses CSI-like tech

A Canadian company that specializes in infrared technologies for breath analysis says it's come up with a test that can detect lung cancer with 98.5% accuracy.

The Picomole breath test for lung cancer is based on the quantitative analysis of a small set of
trace chemicals found in exhaled breath samples.

The pilot study of 40 clinical samples included healthy controls as well as patients diagnosed with other pulmonary diseases.

The results indicated the test had a sensitivity of 100% and a specificity of 97% in the detection of lung cancer.

“The results of the pilot study are very promising. From a clinical point of view, the breath test is
a fast and non-invasive method to detect disease-specific metabolomic abnormalities,” says
Picomole founder Dr. John Cormier, PhD, who will present the results of the pilot study at an
upcoming conference. “The chemicals in the Picomole breath test include novel biomarkers that
were not previously identified in any lung cancer study, demonstrating the power of our infrared
technology.”

"A rapid and non-invasive test for the early detection of lung cancer such as the breath test
being developed by Picomole could have a tremendous effect on decreasing the morbidity and
mortality associated with lung cancer,” says Dr. Ali Mahtabifard, MD, an expert in minimally
invasive surgery for lung cancer at Cedars-Sinai Medical Center. “The clinical significance of
such a test cannot be overstated."

“Most lung cancers do not cause any symptoms until they have spread too far to be cured.
Current technologies used in the detection of lung cancer are inadequate for mass screening
applications. As a result, lung cancers exact a staggering toll, killing roughly 1.4 million people
each year worldwide,” says Michael Tripp, Picomole Vice-President of Corporate Development.
“In the foreseeable future, a Picomole breath test could become an important tool in the fight
against lung cancer, one that is safe, low-cost, and does not expose patients to radiation.”

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New immune cells hint at cause of eczema and allergic skin diseases

Photo: Allergic Dermatitis / Arztsanui

Sydney researchers have discovered a new type of immune cell in skin that plays a role in fighting off parasitic invaders such as ticks, mites, and worms, and could be linked to eczema and allergic skin diseases.

The team from the Immune Imaging and T cell Laboratories at the Centenary Institute worked with colleagues from SA Pathology in Adelaide, the Malaghan Institute in Wellington, New Zealand and the USA.

The new cell type is part of a family known as group 2 innate lymphoid cells (ILC2) which was discovered less than five years ago in the gut and the lung, where it has been linked to asthma. But this is the first time such cells have been found in the skin, and they are relatively more numerous there.

“Our data show that these skin ILC2 cells can likely supress or stimulate inflammation under different conditions,” says Dr Ben Roediger, a research officer in the Immune Imaging Laboratory at Centenary headed by Professor Wolfgang Weninger. “They also suggest a potential link to allergic skin diseases.”

The findings have been published in the respected journal Nature Immunology.

“There’s a great deal we don’t understand about the debilitating skin conditions of allergies and eczema,” says Professor Weninger, “but they affect hundreds of millions of people worldwide. Dermal ILC2 cells could be the clue we need to start unravelling the causes of these diseases.”

The Weninger lab, which has developed techniques for marking different cells of the immune system and tracking them live under the microscope, actually discovered the new dermal cells some years back. “We just didn’t know what they were,” Roediger says.

The Centenary researchers, however, suspected they might be associated with type 2 immunity, the part of the immune system that deals with infection by parasitic organisms. So they contacted Professor Graham Le Gros at the Malaghan Institute, one of the world’s foremost researchers into type 2 immunity.

Not only did Professor Le Gros and his team confirm that the Centenary researchers had found a new form of ILC2 cell, but they were able to provide a new strain of mouse developed in the USA that provided insight into the function of these cells.

“Using these mice, we found that ILC2 cells were the major population in the skin that produced interleukin 13, a molecule that has been linked to a number of allergic diseases, including eczema.” Roediger says.

Using their sophisticated live imaging techniques, the Centenary researchers were also able to watch the behaviour of the ILC2 cells in the skin, where they moved in a characteristic way—in random spurts punctuated by stoppages.

“A halt in movement usually indicates some sort of interaction with another cell,” Roediger says. In this case, the ILC2 cells always seemed to stop in close proximity to mast cells, which are known to play a key role in controlling parasitic infections and to be associated with allergies.

As well as the interaction with mast cells, the Centenary team were able to show that ILC2 cells could be stimulated to spread quickly and were capable of generating the inflammatory skin disease.

“We now have experiments underway in which we are actively looking for the direct involvement of these cells in the sort of skin diseases you would predict based on these findings,” says Roediger.
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Free Mold Removal Training Classes for New Jersey Residents Recovering from Superstorm Sandy: April 27th, 29th, May 4th

With mold being a pervasive problem for residents recovering from Superstorm Sandy, the New Jersey Department of Health has provided UMDNJ-School of Public Health with a $125,000 grant to provide free training on mold assessment and removal for homeowners.

Registration information for classes for homeowners and volunteers can be found on the UMDNJ-School of Public Health website http://ophp.umdnj.edu/moldtraining and the Department of Health Hurricane Recovery website at http://nj.gov/health/er/hurricane_recovery_resources.shtml.

Topics covered in this training includes awareness of mold, safe work practices, personal protective equipment, respiratory protection and best practices for remediation.
 
Upcoming dates for free training for residents are:

• April 27: Atlantic County Training Center, Egg Harbor Twp.
• April 29: Rockaway Township Municipal Building, Rockaway
• May 4: Stafford Municipal Building, Manahawkin

For more information on these classes, please contact Mitchel Rosen at the UMDNJ-School of Public Health at mrosen@umdnj.edu.

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Take the train? Microscopic subway dust may pose health risk

New research from the University of Southampton in the UK has found that working or traveling on an underground railway for a sustained period of time could have health implications.

Matt Loxham, PhD student at the University of Southampton, explains: "We studied the ultrafine dust (or particulate matter) found in an underground station in Europe. Typically, ultrafine dust is composed of inert matter that does not pose much of a risk in terms of its chemical composition. However, in the underground station we studied, the ultrafine dust was at least as rich in metals as the larger dust particles and therefore, taken together with their increased surface area to volume ratio, it is of potential significance in understanding the risks of working and travelling in the underground. These tiny dust particles have the potential to penetrate the lungs and the body more easily, posing a risk to someone's health."

While coarse dust is generally deposited in the nasal passages and bronchi, fine dust generally can reach the bronchioles (smaller airways). The ultrafine dust meanwhile, is able to reach the deepest areas of the lungs, into the alveoli. There is evidence that this ultrafine dust may be able to evade the protective barrier lining the airways, and enter underlying tissue and circulation, meaning that the toxicity of ultrafine particles may not be limited to the airways but may involve the cardiovascular system, liver, brain, and kidneys.

"Underground rail travel is used by great numbers of people in large cities all over the world, for example, almost 1.2 billion journeys are made per year on the London Underground. The high level of mechanical activity in underground railways, along with very high temperatures is key in the generation of this metal-rich dust, and the number of people likely to be exposed means that more studies into the effects of particulate matter in the underground railway environment are needed, as well as examining how the levels of dust and duration of exposure might translate to effects on health."

Further work is now being performed to examine the effects of underground dust on airway cells in more detail and the potential mechanisms by which cells may be able to protect themselves.

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Air pollution speeds up hardening of arteries

Long term exposure to air pollution may be linked to heart attacks and strokes by speeding up atherosclerosis, or "hardening of the arteries", according to a study by U.S. researchers published in this week's PLOS Medicine.

The researchers, led by Sara Adar, John Searle Assistant Professor of Epidemiology, University of Michigan School of Public Health, and Joel Kaufman, Professor of Environmental and Occupational Health Sciences and Medicine, University of Washington, found that higher concentrations of fine particulate air pollution (PM2.5) were linked to a faster thickening of the inner two layers of the common carotid artery, an important blood vessel that provides blood to the head, neck, and brain. They also found that reductions of fine particulate air pollution over time were linked to slower progression of the blood vessel thickness. The thickness of this blood vessel is an indicator of how much atherosclerosis is present in the arteries throughout the body, even among people with no obvious symptoms of heart disease.

"Our findings help us to understand how it is that exposures to air pollution may cause the increases in heart attacks and strokes observed by other studies," Adar said.

The authors reached these conclusions by following 5362 people aged between 45 to 84 years old from six U.S. metropolitan areas as part of the Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air). The researchers were able to link air pollution levels estimated at each person's house with two ultrasound measurements of the blood vessels, separated by about three years. All participants in their study were without known heart disease.

After adjusting for other factors such as smoking, the authors found that on average, the thickness of the carotid vessel increased by 14 µm each year. The vessels of people exposed to higher levels of residential fine particulate air pollution, however, thickened faster than others living in the same metropolitan area.

"Linking these findings with other results from the same population suggests that persons living in a more polluted part of town may have a 2 percent higher risk of stroke as compared to people in a less polluted part of the same metropolitan area," Adar said.

"If confirmed by future analyses of the full 10 years of follow-up in this cohort, these findings will help to explain associations between long-term PM2.5 concentrations and clinical cardiovascular events," the authors wrote.

Study Shows Reproductive Effects of Pesticide Exposure Span Generations

Photo: freedigitalphotos.net

North Carolina State University researchers studying aquatic organisms called Daphnia have found that exposure to a chemical pesticide has impacts that span multiple generations – causing the so-called “water fleas” to produce more male offspring, and causing reproductive problems in female offspring.

“This work supports the hypothesis that exposure to some environmental chemicals during sensitive periods of development can cause significant health problems for those organisms later in life – and affect their offspring and, possibly, their offspring’s offspring,” says Dr. Gerald LeBlanc, a professor of environmental and molecular toxicology at NC State and lead author of a paper on the work. “We were looking at a model organism, identified an important pathway for environmental sex determination, and found that there are chemicals that can hijack that pathway.”

Environmental cues normally determine the sex, male or female, of Daphnia offspring, and researchers have been working to understand the mechanisms involved. As part of that work, LeBlanc’s team had previously identified a hormone called methyl farnesoate (Mf) that Daphnia produce under certain environmental conditions.

The researchers have now found that the hormone binds with a protein receptor called the Mf receptor, which can regulate gene transcription and appears to be tied to the production of male offspring.

In experiments, the researchers exposed Daphnia to varying levels of an insecticide called pyriproxyfen, which mimics the Mf hormone. The pyriproxyfen exposure resulted in Daphnia producing more male offspring and fewer offspring in total, with higher doses exacerbating both effects.

“At high concentrations, we were getting only male offspring, which is not good,” LeBlanc says. “Producing fewer offspring, specifically fewer female offspring, could significantly limit population numbers for Daphnia.”

And low exposure concentrations had significant impacts as well. At pyriproxyfen concentrations as low as 71 nanograms per liter, or 71 parts per trillion, the Daphnia would still produce some female offspring. But those females suffered long-term reproductive health effects, producing significantly smaller numbers of offspring – despite the fact that they had not been exposed to pyriproxyfen since birth.

“We now want to know specifically which genes are involved in this sex determination process,” LeBlanc says. “And, ecologically, it would be important to know the impact of changes in population dynamics for this species. Daphnia are a keystone species – an important food source for juvenile fish and other organisms.”

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Even a few cigarettes a day increases risk of rheumatoid arthritis

The number of cigarettes smoked per day and the number of years a person has smoked, increase the risk of rheumatoid arthritis (RA), finds research in BioMed Central's open access journal Arthritis Research & Therapy. The risk decreases after giving up smoking but, compared to people who have never smoked, this risk is still elevated 15 years after giving up.

Researchers from the Karolinska Institutet and Karolinska University Hospital analyzed data from the Swedish Mammography Cohort, which included 34,000 women aged between 54 and 89, 219 of which had RA. Results of the study showed that even light smoking is associated with an increased risk of RA - smoking 1 to 7 cigarettes a day more than doubled this risk. When the team compared people who had never smoked, to women who had smoked for up to 25 years, they found that the risk also increased with length of smoking.

Stopping smoking did decrease chances of developing RA, with the risk continuing to decrease over time - 15 years after giving up the risk of RA had decreased by a third. However, compared to people who had never smoked, this risk remained significantly higher at 15 years after giving up.

Daniela Di Giuseppe, who led this study, commented, "Stopping smoking is important for many health reasons, including the increased risk of RA for smokers. But the clearly increased risk of developing RA, even many years after giving up, is another reason to stop smoking as soon as possible, and highlight the importance of persuading women not to start at all."

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Air Quality News: Why your garage could pose a health threat

Source: CTV

If you have a garage attached to your house, you could be at higher risk of developing leukemia or other forms of cancer.

Health Canada has expressed concern that benzene from car exhaust and other fumes could be entering homes. It’s now working on guidelines to help homeowners prevent the toxic gas from seeping into their homes.

Benzene is a volatile organic compound, or VOC, that’s found naturally in crude oil and thus in gasoline and vehicle exhaust.

There are already low levels of benzene in the air all around us due to air pollution from motor vehicle exhaust. But now Health Canada wants to make our homes safer.

Most Canadians know about the risks of carbon monoxide in their homes, but many aren’t as familiar with the risk of benzene exposure.

Deborah Schoen, the head of Health Canada’s indoor air section, says the agency has conducted studies measuring levels of the gas in homes across Canada. Those studies found that the levels were generally low, whether the houses had attached garages or not.

“On average, benzene levels in houses with attached garages are three times higher than of other houses,” Schoen told CTV News Channel this week from Ottawa.

Most drivers know not to run their vehicles after entering and closing the garage. What they may not know: after a car is turned off, the engine will continue to emit benzene into the air as it sits in the garage.

As well, the paints and solvents that many homeowners store in their garage also emit benzene as they slowly evaporate.

Schoen says that for the most part, the risk of long-term health effect is not high.

“The cancer risk is extremely low. But Health Canada and the World Health Organization and the European Commission recommend people reduce their exposure to benzene as much as possible,” she says.

“So for this reason, Health Canada advises people to reduce benzene exposure as much as possible.”

Studies have shown that benzene can definitely cause problems if people are exposed to high levels over long periods of time. Workers in industrial settings exposed to high levels of benzene have been shown to have a much higher risk of leukemia.

Benzene is dangerous because of the damage it can do to the blood. It causes bone marrow not to produce enough red blood cells, while also damaging the immune system by not creating enough white blood cells.

Thanks to regulations brought in in the 1990s that reduced the amount of benzene in gasoline, Canadians’ exposure to benzene has been dropping in recent decades.

But Schoen says it’s important to keep looking for ways to reduce our exposure to the gas even further, which is why Health Canada is focusing on the indoor air quality of homes with attached garages.

The guidelines are expected to advised homeowner to never idle a vehicle inside a garage, but to let it warm up outside.

“People might open the garage door and figure that’s enough,” Schoen said.

But even with the door open, a range of pollutants from vehicle exhaust– not just benzene but carbon monoxide and other pollutants-- accumulate when you idle your car in an attached garage.”

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Does your child have a pollen allergy?

Photo: Chris Roll/freedigitalphotos.net

When warmer weather starts to roll in, most kids are ready to shake off cabin fever and get outside to play. It’s also the time when trees and plants are pollinating − a bad combination for a child with a pollen allergy.

“Spring is a problem for lots of people with allergies because it’s when trees and other plants start releasing pollens into the air,” said Joyce Rabbat, MD, pediatric allergist at Loyola University Health System and assistant professor in the department of pediatrics at Loyola University Chicago Stritch School of Medicine. “There are different types of allergies, but if you notice that your child has more symptoms and reactions during the spring it’s a clue that they have a pollen allergy.”

According to Rabbat, allergy symptoms include:
• Itchy eyes
• Sneezing
• Stuffy and/or runny nose
• Coughing
• Asthma

“It’s great to get kids outside and exercising, but if your child has outdoor allergies just be sure to keep an eye on them in case of a reaction,” Rabbat said. For children with allergies to pollen, symptoms most likely will be worse on dry, windy days. Rabbat suggests the following to help limit reactions.

• Check pollen counts and try to spend less time outside when the counts are high. Loyola has an official allergy count you can follow on Twitter @GottliebAllergy
• Keep windows and doors closed, especially on high count days, to limit the amount pollen that settles onto furniture and carpet
• Use the air conditioner to filter pollens from the air inside your house
• When children come in from outdoors have them wash their face and hands; consider having them take a shower and change their clothes to get pollen off the body.

“If your child is active outdoors or in sports, make sure he or she takes allergy medication before heading outside,” Rabbat said.
Rabbat warns parents to keep an eye out for asthma symptoms as many children who deal with allergies have allergic asthma as well.

Allergic asthma symptoms include:
• Couging
• Wheezing
• Shortness of breath
• Rapid breathing
• Feeling a tightness in the chest

“Often treating children’s allergies helps to control their asthma as well. Kids may need to take an allergy medicine before going outside, or they may need daily allergy medication. It’s also important to get ahead of your allergy symptoms. Once allergies are flaring, they become more difficult to treat. If you are on a good medication regimen before the pollens peak, it makes for a much more enjoyable season,” Rabbat.
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Following a Western style diet may lead to greater risk of premature death

Photo:freedigitalphotos.net

Data from a new study of British adults suggest that adherence to a "Western-style" diet (fried and sweet food, processed and red meat, refined grains, and high-fat dairy products) reduces a person's likelihood of achieving older ages in good health and with higher functionality. Study results appear in the May issue of The American Journal of Medicine.

"The impact of diet on specific age-related diseases has been studied extensively, but few investigations have adopted a more holistic approach to determine the association of diet with overall health at older ages," says lead investigator Tasnime Akbaraly, PhD, Inserm, Montpellier, France. "We examined whether diet, assessed in midlife, using dietary patterns and adherence to the Alternative Healthy Eating Index (AHEI), is associated with aging phenotypes, identified after a mean 16-year follow-up."

The AHEI is a validated index of diet quality, originally designed to provide dietary guidelines with the specific intention to combat major chronic conditions such as cardiovascular diseases and diabetes.

Investigators analyzed findings from the British Whitehall II cohort study, which suggest that following the AHEI can double the odds of reversing metabolic syndrome, a condition known to be a strong predictor of heart disease and mortality. The research team sought to identify dietary factors that can not only prevent premature death, but also promote ideal aging.

Researchers followed 3,775 men and 1,575 women from 1985-2009 with a mean age of 51 years from the Whitehall II study. Using a combination of hospital data, results of screenings conducted every five years, and registry data, investigators identified mortality and chronic diseases among participants. The outcomes at follow-up stage, classified into 5 categories were:

1. Ideal aging, defined as free of chronic conditions and high performance in physical, mental, and cognitive functioning tests – 4.0 percent
2. Nonfatal cardiovascular event – 12.7 percent
3. Cardiovascular death – 2.8 percent
4. Noncardiovascular death – 7.3 percent
5. Normal aging -- 73.2 percent

The study determined that participants with low adherence to the AHEI increased their risk of cardiovascular and noncardiovascular death. Those who followed a "Western-type diet" consisting of fried and sweet food, processed food and red meat, refined grains, and high-fat dairy products lowered their chances for ideal aging.

"We showed that following specific dietary recommendations such as the one provided by the AHEI may be useful in reducing the risk of unhealthy aging, while avoidance of the 'Western-type foods' might actually improve the possibility of achieving older ages free of chronic diseases and remaining highly functional," notes Dr. Akbaraly. "A better understanding of the distinction between specific health behaviors that offer protection against diseases and those that move individuals towards ideal aging may facilitate improvements in public health prevention packages."
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Cutting Specific Pollutants Would Slow Sea Level Rise

Photo: Evgeni Dinev/freedigitalphotos.net

With coastal areas bracing for rising sea levels, new research indicates that cutting emissions of certain pollutants can greatly slow down sea level rise this century.

The research team found that reductions in four pollutants that cycle comparatively quickly through the atmosphere could temporarily forestall the rate of sea level rise by roughly 25 to 50 percent.

“To avoid potentially dangerous sea level rise, we could cut emissions of short-lived pollutants even if we cannot immediately cut carbon dioxide emissions,” says Aixue Hu of the National Center for Atmospheric Research (NCAR), the first author of the study. “This new research shows that society can significantly reduce the threat to coastal cities if it moves quickly on a handful of pollutants.”

The study, a collaboration of the Scripps Institution for Oceanography, NCAR, and Climate Central, is being published this week in the journal Nature Climate Change. It was funded by the National Science Foundation and the Department of Energy.

“It is still not too late, by stabilizing carbon dioxide concentrations in the atmosphere and reducing emissions of shorter-lived pollutants, to lower the rate of warming and reduce sea level rise,” says Veerabhadran Ramanathan of Scripps, who led the study. “The large role of the shorter-lived pollutants is encouraging since technologies are available to drastically cut their emissions.”

Protecting the coasts

The potential impact of rising oceans on populated areas is one of the most concerning effects of climate change. Many of the world’s major cities, such as New York, Miami, Amsterdam, Mumbai, and Tokyo, are located in low-lying areas by the water.

As glaciers and ice sheets melt and warming oceans expand, sea levels have been rising by an average of about 3 millimeters annually in recent years (just more than one-tenth of an inch). If temperatures continue to warm, sea levels are projected to rise between 18 and 59 centimeters (7 to 23 inches) this century, according to a 2007 assessment by the Intergovernmental Panel on Climate Change. Some scientists, however, feel those estimates are too conservative.

Such an increase could submerge densely populated coastal communities, especially when storm surges hit.

Despite the risks, policy makers have been unable to agree on procedures for reducing emissions of carbon dioxide. With this in mind, the research team focused on emissions of four other heat-trapping pollutants: methane, tropospheric ozone, hydrofluorocarbons, and black carbon. These gases and particles last anywhere from a week to a decade in the atmosphere, and they can influence climate more quickly than carbon dioxide, which persists in the atmosphere for centuries.

Previous research by Ramanathan and Yangyang Xu of Scripps, a co-author of the new paper, has shown that a sharp reduction in emissions of these shorter-lived pollutants beginning in 2015 could offset warming temperatures by up to 50 percent by 2050.

Applying those emission reductions to sea level rise, the new research found that the cuts could dramatically slow rising sea levels. Their results showed that total sea level rise would be reduced by an estimated 22 to 42 percent by 2100, depending on the extent to which emissions were reduced.

However, the new study also found that delaying emissions cuts until 2040 would reduce the beneficial impact on year-2100 sea level rise by about a third.

If society were able to substantially reduce both emissions of carbon dioxide as well as the four other pollutants, total sea level rise would be lessened by at least 30 percent by 2100, the researchers concluded.

The researchers used mostly percentage changes for sea level rise, rather than actual estimates in centimeters, because of uncertainties over future temperature increases and their impacts on rising sea levels.

“We still have some control over the amount of sea level rise that we are facing,” Hu says.

Another co-author, Claudia Tebaldi of Climate Central, adds:

"Without diminishing the importance of reducing carbon dioxide emissions in the long term, this study shows that more immediate gains from shorter-lived pollutants are substantial. Cutting emissions of those gases could give coastal communities more time to prepare for rising sea levels. As we have seen recently, storm surges in very highly populated regions of the East Coast show the importance of both making such preparations and cutting greenhouse gases."

To conduct the study, Hu and his colleagues turned to the NCAR-based Community Climate System Model, as well as a second computer model that simulates climate, carbon, and geochemistry. They also drew on estimates of future emissions of heat-trapping gases under various social and economic scenarios and on computer models of melting ice and sea level rise.

The study assumes that society could reduce emissions of the four gases and particles by 30 to 60 percent over the next several decades. That is the steepest reduction believed achievable by economists who have studied the issue at Austria’s International Institute for Applied Systems Analysis, one of the world’s leading research centers into the impact of economic activity on climate change.

“It must be remembered that carbon dioxide is still the most important factor in sea level rise over the long term,” says NCAR scientist Warren Washington, a co-author. “But we can make a real difference in the next several decades by reducing other emissions.”

The University Corporation for Atmospheric Research manages the National Center for Atmospheric Research under sponsorship by the National Science Foundation. Any opinions, findings and conclusions, or recommendations expressed in this publication are those of the author(s) and do not necessarily reflect the views of the National Science Foundation.

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Scientists explain how ozone causes respiratory problems and premature death

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A research team from Birkbeck, University of London, Royal Holloway University and Uppsala University in Sweden, have helped explain how ozone causes severe respiratory problems and thousands of cases of premature death each year by attacking the fatty lining of our lungs.

In a study published in Langmuir, the team used neutrons from the Institut Laue-Langevin in Grenoble and the UK's ISIS Neutron Source to observe how even a relatively low dose of ozone attacks lipid molecules that line the lung's surface. The presence of the lipid molecules is crucial for the exchange of oxygen and carbon dioxide, as they prevent the wet surfaces of the lung from collapsing.

Ozone is mostly produced in the upper atmosphere as the sun's UV light splits oxygen molecules, but it can also form at ground level from burning fossil fuels. It is known to harm our respiratory systems and is linked to asthma, bronchitis, heart attacks, and other cardiopulmonary problems. A recent study published by the Bloomberg School's Department of Environmental Health Sciences found that stricter ozone emission regulations in the US could prevent over a thousand premature deaths and over a million complaints of respiratory problems each year [1].

However, it remains unclear how exactly ozone causes this damage. One theory is it attacks the lung's surface layers which consist of a layer of water sitting below a mixture of fatty molecules called lipids and proteins that are together known as lung surfactant. The surfactant aids the exchange of oxygen and carbon dioxide during breathing. It does this by reducing surface tension, i.e. the attraction that molecules feel for each other, in the liquid surface layer above, causing these fluids to spread out and provide a greater surface area for gas exchange.

Critically, a lack of adequate surfactant, a deficiency often found naturally in babies born prematurely, can produce similar respiratory health complaints to those mentioned above, even resulting in death in some cases.

This link was further established in 2011 by the same team from Birkbeck who demonstrated that ozone reacted very strongly with the lipid layer, damaging it. However, what exactly is going on and how these reactions might impede the surfactant from doing its job was still unclear.

To investigate further Dr Katherine Thompson from Birkbeck and her team ran neutron reflection studies at the Institut Laue-Langevin in Grenoble and ISIS Neutron Source in Oxfordshire on an artificial lipid monolayer, created to mimic the lung surface. The lipid layer was exposed to a dilute gaseous mixture of ozone, and changes in its structure or surface tension were studied in real time. The concentration of ozone was around 100 parts per billion (0.1 ppm), equivalent to what you might get in a polluted city in the summer.

The use of neutrons meant that Dr Thompson could label different parts of the sample using deuteration, a process whereby a heavier isotope of hydrogen, deuterium, is introduced and contrasted with undeuterated samples to pick out the location of hydrogen atoms. This allowed them to monitor different parts of the molecule separately as they reacted with the ozone.

Using this technique Dr Thompson's team showed that one of the lipid's upwards-facing tails, known as the C9 portion, breaks off during the ozone degradation and is lost from the surface completely. The portion still attached to the lipid head then re-orientates itself and penetrates into the air‐water interface. The loss of the C9 portion causes an initial decrease in surface tension which temporarily increases surface area for gas exchange and efficient respiration. However this effect is short-lived as the penetration of the rest of the molecule into the water results in a slow but pronounced rise in surface tension, producing an overall net increase.

The next step for Katherine and her colleagues is to look at adapting the model, to represent the condition of people with various forms of chronic respiratory problem and attempt to understand why ozone seems to affect them worse than others.

Dr Katherine Thompson, Birkbeck, University of London said: "We are not completely sure what causes the second stage of tension increase. The damaged lipid might be slowly dissolving in the water and leaving the interface entirely, or a slow reaction might be occurring that is damaging another part of the lipid not directly attacked by ozone. What we can say is that the slow increase in surface tension that occurs as a result of the ozone exposure would certainly damage the ability of our lungs to process oxygen and carbon dioxide, and could account for the respiratory problems associated with ozone poisoning."

Dr Martin King from Royal Holloway University said: "This important study shows how a key air pollutant has a detrimental effect on the human lung and could impair breathing. It is essential that a complex mixture of air pollutants - for example Ozone and nitrogen oxides - and the effect of inhaled particulate matter on the lung, is looked at next."

Dr Richard Campbell from the Institut Laue-Langevin said: "Neutrons are an ideal tool for studying biological materials, particularly their reactions and interactions on surfaces and across interfaces. They are highly sensitive to lighter atoms such as carbon, hydrogen and oxygen that make up these organic molecules and isotopic labelling can be used to determine the structure and composition of interfacial layers. As one of the world's brightest neutron sources, the ILL has a long history of modelling important micro-scale processes that take place inside our bodies and providing ground-breaking insights that inform the next generation of treatments."

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High Levels of Lead Found in Imported Rice and Baby Food

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Rice imported from certain countries contains high levels of lead that could pose health risks, particularly for infants and children, who are especially sensitive to lead’s effects, and adults of Asian heritage who consume large amounts of rice, scientists said here today. Their research, which found some of the highest lead levels in baby food, was among almost 12,000 reports scheduled for the 245th National Meeting & Exposition of the American Chemical Society, the world’s largest scientific society, which continues through Thursday.

Tsanangurayi Tongesayi, Ph.D., who headed the analysis of rice imported from Asia, Europe and South America, pointed out that imports account for only 7 percent of the rice consumed in the United States. With vast rice fields in Louisiana, California, Texas, Arkansas and Mississippi, the U.S. is a major producer and exporter of the grain. However, imports of rice and rice flour are increasing ― by more than 200 percent since 1999 ― and rice is the staple food for 3 billion people worldwide, he added.
“Such findings present a situation that is particularly worrisome given that infants and children are especially vulnerable to the effects of lead poisoning,” Tongesayi said. “For infants and children, the daily exposure levels from eating the rice products analyzed in this study would be 30-60 times higher than the FDA’s provisional total tolerable intake (PTTI) levels. Asians consume more rice, and for these infants and children, exposures would be 60-120 times higher. For adults, the daily exposure levels were 20-40 times higher than the PTTI levels.”

The research was part of a symposium titled “Food and Its Environment: What Is In What We Eat?”

Tongesayi’s team, which is with Monmouth University in N.J., found that levels of lead in rice imported into the United States ranged from 6 to 12 milligrams/kilogram. From those numbers, they calculated the daily exposure levels for various populations and then made comparisons with the FDA’s PTTI levels for lead. They detected the highest amounts of lead in rice from Taiwan and China. Samples from the Czech Republic, Bhutan, Italy, India and Thailand had significantly high levels of lead as well. Analysis of rice samples from Pakistan, Brazil and other countries were still underway.

Because of the increase in rice imports into the United States, Tongesayi said that rice from other nations has made its way into a wide variety of grocery stores, large supermarket chains and restaurants, as well as ethnic specialty markets and restaurants.

The American Chemical Society is a nonprofit organization chartered by the U.S. Congress. With more than 163,000 members, ACS is the world’s largest scientific society and a global leader in providing access to chemistry-related research through its multiple databases, peer-reviewed journals and scientific conferences. Its main offices are in Washington, D.C., and Columbus, Ohio.
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UCLA researchers find potential link between auto pollution, some childhood cancers

Scientists from UCLA's Fielding School of Public Health led by Julia Heck, an assistant researcher in the school's epidemiology department and a member of UCLA's Jonsson Comprehensive Cancer Center, have found a possible link between exposure to traffic-related air pollution and several childhood cancers.

The results of their study — the first to examine air pollution from traffic and a number of rarer childhood cancers — were presented on April 9 in an abstract at the annual meeting of the American Association for Cancer Research in Washington, D.C.

For the study, the UCLA researchers utilized data on 3,950 children who were enrolled in the California Cancer Registry and who were born in the state between 1998 and 2007. They estimated the amount of local traffic the children had been exposed to using California LINE Source Dispersion Modeling, version 4 (CALINE4).

Pollution exposure was estimated for the area around each child's home for each trimester of their mother's pregnancy and during their first year of life. The estimates included information on gasoline and diesel vehicles within a 1,500-meter radius buffer, traffic volumes, roadway geometry, vehicle emission rates and weather. Cancer risk was estimated using a statistical analysis known as unconditional logistic regression.

The researchers found that heightened exposure to traffic-related air pollution was associated with increases in three rare types of childhood cancer: acute lymphoblastic leukemia (white blood cell cancer), germ-cell tumors (cancers of the testicles, ovaries and other organs) and retinoblastoma (eye cancer), particularly bilateral retinoblastoma, in which both eyes are affected.

The pollution-exposure estimates were highly correlated across pregnancy trimesters and the first year of life, meaning that even in areas of high exposure, no particular period stood out as a higher-exposure time. This, the scientists said, made it difficult to determine if one period of exposure was more dangerous than any other.

"Much less is known about exposure to pollution and childhood cancer than adult cancers," Heck said. "Our innovation in this study was looking at other, more rare types of childhood cancer, such as retinoblastoma, and their possible connection to traffic-related air pollution."

Because these are rare diseases, Heck cautions that the findings need to be replicated in further studies.

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Doctors not informed of harmful effects of drugs by pharma reps

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The majority of family doctors receive little or no information about harmful effects of medicines when visited by drug company representatives, according to an international study involving Canadian, U.S. and French physicians.

Yet the same doctors indicated that they were likely to start prescribing these drugs, consistent with previous research that shows prescribing behaviour is influenced by pharmaceutical promotion.

The study, which had doctors fill out questionnaires about each promoted medicine following sales visits, was published online today in the Journal of General Internal Medicine. It shows that sales representatives failed to provide any information about common or serious side effects and the type of patients who should not use the medicine in 59 per cent of the promotions. In Vancouver and Montreal, no potential harms were mentioned for 66 per cent of promoted medicines.

"Laws in all three countries require sales representatives to provide information on harm as well as benefits," says lead author Barbara Mintzes of the University of British Columbia. "But no one is monitoring these visits and there are next to no sanctions for misleading or inaccurate promotion."

Serious risks were mentioned in only six percent of the promotions, even though 57 per cent of the medications involved in these visits came with US Food and Drug Administration "black box" or Health Canada boxed warnings – the strongest drug warning that can be issued by both countries.

"We are very concerned that doctors and patients are left in the dark and patient safety may be compromised," says Mintzes, an expert on drug advertising in UBC's School of Population and Public Health.

Doctors in Toulouse were more likely to be told of a harmful effect in a promotional visit, compared to doctors in Canada and the U.S., according to the study. Researchers suggested that this may reflect stricter regulatory standards for promotion of medicines in France.
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Higher mercury levels in humans associated with increased risk for diabetes

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A new study found that higher levels of mercury exposure in young adults increased their risks for type 2 diabetes later in life by 65 percent. The study, led by Indiana University School of Public Health-Bloomington epidemiologist Ka He, is the first to establish the link between mercury and diabetes in humans.

The study paints a complicated nutritional picture because the main source of mercury in humans comes from the consumption of fish and shellfish, nearly all of which contain traces of mercury. Fish and shellfish also contain lean protein and other nutrients, such as magnesium and omega-3 polyunsaturated fatty acids, that make them important to a healthy diet.

In the study, published online early in the journal Diabetes Care, the people with the highest levels of mercury also appeared to have healthier lifestyles -- lower body mass indexes and smaller waist circumferences, more exercise -- than other study participants. They also ate more fish, which is a possible marker of healthy diet or higher social economic status. Risk factors for type 2 diabetes include being overweight.

The study, which involved 3,875 men and women, established the link between mercury levels and type 2 diabetes risk after controlling for lifestyle and other dietary factors such as magnesium and omega-3 polyunsaturated fatty acids, which could counter the effects of the mercury.

These findings, said He, point to the importance of selecting fish known to have low levels of mercury, such as shrimp, salmon and catfish, and avoiding fish with higher levels, such as swordfish and shark. FDA and EPA guidelines for fish consumption highlight this, particularly for women who are pregnant or of childbearing age and for young children.

"It is likely that the overall health impact of fish consumption may reflect the interactions of nutrients and contaminants in fish. Thus, studying any of these nutrients and contaminants such as mercury should consider confounding from other components in fish," He and the authors wrote in the study. "In the current study, the association between mercury exposure and diabetes incidence was substantially strengthened after controlling for intake of LCn-3PUFAs (omega-3) and magnesium."

The study participants were recruited from Birmingham, Ala., Oakland, Calif., Chicago and Minneapolis,and then followed for 18 years as part of the Coronary Artery Risk Development in Young Adults Study. He, chair of the Department of Epidemiology and Biostatistics in the IU School of Public Health-Bloomington, is principal investigator of the ancillary study, the CARDIA Trace Element Study, which is funded by the National Institutes of Health.
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Marker in the blood of male smokers linked to higher risk of lung cancer; May help with earlier detection

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Elevated levels of bilirubin in the blood get attention because they often indicate that something has gone wrong with the liver. Now researchers have found that male smokers with low levels of the yellow-tinged chemical are at higher risk for lung cancer and dying from the disease.

A team led by researchers at The University of Texas MD Anderson Cancer Center reported its findings in a late-breaking abstract at the AACR Annual Meeting 2013 in Washington, D.C.

"Our study indicates male smokers with low levels of bilirubin are a high-risk group that can be targeted with smoking cessation help, low-dose spiral CT screening of their lungs and other preventive measures," said senior author Xifeng Wu, M.D., Ph.D., professor and chair of MD Anderson's Department of Epidemiology and the Betty B. Marcus Chair in Cancer Prevention.

Lung cancer usually is diagnosed at a late stage, when tumors are inoperable and treatments largely ineffective. The overall five-year survival rate is 15 percent, but it falls to 5 percent for stage 3 lung cancer patients and 1 percent for those with stage 4 disease.

Spiral CT scans catch cancer early, biomarker could reduce false positives

The National Lung Screening Trial found that low-dose spiral computed tomography screening reduces mortality among heavy smokers by 20 percent. However, 95 percent of growths found by spiral CT are false positives, a barrier to large-scale screening.

"Validated biomarkers are urgently needed to improve risk prediction for lung cancer and to reduce false positives, shifting the balance toward more effective and efficient CT screening for cancer detection," Wu said.

The researchers started with an objective analysis of levels of metabolites — substances produced during metabolism. Bilirubin is produced during the breakdown of old blood cells.

They analyzed 60 samples divided into three groups known as "trios" — normal controls, early stage and late stage non-small cell lung cancer patients. The top three metabolites were validated in two more groups of 50 and 123 trios.

When bilirubin emerged as the most significant metabolite, another validation study was done in a prospective cohort of 435,985 people with 208,233 men in Taiwan.

Men were divided into four groups according to their serum bilirubin levels. Lower bilirubin level was associated with significantly higher rates of both lung cancer incidence and mortality.

In the Taiwanese cohort, the incidence rate per 10,000 person-years in men was 7.02 for those in the lowest bilirubin quartile (.68 mg/dL or less), compared to 3.73 in the highest quartile of bilirubin level (1.12 mg/dL or more). The mortality rate per 10,000 person-years was 4.84 for the lowest level compared with 2.46 in the highest bilirubin quartile.

Next step: Establish a risk prediction model in heavy smokers

Bilirubin makes sense as a protective agent because of its anti-oxidant, anti-inflammatory and anti-proliferative effects. "It's plausible that bilirubin protects against lung cancer by scavenging free radicals and carcinogens associated with smoking," said study presenter Fanmao Zhang, a doctoral candidate in epidemiology.

Indeed, a Belgian study showed that bilirubin in the high normal range lowered cancer mortality in men. A study in the United Kingdom showed higher bilirubin levels in the normal range were associated with lower risks of chronic obstructive pulmonary disease, lung cancer and all-cause mortality. Neither of those studies stratified their analysis of bilirubin by smoking status.

"We expected that bilirubin might be protective, but our finding that bilirubin levels affect only smokers was somewhat of a surprise," Wu said. "Our discovery that low levels increase lung cancer risk is unique."

Smokers in the two middle cohorts of bilirubin levels also had higher lung cancer risk than those in the highest quartile. As an objective risk index for lung cancer and all-cause mortality, low levels of bilirubin should send an urgent message to quit smoking, said Chi Pang Wen, M.D., Ph.D., co-lead author from National Health Research Institutes, Taiwan.

The next step, Wu said, is to evaluate the predictive value of serum bilirubin in heavy smokers and to establish a risk prediction model that incorporates bilirubin and other biomarkers with clinical and epidemiological data to improve the efficiency of lung cancer risk prediction.

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Air pollution stunts coral growth

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A new study has found that air pollution from fine particles – mainly the result of burning coal or volcanic eruptions – can shade corals from sunlight and cool the surrounding water resulting in reduced growth rates.

Although coral reefs grow under the sea it seems that they have been responding to changes in the concentration of particulate pollution in the atmosphere, according to a paper published in the journal Nature Geoscience by a team of climate scientists and coral ecologists from the UK, Australia and Panama. Corals are colonies of simple animal cells but most rely on photosynthetic algae for their energy and nutrients.

Lead author Lester Kwiatkowski, a PhD student from Mathematics at the University of Exeter, said: "Coral reefs are the most diverse of all ocean ecosystems with up to 25% of ocean species depending on them for food and shelter. They are believed to be vulnerable to climate change and ocean acidification, but ours is the first study to show a clear link between coral growth and the concentration of particulate pollution in the atmosphere."

Dr Paul Halloran of the Met Office Hadley Centre explained: "Particulate pollution or 'aerosols' reflect incoming sunlight and make clouds brighter. This can reduce the light available for coral photosynthesis, as well as the temperature of surrounding waters. Together these factors are shown to slow down coral growth."

The authors used a combination of records retrieved from within the coral skeletons, observations from ships, climate model simulations and statistical modelling. Their analysis shows that coral growth rates in the Caribbean were affected by volcanic aerosol emissions in the early 20th century and by aerosol emissions caused by humans in the later 20th century.

The researchers hope that this work will lead to a better understanding of how coral growth may change in the future, taking into account not just future carbon dioxide levels, but also localized sources of aerosols such as industry or farming.

Professor Peter Mumby of the University of Queensland put the study in the context of global environmental change: "Our study suggests that coral ecosystems are likely to be sensitive to not only the future global atmospheric carbon dioxide concentration but also the regional aerosol emissions associated with industrialisation and decarbonisation."

Home Depot Agrees to Pay $8 Million to Settle Air Quality Violations in California

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The Home Depot has agreed to pay $8 million to settle air quality violations for allegedly selling tens of thousands of gallons of non-compliant paint and other coatings to California consumers.

Home Depot, the nation’s largest home improvement chain, allegedly sold paints, sealers, primers and other products in 2009 to 2010 containing illegal levels of smog-forming volatile organic compounds (VOCs).

"Paints and other coatings are one of our largest sources of air pollution,” said Barry Wallerstein, executive officer of the South Coast Air Quality Management District. (SCAQMD) “Since the Southland has the most severe air pollution problem in the nation, our standards limiting the polluting ingredients must be enforced.”

Home Depot signed a settlement agreement this week with SCAQMD as well as the Los Angeles City Attorney’s Office and the district attorneys of Orange, Riverside and San Bernardino counties. Of the $8 million, $1.98 million will be paid to SCAQMD and a total of $6.02 million to Los Angeles and the three counties. The agreement settles a lawsuit filed in June 2011 against Home Depot for violations of SCAQMD’s Rule 1113 governing architectural coatings as well as violations of state law prohibiting unfair competition and false and misleading advertising.

From September 2009 through April 2010, SCAQMD inspectors found numerous paint and coating products with VOC content exceeding SCAQMD limits at Home Depot stores in Brea, Irvine, Laguna Hills, Lake Elsinore, Lake Forest, Mission Viejo, Moreno Valley, Panorama City, Pomona, Rialto, Santa Ana, Tustin, West Hills, Whittier and Woodland Hills. Violating products included clear wood finishes, acrylic paints, sealers, lacquers, roof coatings, primers and base paints.

In numerous cases Home Depot stores continued to sell illegal products even after SCAQMD officials warned them to stop doing so and the chain claimed to have remedied the problem. As a result of the settlement, Home Depot has agreed to develop and implement a new computerized tracking system to ensure that only compliant coatings are sold in the future.

All paints and other coatings in the region emit a total of 15 tons of VOCs per day – equivalent to VOC emissions from more than 1.1 million cars. VOCs combine with nitrogen oxides to form ground-level ozone, a pollutant responsible for a wide range of health effects from increased school absences and hospitalizations to increased risk for asthma.

AQMD is the air pollution control agency for Orange County and major portions of Los Angeles, San Bernardino and Riverside counties.

Have Asthma? You Likely Have an Allergy as Well

Asthma is becoming an epidemic in the United States. The number of Americans diagnosed with asthma grows annually, with 26 million currently affected. And according to a new study, nearly two-thirds or more of all asthmatics also have an allergy, which can make this spring season particularly bothersome.

The study, which is published in the April issue of Annals of Allergy, Asthma & Immunology, the scientific journal of the American College of Allergy, Asthma and Immunology (ACAAI), found that an astonishing 75 percent of asthmatic adults aged 20- to 40-years-old, and 65 percent of asthmatic adults aged 55 years and older, have at least one allergy.

“Allergists have known the prevalence of allergies among asthmatic children is high at 60 to 80 percent, but it was thought allergies were not as common in asthmatic adults,” said allergist Paula Busse, MD, lead study author. “These findings are important, and can help lead to proper diagnosis and treatment.”

A total of 2,573 adults were studied in a National Health and Nutrition Examination Survey (NHANES). A panel of 19 allergens was used to detect allergy among asthmatics.

While asthma is frequently associated with children, it is not uncommon among adults 60 years and older, affecting three to seven percent. This number is likely higher, however, because asthma is often underdiagnosed in older adults.

“Both asthma and allergies can strike at any age, and are serious diseases,” said allergist Richard Weber, MD, ACAAI president. “Anyone who thinks they may be having symptoms of an allergy or asthma should see a board-certified allergist. Allergists are experts in diagnosing and treating both conditions.”

According to the ACAAI, more than 50 million Americans have an allergy, a number which is also on the rise. Is the link between asthma and allergies a reason?

“It could be one of many creating this perfect storm for allergies,” said Dr. Weber. “Other factors, such as the hygiene hypothesis, climate change and an increase in awareness and education can also be reasons for this growth.”

Those that have symptoms of asthma or allergy can get tested for free, through the ACAAI Nationwide Asthma Screening Program. Allergists will hold screenings at about 100 locations nationwide. Screenings can be found by visiting www.acaai.org/nasp.
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2013 list of the most miserable U.S. cities for allergy sufferers...

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Just in time for this year's pollen-apocalypse, the Asthma and Allergy Foundation of America (AAFA) has released their 11th annual ranking of the most miserable U.S. cities to live in if  you suffer from seasonal allergies.

Jackson, MS, claimed the top spot , followed by Knoxville, TN (#2) and Chattanooga, TN (#3).

Residents across the United States can actually expect more severe allergy conditions this year as an unusually wet winter and early warm temperatures lead to earlier tree pollination and higher levels of pollen and outdoor mold. Cities predicted to face a more challenging spring allergy season compared to one year ago include: Buffalo, NY (rising 10 spots to #15 out of 100 cities), Springfield, MA (rising from #74 to #18), Richmond, VA (rising from #46 to #22), Detroit, MI (rising from #50 to #26) and Toledo, OH (rising from #57 to #29).

"Severe weather patterns can bring higher temperatures, higher pollen levels and increased exposure to outdoor mold, resulting in spring allergies that can peak stronger and last longer," said Bill Berger , MD, Allergy and Asthma Associates of Southern California.

Recent hurricanes, severe storms and tornadoes can also affect the severity of spring allergies. The increased presence of mold in areas damaged by floods can trigger allergic reactions. Major urban areas and locations with significant construction may also see an increased risk for severe allergies, because pollen from weeds proliferates in places with development projects. Finally, ground-level ozone pollution can affect allergy symptoms.

This year's ranking shows that nasal allergies are a problem nationwide, especially in southern states. Overall, 15 of the top 25 cities on this year's ranking are in the South. These findings are consistent with research showing that spring now arrives 10 to 14 days earlier than it did just 20 years ago, bringing with it increased pollen counts.

An interactive map of 100 cities, resources about diagnosis, prevention and treatment options, resources for physicians, and more information on the study methodology are available at www.AllergyCapitals.com.

Here are the top 10:

1. Jackson, Mississippi

2. Knoxville, Tennessee

3. Chattanooga, Tennessee

4. McAllen, Texas

5. Louisville, Kentucky

6. Wichita, Kansas

7. Dayton, Ohio

8. Memphis, Tennessee

9. Oklahoma City, Oklahoma

10. Baton Rouge, Louisiana

Photo: freedigitalphotos.net

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Streams stressed by pharmaceutical pollution

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Pharmaceuticals commonly found in the environment are disrupting streams, with unknown impacts on aquatic life and water quality. So reports a new Ecological Applications paper, which highlights the ecological cost of pharmaceutical waste and the need for more research into environmental impacts.

Lead author Dr. Emma Rosi-Marshall, a scientist at the Cary Institute of Ecosystem Studies, comments: "Pharmaceutical pollution is now detected in waters throughout the world. Causes include aging infrastructure, sewage overflows, and agricultural runoff. Even when waste water makes it to sewage treatment facilities, they aren't equipped to remove pharmaceuticals. As a result, our streams and rivers are exposed to a cocktail of synthetic compounds, from stimulants and antibiotics to analgesics and antihistamines."

With colleagues from Indiana University and Loyola University Chicago, Rosi-Marshall looked at how six common pharmaceuticals influenced similar-sized streams in New York, Maryland, and Indiana. Caffeine, the antibiotic ciprofloxacin, the antidiabetic metformin, two antihistimines used to treat heartburn (cimetidine and ranitidine), and one antihistamine used to treat allergies (diphenhydramine) were investigated, both alone and in combinations, using pharmaceutical-diffusing substrates.

Rosi-Marshall explains, "We focused on the response of biofilms – which most people know as the slippery coating on stream rocks – because they're vital to stream health. They might not look like much to the naked eye, but biofilms are complex communities composed of algae, fungi, and bacteria all living and working together. In streams, biofilms contribute to water quality by recycling nutrients and organic matter. They're also a major food source for invertebrates that, in turn, feed larger animals like fish."

Healthy streams are slippery streams. And it turns out that antihistamines dry more than our noses. The most striking result of the study was diphenhydramine's effects on algal production and microbial respiration. Exposure caused biofilms to experience up to a 99% decrease in photosynthesis, as well as significant drops in respiration. Diphenhydramine also caused a change in the bacterial species present in the biofilms, including an increase in a bacterial group known to degrade toxic compounds and a reduction in a group that digests compounds produced by plants and algae.

Results suggest that this antihistamine is disrupting the ecology of these sensitive biofilm communities. Rosi-Marshall notes, "We know that diphenhydramine is commonly found in the environment. And its effect on biofilms could have repercussions for animals in stream food webs, like insects and fish. We need additional studies looking at the concentrations that cause ecosystem disruption, and how they react with other stressors, such as excess nutrients."

The other pharmaceuticals investigated also had a measurable effect on biofilm respiration, both alone and in combinations. More work is needed to understand how drug mixtures, which most natural streams experience, impact freshwater systems.

Society's dependence on pharmaceuticals is not likely to wane. Nor is its need for clean, fresh water. This study adds another piece of evidence to the case calling for innovations in the way we manage waste water. Currently, only a fraction of the world's waste water is treated, and the infrastructure in many developed nations is aging.
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