The pros and cons of HEPA air purifiers

HEPA or High Efficiency Particulate Arresting air purifiers use a fibrous filter to trap ultrafine particles. HEPA filtration was actually born from an infamous and historically significant event; the development of the atomic bomb. It was created to prevent the spread of minute radioactive particles. Today, HEPA plays an equally important role in home air purifiers, filtering dangerous particles from air pollution and smoke that have been linked to heart disease, cancer and respiratory illnesses. While widely recommended, HEPA-only air purifiers have a significant disadvantage; they cannot filter out other worrisome modern-day pollutants like chemicals, gases and odors.

What exactly is HEPA?

HEPA filters are comprised from tightly arranged fibres that trap hazardous fine particles that could otherwise be inhaled and settle in the body. To be classified as HEPA, the filter must remove at least 99.97% of all particles greater than 0.3 micrometers. Air purifiers that claim to be "HEPA-type" or “HEPA-like” may not have been adequately tested and could provide inferior air filtration. 

Why can’t HEPA air purifiers filter all types of contaminants?

While the design of the HEPA filter is ideal for trapping ultrafine particles, other pollutants like gases, fumes, chemicals and odors pass right through.  Air purifiers that trap a wider range of contaminants combine HEPA filtration with another filtration media. 

Air purifiers with activated carbon

The most efficient filter material for trapping gaseous pollutants is activated carbon. Like HEPA, activated carbon was developed by the military, and then commercialized for residential use.  It’s so effective, that activated carbon is widely used by heavy industry to trap toxic chemicals and is also used in water filtration. As home air quality concerns shift to dangerous airborne chemicals, some manufacturers have unfortunately used carbon as marketing ploy. These types of inefficient air purifiers use only a thin carbon mesh and claim their units can remove odors and chemicals. The adsorption capacity of carbon-mesh is so limited that these types of filters may be full within only weeks or days of use, depending on the level of pollutants in the environment. Only air purifiers with pounds of deep-bed activated carbon can provide lasting adsorption of chemicals, gases and odors.

How does activated carbon work?

The carbon used in air purifiers has been specially treated to open up millions of microscopic pores that attract and trap chemicals, gases and odors. Only a handful of granular activated carbon has a surface area larger than most suburban shopping malls. 

Hybrid Air Purifiers

The most effective air purifiers for today’s air quality challenges combine both of these excellent filtration methods into one unit.  When used together, a HEPA and deep-bed activated carbon air cleaner can remove a wider range of airborne contaminants including allergens like dust, pollen and dander as well as smoke, cleaning chemicals, VOCs (volatile organic compounds) and strong odors.

Learn More

For more information on hybrid HEPA-carbon air purifiers speak with an AllerAir air quality expert at 1-888-852-8247 or connect via the live chat link at www.allerair.com.

Study: Indoor air pollution puts female nonsmokers at increased lung cancer risk, especially in China

The hazards of breathing outdoor air in some  cities have been well-documented. Now a University at Buffalo study confirms that breathing indoor air also carries significant cancer risks, especially for Chinese women.

The UB study, published online this month, in the journal Cancer Causes & Control, found that indoor air pollution that generates fine particulate matter is a key contributor to the high rates of lung cancer among Chinese women, despite the fact that few of them smoke.

The research found indoor particulate matter levels that are at least double the maximum level considered acceptable by World Health Organization guidelines. The study is the first to measure particulate matter (PM) levels inside the home and to link it with the incidence of lung cancer in Chinese women.

“Our results show that besides smoking, indoor air pollution contributes significantly to women’s lung cancer risk in China,” says Lina Mu, MD, PhD, assistant professor of social and preventive medicine in the UB School of Public Health and Health Professions and lead author on the paper.

While around 60 percent of Chinese men smoke, Chinese women have extremely low smoking rates – approximately 4 percent. However, women’s rates of lung cancer in China are among the highest in the world, approximately 21 cases per 100,000, while smoking accounts for less than 20 per cent of lung cancer cases in Chinese women, says Mu.

“That’s why we wanted to find out how much indoor air pollution contributes to lung cancer risk among Chinese women,” says Mu. “It has been suspected but not measured.”

The paper notes that since women tend to be home for longer periods of time and to cook more frequently, housing-related exposure is more of a factor among women than men.

The case-control study includes 429 Chinese women: 197 who had lung cancer and 232 who were controls. Of the 197 with lung cancer, 164 were nonsmokers while there were 218 nonsmokers in the control group.

The study was conducted in Taiyuan city, one of the top 10 air polluted cities in the world according to Asian Development Bank’s 2012 annual report. Taiyuan is a large industrial city in northern China, which is home to heavy industry, including steel, coal mining and processing and electronics plants.

The study found that among the nonsmokers, lung cancer was strongly associated with multiple sources of indoor air pollution, which included exposure to tobacco smoke at work, frequent cooking and the use of solid fuel, primarily coal, for cooking and heating.

A particle mass monitor was used to measure PM levels inside the homes – mostly apartments – of study participants.

“We found that the smallest type of particulate matter is the type associated with the higher risk of lung cancer among nonsmoking Chinese women,” she says. “For every additional 10 micrograms per square meter of fine particular matter, there is an associated 45 percent increased risk of lung cancer.”

The paper notes that increased lung cancer risk among women was strongly attributed to the fine particles produced by coal combustion for heating and cooking, and from passive smoking.

Mu says that kitchen ventilation systems, such as fans, are not common in China and that people are reluctant to open windows because they want to keep heat in and prevent outdoor pollution from coming inside.

She adds that hot oil, a staple in traditional Chinese stir-frying and deep-frying, produces carcinogens, and is a key contributor.

“Women are at high risk because they are exposed to solid fuel emissions from heating and cooking as well as from passive smoking,” she says, adding that smoking is a key social ingredient in China. “Men tend to gather and smoke together, often in small, enclosed spaces, especially in offices.”

Mu notes that while in large cities, some restaurants have begun to segregate smokers, people smoke freely in most public places in China.

She says that improvements will depend on significant changes, such as a switch to clean energy sources, the installation of better ventilation systems as well as public education about the benefits of keeping windows open and curbing passive smoking.

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Harvard researchers say better air quality means improved U.S. life expectancy

A study led by researchers at the Harvard School of Public Health (HSPH) has found an association between reductions in fine particulate matter and improved life expectancy in 545 counties in the U.S. from 2000 to 2007. It is the largest study to date to find beneficial effects to public health of continuing to reduce air pollution levels in the U.S.

“Despite the fact that the U.S. population as a whole is exposed to much lower levels of air pollution than 30 years ago—because of great strides made to reduce people’s exposure—it appears that further reductions in air pollution levels would continue to benefit public health,” said lead author Andrew Correia, a PhD candidate in the Department of Biostatistics at HSPH.

The study looked at the effects on health of fine particulate matter, small particles of 2.5 micrometers or less in diameter—referred to as PM2.5. Numerous studies have shown associations between acute and chronic exposure to fine particle air pollution and cardiopulmonary disease and mortality. Studies have also shown that reductions in air pollution are associated with reductions in adverse health effects and improved life expectancy. Air pollution has been declining steadily in the U.S. since 1980, but the rate has slowed in the years since 2000. The HSPH researchers wanted to know whether the relatively smaller decreases in PM2.5 levels since 2000 are still improving life expectancy.

Controlling for socioeconomic status, smoking prevalence, and demographic characteristics, the results showed that a decrease of 10 micrograms per cubic meter (10 ?g/m3) in the concentration of PM2.5 during the period 2000 to 2007 was associated with an average increase in life expectancy of 0.35 years in 545 U.S. counties.

The research expanded on a 2009 study published in the New England Journal of Medicine by some of the same authors (Pope, Ezzati, and Dockery) that found that reduced air pollution was associated with increased life expectancy in 211 urban counties. This new study looked at more recent data, more than two-and-a-half times as many counties, and included both rural and urban areas. The findings showed that there’s a stronger association between declining air pollution and increased life expectancy in more urban, densely populated areas than in rural areas. The results also suggested that reduced levels of air pollution may be more beneficial to women than to men.

As to why there was a stronger association between reductions in fine particulate matter and improvements in life expectancy in urban areas, the researchers speculated that the composition of the particulates there may be different from that in rural areas.

“Since the 1970s, enactment of increasingly stringent air quality controls has led to improvements in ambient air quality in the United States at costs that the U.S. Environ­mental Protection Agency has estimated as high as $25 billion per year. However, the extent to which more recent regulatory actions have benefited public health remains in question. This study provides strong and compelling evidence that continuing to reduce ambient levels of PM2.5 prolongs life,” said senior author Francesca Dominici, professor of biostatistics at HSPH.

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BPA may be associated with hyperactivity

Female mice exposed to Bisphenol A through their mother's diet during gestation and lactation were found to be hyperactive, exhibit spontaneous activity and had leaner body mass than those with no BPA chemical exposure.

BPA is a chemical most commonly found in the lining of food cans and cash register receipts. It once was in many hard plastic bottles, including baby bottles, but many companies have removed it as concerns about exposure have come to light in recent years.

These latest findings from researchers at the University of Michigan School of Public Health seem to contradict previous studies on BPA that found the chemical to be a factor in obesity. But Dana Dolinoy, the John G. Searle Assistant Professor of Environmental Health Sciences and senior/corresponding author of the study, says research shows that many factors impact how the body reacts to the chemical.

"Our hypothesis going into this study was that BPA would act as an obesogenic agent. And there is some preliminary evidence that it does," Dolinoy said. "But there are differences in exposure, duration and when you actually measure the individual.

"Recent evidence in humans only looks at one time point. What we're really interested in is BPA exposure during early development, and how that affects health throughout life. So those are two very different questions."

The researchers exposed mothers to three different levels of BPA in the diet then followed the offspring through adulthood at three, six and nine months of age. The average lifespan of a mouse is two years, so by three months they are young adults.

"We looked at several different metabolic phenotypes, including spontaneous activity, food intake, energy expenditure and body composition. I think the most striking result we saw was the increased activity in these animals," said Olivia Anderson, doctoral student in environmental health sciences and lead author on the paper published online in the Journal of the Federation of American Societies for Experimental Biology.

"There are several things we need to look at in evaluating studies investigating BPA as an obesogen, such as composition of the diet. Not all these diets are similar throughout these studies. Some may have high-fat diets. Some may have diets with different protein levels. Then there is the difference in exposure timing and doses of exposure of BPA. It's important to dig a little deeper and actually look at the mechanism that BPA is acting upon."

As to why only females exhibited the excessive activity and lean bodies, Dolinoy says it bears more study, but because BPA is known to impact estrogen and thyroid hormone, most likely it is affecting these natural hormones in the females.

Dolinoy's lab is dedicated to the study of environmental epigenetics and nutrition—learning about how exposure to chemical, nutritional and behavioral factors alters gene expression and impacts health and disease.

In December, she and colleagues released a study that found BPA in human fetal liver tissue, demonstrating that there is considerable exposure to the chemical during pregnancy. That research also found that the BPA in fetuses was in a form not eliminated from the body, unlike previous studies that showed adult humans metabolize and rid their bodies of the chemical.

Study shows climate change could affect onset and severity of flu seasons

The American public can expect to add earlier and more severe flu seasons to the fallout from climate change, according to a new study.

A team of scientists led by Sherry Towers, research professor in the Mathematical, Computational and Modeling Sciences Center at Arizona State University, studied waves of influenza and climate patterns in the U.S. from the 1997-1998 season to the present.

The team's analysis, which used Centers for Disease Control data, indicates a pattern for both A and B strains: warm winters are usually followed by heavy flu seasons.

"It appears that fewer people contract influenza during warm winters, and this causes a major portion of the population to remain vulnerable into the next season, causing an early and strong emergence," says Towers. "And when a flu season begins exceptionally early, much of the population has not had a chance to get vaccinated, potentially making that flu season even worse."

The current flu season, which is still in high gear in parts of the nation, began early and fiercely. It followed a relatively light 2011 season, which saw the lowest peak of flu since tracking efforts went into effect, and coincided with the fourth warmest winter on record. According to previous studies, flu transmission decreases in warm or humid conditions.

If global warming continues, warm winters will become more common, and the impact of flu will likely be more heavily felt, say the study's authors.

Mathematical epidemiologist Gerardo Chowell-Puente, an associate professor in the School of Human Evolution and Social Change in the College of Liberal Arts and Sciences, adds that the findings could inform preparedness efforts following mild winters: "The expedited manufacture and distribution of vaccines and aggressive vaccination programs could significantly diminish the severity of future influenza epidemics."

Research ties lightning to onset of migraines; may increase in pollution

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University of Cincinnati (UC) researchers have found that lightning may affect the onset of headache and migraines.

These results, published in the online edition of the journal Cephalalgia, are the first tying lightning to headache and could help chronic sufferers more efficiently anticipate headache and migraine arrival and begin preventive treatment immediately.

Geoffrey Martin, fourth-year medical student at UC, and his father Vincent Martin, MD, professor in the division of general internal medicine, UC Health physician and headache expert, led the study which showed that there was a 31 percent increased risk of headache and 28 percent increased risk of migraine for chronic headache sufferers on days lighting struck within 25 miles of study participant's homes.

In addition, new-onset headache and migraine increased by 24 percent and 23 percent in participants.

"Many studies show conflicting findings on how weather, including elements like barometric pressure and humidity, affect the onset of headaches," Geoffrey Martin says. "However, this study very clearly shows a correlation between lightning, associated meteorological factors and headaches."

Participants who fulfilled the criteria for International Headache Society-defined migraines were recruited from sites located in Ohio and Missouri and recorded their headache activity in a daily journal for three to six months.

During this time, the location where lightning struck within 25 miles of participant's homes as well as the magnitude and polarity of lightning current was recorded.

"We used mathematical models to determine if the lightning itself was the cause of the increased frequency of headaches or whether it could be attributed to other weather factors encountered with thunderstorms," says Vincent Martin. "Our results found a 19 percent increased risk for headaches on lightning days, even after accounting for these weather factors. This suggests that lightning has its own unique effect on headache."

He says that negatively charged lightning currents were also particularly associated with a higher chance of headache.

"There are a number of ways in which lightning might trigger headaches," he says. "Electromagnetic waves emitted from lightning could trigger headaches. In addition, lightning produces increases in air pollutants like ozone and can cause release of fungal spores that might lead to migraine."

"This study gives some insight into the tie between headaches or migraines, lightning and other meteorologic factors," says Geoffrey Martin. "However, the exact mechanisms through which lightning and/or its associated meteorologic factors trigger headache are unknown, although we do have speculations. Ultimately, the effect of weather on headache is complex, and future studies will be needed to define more precisely the role of lightning and thunderstorms on headache."

BPA substitute could spell trouble

A few years ago, manufacturers of water bottles, food containers, and baby products had a big problem. A key ingredient of the plastics they used to make their merchandise, an organic compound called bisphenol A, had been linked by scientists to diabetes, asthma and cancer and altered prostate and neurological development. The FDA and state legislatures were considering action to restrict BPA's use, and the public was pressuring retailers to remove BPA-containing items from their shelves.

The industry responded by creating "BPA-free" products, which were made from plastic containing a compound called bisphenol S. In addition to having similar names, BPA and BPS share a similar structure and versatility: BPS is now known to be used in everything from currency to thermal receipt paper, and widespread human exposure to BPS was confirmed in a 2012 analysis of urine samples taken in the U.S., Japan, China and five other Asian countries.

According to a study by University of Texas Medical Branch at Galveston researchers, though, BPS also resembles BPA in a more problematic way. Like BPA, the study found, BPS disrupts cellular responses to the hormone estrogen, changing patterns of cell growth and death and hormone release. Also like BPA, it does so at extremely low levels of exposure.

"Our studies show that BPS is active at femtomolar to picomolar concentrations just like endogenous hormones —that's in the range of parts per trillion to quadrillion," said UTMB professor Cheryl Watson, senior author of a paper on the study now online in the advance publications section of Environmental Health Perspectives. "Those are levels likely to be produced by BPS leaching from containers into their contents."

Watson and graduate student René Viñas conducted cell-culture experiments to examine the effects of BPS on a form of signaling that involves estrogen receptors — the "receivers" of a biochemical message — acting in the cell's outer membrane instead of the cell nucleus. Where nuclear signaling involves interaction with DNA to produce proteins and requires hours to days, membrane signaling (also called "non-genomic" signaling) acts through much quicker mechanisms, generating a response in seconds or minutes.

Watson and Viñas focused on key biochemical pathways that are normally stimulated when estrogen activates membrane receptors. One, involving a protein known as ERK, is linked to cell growth; another, labeled JNK, is tied to cell death. In addition, they examined the ability of BPS to activate proteins called caspases (also linked to cell death) and promote the release of prolactin, a hormone that stimulates lactation and influences many other functions.

"These pathways form a complicated web of signals, and we're going to need to study them more closely to fully understand how they work," Watson said. "On its own, though, this study shows us that very low levels of BPS can disrupt natural estrogen hormone actions in ways similar to what we see with BPA. That's a real cause for concern."

Residents near e-waste site face greater cancer risk

Residents living near an e-waste recycling site in China face elevated risks of lung cancer, according to a recent study co-authored by Oregon State University researchers.

Electronic trash, such as cell phones, computers and TVs, is collected in dumps in developing countries and crudely incinerated to recover precious metals, including silver, gold, palladium and copper. The process is often primitive, releasing chemical fumes with a range of toxic substances, including polycyclic aromatic hydrocarbons, or PAHs, a group of more than 100 chemicals.

PAHs, many of which are recognized as carcinogenic and linked to lung cancer when inhaled, were the focus of the study. Over the course of a year, researchers collected air samples from two rooftops in two areas in China.

One was in a rural village in the southern province of Guangdong less than a mile from an active e-waste burning site and not surrounded by any industry. The other was Guangzhou, a city heavily polluted by industry, vehicles and power plants but not e-waste.

The scientists concluded that those living in the e-waste village are 1.6 times more likely to develop cancer from inhalation than their urban-dwelling peers.

"In the village, people were recycling waste in their yards and homes, using utensils and pots to melt down circuit boards and reclaim metals," said Staci Simonich, a co-author of the study and a professor of environmental and molecular toxicology at OSU. "There was likely exposure through breathing, skin and food – including an intimate connection between e-waste and the growing of vegetables, raising of chickens and catching of fish."

The researchers estimated that of each million people in the e-waste area, 15 to 1,200 would develop lung cancer on account of PAHs over their lifetimes, while the likelihood in the city is slightly lower at 9 to 737 per million. These approximations do not include lung cancer caused by smoking.

The study also found that the level of airborne carcinogenic PAHs exceeded China's air quality standards 98 percent of the time in the e-waste area and 93 percent of the time in the city.

The study was published in the journal Environmental Science and Technology. The OSU Superfund Research Program provided assistance for the study. The National Institute of Environmental Health Sciences (NIEHS) and the National Institutes of Health (NIH) provided funding for the study. Eight researchers collaborated on the project, including OSU graduate student Leah Gonzales and scientists from China.

Researchers find link between air pollution and happiness

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Researchers in Canada have found a correlation between air pollution and people's happiness.

Economists at Trent University in Ontario, Canada, have taken an outside view of fourteen European countries to see whether or not there is a causal link between levels of air pollution and the happiness of citizens of those countries. Byron Lew and Mak Arvin explain that their research is not about the determinants of life satisfaction or air pollution but the primary goal is to focus on the causal relationships between these two factors.

The researchers looked at recorded data on pollution levels in Belgium, Denmark, France, Germany, Greece, Ireland, Italy, Luxembourg, Netherlands, Portugal, Romania, Russia, Spain and the UK. They analysed per capita carbon dioxide emissions as a proxy for overall pollution given that its main source is the burning of fossil fuels and looked for causality using a statistical formula, the Granger causality test, with citizen happiness as determined from survey data.

The findings do not offer a mechanism by which air pollution levels cause unhappiness and vice versa. However, they do suggest that policy changes that encourage less pollution will have a positive effect.

"A stronger case can be made for further regulation of the state of the environment in general and air quality in particular," the team says. "Cleaner air will elevate the level of happiness of citizens in Europe and we suspect in other regions around the globe."

Their analysis, is reported in the latest issue of the International Journal of Green Economics. 

Asthma researchers make breakthrough in attacks related to colds and allergens

Pediatric and respiratory researchers from the University of Newcastle, along with national and international collaborators, are a step closer to identifying the source of serious virus-and allergen-induced asthma attacks after detecting important molecular signals generated very early in the disease process.

Led by Professor Joerg Mattes, the team of researchers and clinicians spent several years investigating the mechanisms that trigger airway inflammation and cause asthma attacks.

The pre-clinical study targeted the common cold (rhinovirus), which is the virus that causes most asthma attacks; and the effects caused by allergens such as house dust mites.

“Asthmatics experience severe and prolonged symptoms when infected with the common cold virus or exposed to allergens, both of which promote inflammation in the lungs and production of mucus," Professor Mattes said.

“Asthma attacks are currently treated similarly regardless of whether they are caused by viruses or allergens. However virus-induced effects are much less responsive to current therapies, which is why this investigation is so important.”

A comprehensive gene expression analysis led to the initial discovery of the signals – proteins otherwise known as midline 1 and protein phosphatase 2A.

“The proteins are generated in the innermost layer of the airways, where the body has first contact with allergens and viruses, and once activated they appear to modulate many other disease factors,” Dr Adam Collison**, one of the study authors from Professor Mattes’ research team, said. “Obviously it is better to target these earlier signals rather than the hundreds of downstream effects.”

The researchers have already begun testing therapeutic strategies to modify the pathway, setting a platform for the development of targeted drugs ahead of full clinical trialling.

“We have seen that this pathway operates in the cells of asthmatics, and our pre-clinical disease models showed that we can inhibit the pathway and protect against the development of both virus- and allergen-induced asthma,” Professor Mattes said.

He advised sufferers to be vigilant with their asthma management during late summer and winter, the worst times for cold epidemics.

The results are published in Nature Medicine, the world’s leading journal for biomedical research. Researchers from the University of New South Wales, the University of Cincinnati and the Imperial College London took part in the investigation. 

Loneliness, like chronic stress, taxes the immune system

New research links loneliness to a number of dysfunctional immune responses, suggesting that being lonely has the potential to harm overall health.

Researchers found that people who were more lonely showed signs of elevated latent herpes virus reactivation and produced more inflammation-related proteins in response to acute stress than did people who felt more socially connected.

These proteins signal the presence of inflammation, and chronic inflammation is linked to numerous conditions, including coronary heart disease, Type 2 diabetes, arthritis and Alzheimer's disease, as well as the frailty and functional decline that can accompany aging.

Reactivation of a latent herpes virus is known to be associated with stress, suggesting that loneliness functions as a chronic stressor that triggers a poorly controlled immune response.

"It is clear from previous research that poor-quality relationships are linked to a number of health problems, including premature mortality and all sorts of other very serious health conditions. And people who are lonely clearly feel like they are in poor-quality relationships," said Lisa Jaremka, a postdoctoral fellow at the Institute for Behavioral Medicine Research at Ohio State University and lead author of the research.

"One reason this type of research is important is to understand how loneliness and relationships broadly affect health. The more we understand about the process, the more potential there is to counter those negative effects – to perhaps intervene. If we don't know the physiological processes, what are we going to do to change them?"

The results are based on a series of studies conducted with two populations: a healthy group of overweight middle-aged adults and a group of breast cancer survivors. The researchers measured loneliness in all studies using the UCLA Loneliness Scale, a questionnaire that assesses perceptions of social isolation and loneliness.

Jaremka will present the research Saturday (1/19) at the Society for Personality and Social Psychology annual meeting in New Orleans.

The researchers first sought to obtain a snapshot of immune system behavior related to loneliness by gauging levels of antibodies in the blood that are produced when herpes viruses are reactivated.

Participants were 200 breast cancer survivors who were between two months and three years past completion of cancer treatment with an average age of 51 years. Their blood was analyzed for the presence of antibodies against Epstein-Barr virus and cytomegalovirus.

Both are herpes viruses that infect a majority of Americans. About half of infections do not produce illness, but once a person is infected, the viruses remain dormant in the body and can be reactivated, resulting in elevated antibody levels, or titers – again, often producing no symptoms but hinting at regulatory problems in the cellular immune system.

Lonelier participants had higher levels of antibodies against cytomegalovirus than did less lonely participants, and those higher antibody levels were related to more pain, depression and fatigue symptoms. No difference was seen in Epstein-Barr virus antibody levels, possibly because this reactivation is linked to age and many of these participants were somewhat older, meaning reactivation related to loneliness would be difficult to detect, Jaremka said.

Previous research has suggested that stress can promote reactivation of these viruses, also resulting in elevated antibody titers.

"The same processes involved in stress and reactivation of these viruses is probably also relevant to the loneliness findings," Jaremka said. "Loneliness has been thought of in many ways as a chronic stressor – a socially painful situation that can last for quite a long time."

In an additional set of studies, the scientists sought to determine how loneliness affected the production of proinflammatory proteins, or cytokines, in response to stress. These studies were conducted with 144 women from the same group of breast cancer survivors and a group of 134 overweight middle-aged and older adults with no major health problems.

Baseline blood samples were taken from all participants, who were then subjected to stress – they were asked to deliver an impromptu five-minute speech and perform a mental arithmetic task in front of a video camera and three panelists. Researchers followed by stimulating the participants' immune systems with lipopolysaccharide, a compound found on bacterial cell walls that is known to trigger an immune response.

In both populations, those who were lonelier produced significantly higher levels of a cytokine called interleukin-6, or IL-6, in response to acute stress than did participants who were more socially connected. Levels of another cytokine, tumor necrosis factor-alpha, also rose more dramatically in lonelier participants than in less lonely participants, but the findings were significant by statistical standards in only one study group, the healthy adults.

In the study with breast cancer survivors, researchers also tested for levels of the cytokine interleukin 1-beta, which was produced at higher levels in lonelier participants.

When the scientists controlled for a number of factors, including sleep quality, age and general health measures, the results were the same.

"We saw consistency in the sense that more lonely people in both studies had more inflammation than less lonely people," Jaremka said.

"It's also important to remember the flip side, which is that people who feel very socially connected are experiencing more positive outcomes," she said.

VIDEO: Children Raised on Farms Develop Better Immune Systems

Is farm life the secret to healthy living? Watch this report from ABC news:



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Pesticides, Wastewater Contributing to Pollution in the Great Lakes; Affects 8 U.S. States and 2 Canadian Provinces

Toxic releases into surface waters in the Great Lakes Basin increased by 12 percent from 2010 to 2011, according to the U.S. Environmental Protection Agency’s annual Toxics Release Inventory report published today.

“This is a significant increase in toxic releases to our waters – and an indication that the Great Lakes region is lagging behind other parts of the country,” said Susan Hedman, EPA Region 5 Administrator and Great Lakes National Program Manager. “EPA’s Toxic Release Inventory is a valuable tool to help target areas for improvement and we will use this new information to work with municipalities, agricultural producers and manufacturers in the Great Lakes Basin to improve water quality.”

Nitrates and pesticides from municipal wastewater treatment plants and agriculture account for most of the toxic surface water discharges to the Great Lakes Basin. Nitrates were also discharged by primary metals facilities, such as iron and steel mills and smelters, and food and beverage manufacturers.

The Great Lakes Basin consists of Lakes Superior, Michigan, Huron, Erie and Ontario; a number of other smaller lakes and waterways; and the surrounding watershed. The watershed covers parts of Illinois, Indiana, Minnesota, Michigan, New York, Ohio, Pennsylvania and Wisconsin, and parts of Ontario in Canada. The Great Lakes are the largest surface freshwater system in the world.

Despite increases from 2010 to 2011, overall toxic releases in the Great Lakes Basin have decreased about 40 percent since 2003 and are currently at the second-lowest level in a decade.

Nationwide, the 2011 TRI data show total toxic air releases in 2011 declined 8 percent from 2010, mostly because of decreased emissions of hazardous air pollutants. Total releases of toxic chemicals increased for the second year in a row as a result of mining.

EPA’s TRI program collects information on toxic chemical releases to the air, water and land, as well as information on waste management and pollution prevention activities by facilities across the country. Facilities must report their toxic releases to EPA under the Federal Emergency Planning and Community Right-to-Know Act by the beginning of July each year.

Airpocalypse: China's pollution off the charts

Beijing from Space: NASA image 

The fact that it's being discussed openly on TV in China gives some hint as to the gravity of the air pollution currently besieging the country's capital.

At it's peak on January 12th the U.S. embassy measured the airborne fine particle count at a shocking 886 micrograms per cubic meter of air. That's the highest since monitoring began in 2007. The World Health Organization considers the air safe when it is below 25.

The overall air quality index rating was measured at 775. According to the AQI ranking system, anything over 300 is "Hazardous" –  and not just for those with respiratory issues, but for anyone that breathes. 

The situation has been dubbed "Airpocalypse" and is the result of several factors including surrounding mountains which trap pollutants low in the atmosphere, the lack of wind and the proliferation of factories and coal burning.

Study says fast food linked to severe asthma, eczema in teens and kids

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Kids and teens who eat fast food three or more times per week have a much higher risk of suffering from severe asthma and eczema say researchers.

The scientists at the University of Auckland studied data from 319,000 teens in 51 countries and 181,000 children ages 6 and 7 in 31 countries. They found that teens who ate three or more servings per week have a 39% increased chance of developing severe asthma, while kids risk increase by 27%.

The authors say that because fast food was the only dietary category shown to have an association with these conditions, the results may suggest that such a diet may actually cause asthma attacks or eczema outbreaks.



Fast foods contain high levels of trans fatty acids, which are known to affect immune reactions and inflammation.

The researchers also found that eating at least three servings of fruits and vegetables per week had a protective effect and helped reduce the risk of developing asthma and eczema. 

The study was published today in the British medical journal Thorax.

Pollen exposure during pregnancy affects child's risk of early asthma

A woman’s exposure to high pollen levels late in pregnancy increases her risk of having a child with early asthma, according to a new study. 

The researchers at the Division of Occupational and Environmental Medicine at Umeå University in Sweden followed 110,000 pregnancies in the Stockholm area.

They found that high levels of pollen exposure during the last 12 weeks of pregnancy resulted in a significantly increased risk of hospitalization for asthma symptoms in the first year of life for a child. The analysis was adjusted for factors such as maternal smoking and pollen season.

They say there may be several reasons for the association. High pollen exposure of pregnant women with pollen allergies may trigger reactions and asthma symptoms that then affect the unborn child's immune system development. It is also possible that pregnant women with severe reactions to pollen suffer complications and sometimes give birth earlier than they otherwise would have done, which in itself increases the risk of respiratory problems in the child.

Study offers clues to why heavy people and anorexics have higher asthma rates

A new study led by Columbia University researchers has found that leptin, a hormone that plays a key role in energy metabolism, fertility, and bone mass, also regulates airway diameter.

These findings could explain why obese people are prone to asthma and suggest that body-weight–associated-asthma may be relieved with medications which help the body mediate leptin function. The study, conducted in mice, was published in the online edition of the journal Cell Metabolism.

“Our study started with the clinical observation that both obesity and anorexia can lead to asthma,” said Gerard Karsenty MD, PhD, professor and chair of genetics and development and professor of medicine at CUMC, and lead author of the study. “This led us to suspect that there must be a signal coming from fat cells that somehow affects the lungs —directly or indirectly.” The most likely candidate was leptin, a protein made by fat cells that circulates in the bloodstream and travels to the brain.

Extensive evidence shows that obesity can cause narrowing of the airways (bronchoconstriction). When obesity develops in people with asthma, it exacerbates the breathing disorder and hampers its treatment through mechanisms that are poorly understood. The current study was designed to elucidate the genetic and molecular bases of the relationships among obesity, airway diameter, and lung function.

Through mouse studies, the researchers showed that abnormally low or high body weight and fat mass results in bronchoconstriction and diminished lung function. Next, they showed that leptin increases airway diameter independently of, and at a lower threshold than, its regulation of appetite.

Leptin affects the airways by decreasing the activity of the parasympathetic nervous system, a branch of the autonomic nervous system not usually associated with leptin. The researchers also showed that regulation of airway diameter occurs regardless of local inflammation in the bronchi.

The researchers conducted two subsequent experiments to determine if these findings might have bearing on asthma therapy. In one, they took obese, asthmatic mice and administered a substance that increases lung inflammation. When they infused leptin in the brain of these mice for four days, “There was no effect on inflammation, but airway diameter and lung functions were normal,” said Dr. Karsenty. “This showed that, at least in the mouse, you can cure obesity-related asthma without affecting inflammation.” In the second experiment, the researchers treated obese, asthmatic mice with drugs that decrease parasympathetic tone, or rate of neuronal firing. Again, the asthma abated after several days.

“The therapeutic implication is that it may be possible to correct asthma in obese people with drugs that inhibit parasympathetic signaling—and thereby inhibit leptin deficiency-related brain signaling,” said Dr. Karsenty. Such drugs are already available. One is tiotropium bromide, which is used primarily for the treatment of chronic obstructive pulmonary disease. Clinical trials are needed before this or a more active and selective drug can be recommended for the treatment of body weight–associated asthma, Dr. Karsenty added.

U of Florida study uncovers protein key to fighting and preventing obesity

University of Florida researchers and colleagues have identified a protein that, when absent, helps the body burn fat and prevents insulin resistance and obesity.

The discovery could aid development of drugs that not only prevent obesity, but also spur weight loss in people who are already overweight, said Dr. Stephen Hsu, one of the study’s corresponding authors and a principal investigator with the UF Sid Martin Biotechnology Development Institute.

One-third of adults and about 17 percent of children in the United States are obese, according to the Centers for Disease Control and Prevention. Although unrelated studies have shown that lifestyle changes such as choosing healthy food over junk food and increasing exercise can help reduce obesity, people are often unable to maintain these changes over time, Hsu said.

“The problem is when these studies end and the people go off the protocols, they almost always return to old habits and end up eating the same processed foods they did before and gain back the weight they lost during the study,” he said. Developing drugs that target the protein, called TRIP-Br2, and mimic its absence may allow for the prevention of obesity without relying solely on lifestyle modifications, Hsu said.

First identified by Hsu, TRIP-Br2 helps regulate how fat is stored in and released from cells. To understand its role, the researchers compared mice that lacked the gene responsible for production of the protein, with normal mice that had the gene.

They quickly discovered that mice missing the TRIP-Br2 gene did not gain weight no matter what they ate — even when placed on a high-fat diet — and were otherwise normal and healthy. On the other hand, the mice that still made TRIP-Br2 gained weight and developed associated problems such as insulin resistance, type 2 diabetes and high cholesterol when placed on a high-fat diet. The normal and fat-resistant mice ate the same amount of food, ruling out differences in food intake as a reason why the mice lacking TRIP-Br2 were leaner.

“We had to explain why the animals eating so much fat were remaining lean and not getting high cholesterol. Where was this fat going?” Hsu said. “It turns out this protein is a master regulator. It coordinates expression of a lot of genes and controls the release of the fuel form of fat and how it is metabolized.”

When functioning normally, TRIP-Br2 restricts the amount of fat that cells burn as energy. But when TRIP-Br2 is absent, a fat-burning fury seems to occur in fat cells. Although other proteins have been linked to the storage and release of fat in cells, TRIP-Br2 is unique in that it regulates how cells burn fat in a few different ways, Hsu said. When TRIP-Br2 is absent, fat cells dramatically increase the release of free fatty acids and also burn fat to produce the molecular fuel called ATP that powers mitochondria — the cell’s energy source. In addition, cells free from the influence of TRIP-Br2 start using free fatty acids to generate thermal energy, which protects the body from exposure to cold.

“TRIP-Br2 is important for the accumulation of fat,” said Dr. Rohit N. Kulkarni, also a senior author of the paper and an associate professor of medicine at Harvard Medical School and the Joslin Diabetes Center. “When an animal lacks TRIP-Br2, it can’t accumulate fat.”

Because the studies were done mostly in mice, additional studies are still needed to see if the findings translate to humans.

“We are very optimistic about the translational promise of our findings because we showed that only human subjects who had the kind of fat (visceral) that becomes insulin-resistant also had high protein levels of TRIP-Br2,” Hsu said.

“Imagine you are able to develop drugs that pharmacologically mimic the complete absence of TRIP-Br2,” Hsu said. “If a patient started off fat, he or she would burn the weight off. If people are at risk of obesity and its associated conditions, such as type 2 diabetes, it would help keep them lean regardless of how much fat they ate. That is the ideal anti-obesity drug, one that prevents obesity and helps people burn off excess weight.”

Pesticides and Parkinson's: Researchers Uncover Further Proof of a Link

For several years, neurologists at UCLA have been building a case that a link exists between pesticide chemical exposure and Parkinson's disease. To date, paraquat, maneb and ziram — common chemicals sprayed in California's Central Valley and elsewhere — have been tied to increases in the disease, not only among farmworkers but in individuals who simply lived or worked near fields and likely inhaled drifting particles.

Now, UCLA researchers have discovered a link between Parkinson's and another pesticide, benomyl, whose toxicological effects still linger some 10 years after the chemical was banned by the U.S. Environmental Protection Agency.

Even more significantly, the research suggests that the damaging series of events set in motion by benomyl may also occur in people with Parkinson's disease who were never exposed to the pesticide, according to Jeff Bronstein, senior author of the study and a professor of neurology at UCLA, and his colleagues.

Benomyl exposure, they say, starts a cascade of cellular events that may lead to Parkinson's. The pesticide prevents an enzyme called ALDH (aldehyde dehydrogenase) from keeping a lid on DOPAL, a toxin that naturally occurs in the brain. When left unchecked by ALDH, DOPAL accumulates, damages neurons and increases an individual's risk of developing Parkinson's.

The investigators believe their findings concerning benomyl may be generalized to all Parkinson's patients. Developing new drugs to protect ALDH activity, they say, may eventually help slow the progression of the disease, whether or not an individual has been exposed to pesticides.

The research is published in the current online edition of Proceedings of the National Academy of Sciences.

Parkinson's disease is a debilitating neurodegenerative disorder that affects millions worldwide. Its symptoms — including tremor, rigidity, and slowed movements and speech — increase with the progressive degeneration of neurons, primarily in a part of the mid-brain called the substantia nigra. This area normally produces dopamine, a neurotransmitter that allows cells to communicate, and damage to the mid-brain has been linked to the disease. Usually, by the time Parkinson's symptoms manifest themselves, more than half of these neurons, known as dopaminergic neurons, have already been lost.

While researchers have identified certain genetic variations that cause an inherited form of Parkinson's, only a small fraction of the disease can be blamed on genes, said the study's first author, Arthur G. Fitzmaurice, a postdoctoral scholar in Bronstein's laboratory.

"As a result, environmental factors almost certainly play an important role in this disorder," Fitzmaurice said. "Understanding the relevant mechanisms — particularly what causes the selective loss of dopaminergic neurons — may provide important clues to explain how the disease develops."

Benomyl was widely used in the U.S. for three decades until toxicological evidence revealed it could potentially lead to liver tumors, brain malformations, reproductive effects and carcinogenesis. It was banned in 2001.

The researchers wanted to explore whether there was a relationship between benomyl and Parkinson's, which would demonstrate the possibility of long-lasting toxicological effects from pesticide use, even a decade after chronic exposure. But because a direct causal relationship between the pesticide and Parkinson's can't be established by testing humans, the investigators sought to determine if exposure in experimental models could duplicate some of the pathologic features of the disease.

They first tested the effects of benomyl in cell cultures and confirmed that the pesticide damaged or destroyed dopaminergic neurons.

Next, they tested the pesticide in a zebrafish model of the disease. This freshwater fish is commonly used in research because it is easy to manipulate genetically, it develops rapidly and it is transparent, making the observation and measurement of biological processes much easier. By using a fluorescent dye and counting the neurons, the researchers discovered there was significant neuron loss in the fish — but only to the dopaminergic neurons. The other neurons were left unaffected.

Until now, evidence had pointed to one particular culprit — a protein called α-synuclein — in the development of Parkinson's. This protein, common to all Parkinson's patients, is thought to create a pathway to the disease when it binds together in "clumps" and becomes toxic, killing the brain's neurons. (See UCLA research using "molecular tweezers" to break up these toxic aggregations.)

The identification of ALDH activity now gives researchers another target to focus on in trying to stop this disease.

"We've known that in animal models and cell cultures, agricultural pesticides trigger a neurodegenerative process that leads to Parkinson's," said Bronstein, who directs the UCLA Movement Disorders Program. "And epidemiologic studies have consistently shown the disease occurs at high rates among farmers and in rural populations. Our work reinforces the hypothesis that pesticides may be partially responsible, and the discovery of this new pathway may be a new avenue for developing therapeutic drugs."

"Tricorders" closer to becoming a reality

Photo: Peter Norgard, University of Missouri

The hand-held scanners, or tricorders, of the Star Trek movies and television series are one step closer to reality now that a University of Missouri engineering team has invented a compact source of X-rays and other forms of radiation.

 The radiation source, which is the size of a stick of gum, could be used to create inexpensive and portable X-ray scanners for use by doctors, as well as to fight terrorism and aid exploration on this planet and others.

“Currently, X-ray machines are huge and require tremendous amounts of electricity,” said Scott Kovaleski, associate professor of electrical and computer engineering at MU. “In approximately three years, we could have a prototype hand-held X-ray scanner using our invention. The cell-phone-sized device could improve medical services in remote and impoverished regions and reduce health care expenses everywhere.”

Kovaleski suggested other uses for the device. In dentists’ offices, the tiny X-ray generators could be used to take images from the inside of the mouth shooting the rays outward, reducing radiation exposure to the rest of the patients’ heads. At ports and border crossings, portable scanners could search cargoes for contraband, which would both reduce costs and improve security. Interplanetary probes, like the Curiosity rover, could be equipped with the compact sensors, which otherwise would require too much energy.

The accelerator developed by Kovaleski’s team could be used to create other forms of radiation in addition to X-rays. For example, the invention could replace the radioactive materials, called radioisotopes, used in drilling for oil as well as other industrial and scientific operations. Kovaleski’s invention could replace radioisotopes with a safer source of radiation that could be turned off in case of emergency.

“Our device is perfectly harmless until energized, and even then it causes relatively low exposures to radiation,” said Kovaleski. “We have never really had the ability to design devices around a radioisotope with an on-off switch. The potential for innovation is very exciting.”

The device uses a crystal to produce more than 100,000 volts of electricity from only 10 volts of electrical input with low power consumption. Having such a low need for power could allow the crystal to be fueled by batteries. The crystal, made from a material called lithium niobate, uses the piezoelectric effect to amplify the input voltage. Piezoelectricity is the phenomenon whereby certain materials produce an electric charge when the material is under stress.

Kovaleski’s team published “Investigation of the Piezoelectric Effect as a Means to Generate X-Rays” in the journal IEEE Transaction on Plasma Science. Kovaleski is interim department chair of the Electrical & Computer Engineering in MU’s Department of Engineering.


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Study Finds Flame Retardant Pollutants Even in Remote Areas like Nepal

Chemicals used as flame retardants are present as environmental pollutants at locations around the globe, including remote sites in Indonesia, Nepal and Tasmania, according to a study by researchers from the Indiana University School of Public and Environmental Affairs.

The study, published this month in the journal Environmental Science and Technology, makes use of a novel but highly effective sampling technique: measuring concentrations of the chemicals in the bark of trees, which absorbs airborne chemical compounds in both vapor and particle phases.

"These findings illustrate further that flame retardants are ubiquitous pollutants and are found all around the world, not only in biota and humans but also in plants," said Amina Salamova, a research associate in the School of Public and Environmental Affairs at IU Bloomington and co-author of the study with Ronald A. Hites, Distinguished Professor in SPEA and in the Department of Chemistry in the College of Arts and Sciences.

The study measured concentrations of brominated and chlorinated flame retardants collected in tree bark samples at 12 locations around the globe: three sites in Canada and single sites in Iceland, Ireland, Norway, Czech Republic, South Africa, Nepal, Indonesia, Tasmania and American Samoa.

The highest concentrations were found at an urban site: Downsview, Ontario, Canada, near Toronto. However, the second-highest concentration of one type of flame retardant, Dechlorane Plus, was found at a remote site at Bukit Kototabang in Indonesia. Researchers don't know the cause of the relatively high concentrations at the site but suspect it may be near a source.

The study was carried out in cooperation with the Global Atmospheric Passive Sampling network, an international monitoring initiative established in 2004 on six continents.

Brominated and chlorinated flame retardants have been used for several decades in consumer products made of plastic, foam, wood and textiles to prevent combustion and slow the spread of fire. They persist in the environment and bio-accumulate in ecosystems and in human tissues. Exposure to the compounds has been associated with thyroid and other endocrine system disruption and with adverse neurological development. As a result, the production and use of certain flame retardants has been restricted in North America and the European Union.

Researchers measured a variety of flame retardants, including widely used polybrominated diphenyl ethers, or PBDE, as well as nonregulated compounds such as Dechlorane Plus and "older" flame retardants that were used in the 1980s. Findings included:

-- Most of the compounds were detected at all the locations, with concentrations varying widely.
-- Concentrations were associated with population density, suggesting the compounds most likely entered the environment through their use in nearby homes and offices.
-- Concentrations found in tree bark are correlated with those measured in previous atmospheric sampling at the sites by the Global Atmospheric Passive Sampling network.

Higher concentrations of flame retardants in bark and the atmosphere have been found by Hites and others in previous studies of the Great Lakes region, especially urban areas near Chicago and Cleveland, and also at cities in China. Even higher concentrations were found in southern Arkansas and at Niagara Falls, N.Y., near the sites of manufacturing facilities for PBDE and Dechlorane Plus, respectively.

The study also confirms the effectiveness of using tree bark as a sampling medium, a technique that Hites and colleagues have used in previous studies of persistent organic pollutants such as flame retardants.

Bark makes an effective sampling medium because of its large surface area and high lipid content. The samples are easy and inexpensive to collect, an advantage in developing countries that lack funding for extensive environmental monitoring programs. Tree bark also collects both vapor and particle phase pollutants, while other samplers collect one or the other.

Modern parenting may hinder brain development, research shows

Social practices and cultural beliefs of modern life are preventing healthy brain and emotional development in children, according to an interdisciplinary body of research presented recently at a symposium at the University of Notre Dame.

“Life outcomes for American youth are worsening, especially in comparison to 50 years ago,” says Darcia Narvaez, Notre Dame professor of psychology who specializes in moral development in children and how early life experiences can influence brain development.

“Ill-advised practices and beliefs have become commonplace in our culture, such as the use of infant formula, the isolation of infants in their own rooms or the belief that responding too quickly to a fussing baby will ‘spoil’ it,” Narvaez says.

This new research links certain early, nurturing parenting practices — the kind common in foraging hunter-gatherer societies — to specific, healthy emotional outcomes in adulthood, and has many experts rethinking some of our modern, cultural child-rearing “norms.”

“Breast-feeding infants, responsiveness to crying, almost constant touch and having multiple adult caregivers are some of the nurturing ancestral parenting practices that are shown to positively impact the developing brain, which not only shapes personality, but also helps physical health and moral development,” says Narvaez.

Studies show that responding to a baby’s needs (not letting a baby “cry it out”) has been shown to influence the development of conscience; positive touch affects stress reactivity, impulse control and empathy; free play in nature influences social capacities and aggression; and a set of supportive caregivers (beyond the mother alone) predicts IQ and ego resilience as well as empathy.

The United States has been on a downward trajectory on all of these care characteristics, according to Narvaez. Instead of being held, infants spend much more time in carriers, car seats and strollers than they did in the past. Only about 15 percent of mothers are breast-feeding at all by 12 months, extended families are broken up and free play allowed by parents has decreased dramatically since 1970.

Whether the corollary to these modern practices or the result of other forces, an epidemic of anxiety and depression among all age groups, including young children; rising rates of aggressive behavior and delinquency in young children; and decreasing empathy, the backbone of compassionate, moral behavior, among college students, are shown in research.

According to Narvaez, however, other relatives and teachers also can have a beneficial impact when a child feels safe in their presence. Also, early deficits can be made up later, she says.

“The right brain, which governs much of our self-regulation, creativity and empathy, can grow throughout life. The right brain grows though full-body experience like rough-and-tumble play, dancing or freelance artistic creation. So at any point, a parent can take up a creative activity with a child and they can grow together.”

Cornell University: Conditions right for outbreak of new virus in NYC, Atlanta, Miami

Global travel and climate warming could be creating the right conditions for outbreaks of a new virus in this country, according to a new Cornell University computer model.

The model predicts that outbreaks of "chikungunya", a painful virus transported by travelers and spread by the invasive Asian tiger mosquito, could occur in 2013 in New York City during August and September, in Atlanta from June through September, and year-round in Miami. The probability of a disease outbreak is correlated with temperature, as warmer weather allows the Asian tiger mosquito to breed faster and grow in numbers, according to the study published in PLOS Neglected Tropical Diseases.

According to the simulation, there is a high probability of a chikungunya outbreak if a single infected person arrives in New York in July or August and is bitten by an Asian tiger mosquito. The risks are the same, but with wider time frames, for transmission in Atlanta and Miami, according to the paper.

Asian tiger mosquitoes were introduced to the United States in Texas in the 1980s; they are established up the East Coast into New Jersey and are rising in numbers in New York City. The aggressive mosquito outcompetes local varieties and transmits more than 20 pathogens, including chikungunya and dengue, said Laura Harrington, associate professor of entomology and the study’s senior author.

“The virus is moving in people, and resident mosquito populations are picking it up,” Harrington said.

The model estimates that with typical regional temperatures, a chikungunya outbreak in New York would infect about one in 5,000 people, said Diego Ruiz-Moreno, a postdoctoral associate and the paper’s lead author

“However, this number would increase drastically as temperatures rise due to climate change,” Ruiz-Moreno said.

Chikungunya symptoms include a fever, severe joint pain, achiness, headache, nausea and fatigue, as well as “debilitating and prolonged” pain in the small joints of the hands and feet, according to the paper. The virus originated in Central Africa and is endemic in Southeast Asia.

Since no chikungunya vaccine exists, U.S. residents can help prevent an outbreak by removing standing water, wearing long sleeves and repellent during the day when the mosquitoes feed, and knowing the risk and symptoms when traveling, Harrington said.

The study was funded by a National Institute for Food and Agriculture Hatch grant and Cornell’s Atkinson Center for a Sustainable Future Climate Change and Disease Program.

Toys and Training Batons May Expose Dogs to Dangerous Chemicals

Sometimes orange, sometimes white, dog trainers often use plastic fetching batons called bumpers to teach dogs how to retrieve. But researchers at Texas Tech University have discovered that the dogs also may fetch a mouthful of potentially dangerous chemicals at the same time.

Researchers also found these chemicals, though at significantly lower concentrations, in a multitude of plastic chew toys purchased from a pet store.

The research was conducted by Kimberly Wooten, a master’s student using the project as her thesis, and Phil Smith, an associate professor of terrestrial ecotoxicology at The Institute of Environmental and Human Health at Texas Tech. Though unpublished, Wooten presented the results at the Society of Environmental Toxicology and Chemistry conference held in California.

“I raise and train Labrador retrievers and hunt with them as well,” Smith said, explaining what inspired him and Wooten to conduct the experiments. “In the process of training a lab, you do a lot of work with these plastic bumpers. I have a lot of bumpers in my garage, and they spend a lot of time in the mouths of my retrievers. Well, lots of attention has been given to chemicals in plastics lately regarding their effects on humans. Since we all care about our dogs, and we want them to be as healthy and smart and well-behaved as possible, we decided to look into this.”

Wooten and Smith said they predicted the possibility that the bumpers could leach phthalates and bisphenol A (BPA), which are used to give elasticity to plastic and vinyl and are known endocrine disruptors that mimic estrogen or act as anti-androgens and could lead to negative health effects. However, both said the findings have created more questions than answers because hardly any data exists on long-term effects of these chemicals on man’s best friend.

“The whole end goal was to answer the questions, ‘What does this mean for my pet? Is this a concern for our health?’” Wooten said. “We don’t have a good answer yet because there’s no good data to compare to our findings.”

To test for the chemicals, Wooten and Smith created simulated dog saliva, then simulated chewing by squeezing the bumpers and dog toys with stainless steel salad tongs.

Some bumpers and toys were weathered outside as well to see if older toys gave off more chemicals, Smith said.

“We found that the aging or weathering the toys increased concentrations of BPA and phthalates,” Smith said. “The toys had lower concentrations of phthalates than the bumpers, so that’s good news. But they also had some other chemicals that mimicked estrogen. We need to find out what those are.”

Wooten said BPA and phthalates can have effects on developing fetuses and can have a lifelong effect on offspring on lab animals. Some studies on humans conclude that BPA poses no health risks while others cite a number of adverse effects. Because of this, the U.S. government banned the use of BPA in baby bottles in 2012.

Wooten said questions still remain also as to how much of a dose a dog may get from playing with the bumpers, since it was difficult to say how much of these chemicals may actually leach out into a dog’s mouth.

“The interaction of pet health and environmental chemicals is understudied,” Wooten said. “What may be a safe dose for one species isn’t always a good measure for another species. But the amount of BPA and phthalates we found from the bumpers would be considered on the high end of what you might find in children’s toys.”

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Survey Shows That Nearly 1 in 3 Children with Food Allergies Experience Bullying

Photo: Stuart Miles

Nearly a third of children diagnosed with food allergies who participated in a recent study are bullied, according to researchers at the Icahn School of Medicine at Mount Sinai. Almost eight percent of children in the U.S. are allergic to foods such as peanuts, tree-nuts, milk, eggs, and shellfish.

Nearly half of parents surveyed (47.9 percent) were not aware of the bullying—although both the bullied children and their parents reported experiencing higher stress levels and lower quality of life.

The study, titled, “Child and Parental Reports of Bullying in a Consecutive Sample of Children with Food Allergy,” appears in the online issue of Pediatrics on December 24. The study was led by Eyal Shemesh, MD, Associate Professor of Pediatrics and Psychiatry at the Icahn School of Medicine at Mount Sinai. Dr. Shemesh and his team surveyed 251 pairs of parents and children. The patient and parent pairs were consecutively recruited during allergy clinic visits to independently answer questionnaires. Bullying due to food allergy or for any cause, quality of life, and distress in both the child and parent were evaluated using validated questionnaires.

“Parents and pediatricians should routinely ask children with food allergy about bullying,” said Dr. Shemesh. “Finding out about the child’s experience might allow targeted interventions, and would be expected to reduce additional stress and improve quality of life for these children trying to manage their food allergies.” Dr. Shemesh is Director of EMPOWER (Enhancing, Managing, and Promoting Well-being and Resiliency), a program within Mount Sinai’s Jaffe Food Allergy Institute. Dr. Shemesh is also Chief of the Division of Behavioral and Developmental Health in the Department of Pediatrics at The Mount Sinai Medical Center.

“When parents are aware of the bullying, the child’s quality of life is better,” said the senior author, Scott H. Sicherer, MD, Professor of Pediatrics, Chief, Division of Pediatric Allergy, Co-Director, EMPOWER program. “Our results should raise awareness for parents, school personnel, and physicians to proactively identify and address bullying in this population.”

The work for the study was supported by the EMPOWER program, a program funded by a generous donation from the Jaffe Family Foundation, that is devoted to understanding and enhancing the quality of life of persons with food allergy.

Infants with Severe RSV Disease May Be Immunosuppressed

Infants with severe lower respiratory tract infection caused by respiratory syncytial virus (RSV) may have a dysfunctional innate immune response that relates to the severity of their disease. These are the findings from a Nationwide Children’s Hospital study appearing in a recent issue of the Journal of Infectious Diseases.

RSV is the leading cause of lower respiratory tract infection in young children worldwide. The majority of children hospitalized with this condition are previously healthy with no known risk factors for serious disease. Of these infants, up to 20 percent will develop a disease severe enough to require admission to the pediatric intensive care unit (PICU).

It’s suggested that viral factors and the host immune response both contribute to the severity of RSV disease. A child’s functional innate immune response is increasingly being recognized as contributing to disease severity, but few studies have examined this phenomenon.

“For a long time we thought that children with severe RSV disease had higher concentrations of innate immunity cytokines, but it seems to be the opposite,” said the study’s senior author Asuncion Mejias, MD, PhD, physician scientist in Infectious Diseases at Nationwide Children’s Hospital. “When we stimulate the blood of these infants the production of innate immunity cytokines is severely impaired, and more importantly, this weakened response correlates with the more severe forms of the disease.”

To investigate the relationship between innate immunity and RSV disease severity, Dr. Mejias and Octavio Ramilo, MD, chief of Infectious Diseases at Nationwide Children’s in collaboration with Cesar Mella, MD, and Mark Hall, MD, from Critical Care at Nationwide Children’s, sought to determine whether patients with bronchiolitis admitted to the PICU had decreased whole blood functional innate immune responses. They also examined the relationships between innate immune dysfunction and disease outcomes.

The team evaluated 66 previously-healthy children less than two years old who were hospitalized with a first episode of RSV bronchiolitis during the 2010 – 2011 respiratory season. A nasal wash sample and a blood sample were obtained from each patient within 24 hours of admission to confirm RSV infection, and to measure cytokine concentrations before and after LPS stimulation. The team also enrolled healthy infants for control comparison.

They found that critically ill children with RSV admitted to the PICU had a significantly lower production capacity of innate cytokines compared with healthy controls and infants with less severe RSV bronchiolitis hospitalized in the Infectious Diseases unit.

“Whether children who develop severe RSV disease are born with an already impaired immune response, and RSV just uncovers their abnormal immune system will require further studies,” says Dr. Mejias, who is also a faculty member at The Ohio State University (OSU) College of Medicine. “Our study clearly suggests the presence of an inadequate, rather than excessive, functional innate immune response in children with RSV. This inadequate functional innate immune response is directly associated with the severity of the disease.”

Dr. Hall, also with OSU College of Medicine, said that immune monitoring of RSV patients at the time of hospitalization could have important clinical implications.

“Our data suggest that children with the most severe forms of RSV disease may already be immunosuppressed when we meet them in the ICU, raising the possibility of worsening this immunosuppression with the addition of commonly prescribed corticosteroids used to blunt the pro-inflammatory response to RSV,” said Dr. Hall.

Prospective immune monitoring may be helpful to identify children with bronchiolitis at high-risk for severe disease.

The findings also suggest the potential for the use of immune stimulant drugs that have been used with some success in reversing innate immune suppression in critically ill adults and children.

“Further studies are needed to explain the mechanisms responsible for innate immune suppression observed in critically-ill RSV-infected children,” said Dr. Ramilo, also with OSU College of Medicine.

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