Friday, March 29, 2013

Childhood asthma tied to combination of genes and wheezing illness

About 90 percent of children with two copies of a common genetic variation and who wheezed when they caught a cold early in life went on to develop asthma by age 6, according to a study to be published March 28 by the New England Journal of Medicine.

These children, all from families with a history of asthma or allergies, were nearly four times as likely to develop the disease as those who lacked the genetic variation and did not wheeze. The effects of each—the genetic variation and wheezing illness caused by a human rhinovirus infection—are not merely additive but also interactive, the authors say.

The genetic marker studied, a variation on chromosome 17, is common. Half of the children in the study had one copy and 25 percent had two. Colds caused by human rhinoviruses also are extremely common, affecting almost all infants. But the combination of genetic risk plus the wheezing response to rhinovirus infection by children under age 3 was tightly linked to the development of asthma by age 6.

"We found that the interaction between this specific wheezing illness and a gene or genes on a region of chromosome 17 determines childhood asthma risk," said study author Carole Ober, PhD, Blum-Riese Professor of Human Genetics at the University of Chicago. "The combination of genetic predisposition and the child's response to this infection has a huge effect."

Wheezing caused by respiratory syncytial virus (RSV), a more serious but less common childhood infection, did not show this same interaction.

Several genome-wide association studies have linked asthma to genetic variation on a region of chromosome 17, referred to as 17q21. Although this variation applies primarily to early-onset asthma, it still "dwarfs every other asthma-related genetic risk factor," Ober said.

Exactly how the genes and viral infection interact to cause asthma is unclear. Two genes in the 17q21 region may play a role. One of them, known as ORMDL3, is the "most likely candidate," Ober said. The protein produced by ORMDL3 is found in the endoplasmic reticulum membrane, the same component of airway cells that rhinovirus uses to makes more copies of itself. Less is known about the function of the second gene, GSDMB.

The researchers studied two carefully monitored cohorts of children from families at high risk for asthma. All of the 200 children in the COAST cohort, based at the University of Wisconsin under the leadership of Robert Lemanske, MD, principal investigator of the project, had at least one parent with asthma, respiratory allergies, or both. They were followed from birth and evaluated for asthma at age 6. The 297 Danish children in the COPSAC cohort were born to mothers with asthma and evaluated for asthma at age 7.

The researchers first investigated the links between genes, wheezing with viral infection, and asthma in the COAST group, in which they found significant interactions. Less than 30 percent of children in this group who lacked the asthma-related genetic marker were subsequently diagnosed with the disease, compared to 40 percent of children with one at-risk allele and 50 percent with two. Children who had two copies of the asthma-related genetic variation also had far more HRV-related wheezing illnesses.

When the researchers combined both factors, the difference was striking. Only about 25 percent of children who had no wheezing illness from HRV developed asthma. About 40 percent of those who wheezed in the first three years of life but lacked the risk-related genes got asthma. That increased to nearly 60 percent for those with one copy of the asthma-related allele and to 90 percent for those with two copies.

Next they sought to replicate that finding in a similar group, but from a different continent. Although the overall asthma prevalence, based on slightly different criteria in the Danish cohort, was lower, the more-than-additive association between the at-risk genotype, wheezing illness in early life and asthma diagnosis persisted.

To see how exposure to HRV altered expression of genes associated with the 17q21 marker, the University of Chicago researchers recruited 100 normal adult volunteers, collected blood from them and exposed immune-system cells from the blood to HRV. The leading suspect, ORMDL3, had the most robust response, more than doubling its presence in exposed cells.

This result suggests that "higher expression of ORMDL3 may increase the efficiency of the infection or viral replication in respiratory epithelial cells," according to the study's first author, Minal Çalışkan, a graduate student in Ober's laboratory.

"This is the site where rhinovirus infection and replication occur," she explained. "Upregulation of this gene may lessen these cells' ability to repair the airway after an HRV infection, a feature associated with asthma. Our next project is to look more closely at this process in airway epithelial cells."

What can parents do to prevent early onset asthma? At this point, "nothing that we know of," Ober said. Parents can't prevent their children from catching colds, but "perhaps they could work with their pediatricians to find proactive ways to prevent wheezing in young children with the asthma genotype."

Thursday, March 28, 2013

Combinations of estrogen-mimicking chemicals found to strongly distort hormone action

For years, scientists have been concerned about chemicals in the environment that mimic the estrogens found in the body. In study after study, researchers have found links between these "xenoestrogens" and such problems as decreased sperm viability, ovarian dysfunction, neurodevelopmental deficits and obesity. But experimental limitations have prevented them from exploring one of the most serious questions posed by exposure to xenoestrogens: what happens when — as in the real world — an individual is exposed to multiple estrogen-mimicking chemicals at the same time?

Now University of Texas Medical Branch at Galveston researchers have used new techniques to study exposure to low doses of multiple xenoestrogens. And they've come to some disturbing conclusions.

Using cell cultures to test mixtures of three compounds known to affect estrogen signaling, — bisphenol A (found in plastic bottles and the linings), bisphenol S (a supposedly safer replacement for bisphenol A recently found to have similar effects) and nonylphenol (a common component of industrial detergents and surfactants) — the scientists determined that combinations of endocrine disruptors could have a dramatically greater effect than any one of them alone.

"We wanted to see how these persistent, ubiquitous contaminants affect estrogenic signaling when they're mixed together as they are in nature, so we set up a cell-culture system that allowed us to test their influence on signaling by estradiol, the estrogen found in adult, cycling women," said UTMB professor Cheryl Watson, senior author of a paper on the study now online in the journal Environmental Health ( "What we found is that these things gang up on estradiol and thwart its response, which is not a good thing."

Watson and her colleagues tested different mixtures of estrogen-disrupting compounds using rat pituitary cells, cells that are master regulators of the animals' endocrine systems. Their experiments measured the responses of key signaling pathways that lead to cell proliferation, the secretion of the pituitary hormone prolactin and the activation of proteins involved in apoptosis (programmed cell death), comparing the effects of estradiol alone with those of estradiol and mixtures of bisphenol A, bisphenol S and nonylphenol.

"These compounds work at very low concentrations — at the parts per trillion or parts per quadrillion level — and when you mix them together they affect estrogenic signaling differently and more dramatically than they do individually," Watson said. "We need to pay attention to this, because estrogens influence so many things in both males and females — reproduction, the immune system, metabolism, bone growth, all sorts of important biological functions."

Studies have detected measurable levels of bisphenol A and bisphenol S in the urine of more than 90 percent of Americans. According to Watson, modern humans are exposed to dozens of xenoestrogens more or less continually.

"These things are all over the environment, and we need to know what they do so we can start figuring out what we need to change," Watson said. "They're probably disrupting and confusing hormones in people, and it's important to find a way to prevent that as soon as we can. We need to test these compounds for their hormone-disrupting activities before they are put into products, so we can redesign for safety very early in the process."

Wednesday, March 27, 2013

EPA Announces Chemicals for Risk Assessment in 2013, Focus on Widely Used Flame Retardants

Photo: Posterize
The U.S. Environmental Protection Agency (EPA) announced it will begin assessments on 23 commonly used chemicals, with a specific focus on flame retardant chemicals, in order to more fully understand any potential risks to people’s health and the environment. This effort is part of the Toxic Substances Control Act (TSCA) Work Plan which identifies commonly used chemicals for risk assessment.

Americans are often exposed to flame retardant chemicals in their daily lives; flame retardants are widely used in products such as household furniture, textiles, and electronic equipment. Some flame retardant chemicals can persist in the environment, bioaccumulate in people and animals, and have been shown to cause neurological developmental effects in animals.

“EPA is committed to more fully understanding the potential risks of flame retardant chemicals, taking action if warranted, and identifying safer substitutes when possible,” said James J. Jones, Acting assistant administrator for the Office of Chemical Safety and Pollution Prevention. “Though today’s announcement represents a significant step forward on chemical safety, it’s important to remember that TSCA, this country’s chemicals management legislation, remains in dire need of reform in order to ensure that all Americans are protected from toxic chemicals in their environment.”

EPA will begin evaluating 20 flame retardant chemicals, conducting full risk assessments for four of the flame retardants, three of which are on the TSCA Work Plan, and one that was the subject of an Action Plan development under TSCA. In addition, we are assessing eight other flame retardants by grouping flame retardants with similar characteristics together with the chemicals targeted for full assessment. EPA will use the information from these assessments to better understand the other chemicals in the group, which currently lack sufficient data for a full risk assessment.

EPA will also begin analyzing how eight of the 20 flame retardant chemicals transform and move in the environment. These chemicals were selected because they are likely to persist in the environment, bioaccumulate in people and/or have high exposure potential, but there are not adequate data to conduct full risk assessments.

During its review of data on flame retardant chemicals in commerce, EPA also identified approximately 50 flame retardant chemicals that are unlikely to pose a risk to human health, making them possible substitutes for more toxic flame retardant chemicals.

As EPA develops its draft risk assessments, the agency will use information that is available through a wide range of publicly available data sources. EPA also encourages submission of additional relevant information on these chemicals, such as unpublished studies and information on uses and potential exposures. This information should be submitted by May 30, 2013, to ensure that it is included in the agency’s review.

Submit relevant information on these chemicals or find more information on TSCA Work Plan and flame retardant chemicals for risk assessment:

A full list of the chemicals announced for further assessment is available here:

For more stories on chemical exposure and improving your indoor air quality visit or call to speak to an air quality expert about improving the air in your home 1-888-852-8247. Remove 99.97% of particles and the chemicals and odors other air cleaners leave behind.

Tuesday, March 26, 2013

EPA Says More Than Half of the Nation’s Rivers and Streams in Poor Condition

Photo: Karen Harding
The U.S. Environmental Protection Agency has released the results of the first comprehensive survey looking at the health of thousands of stream and river miles across the country, finding that more than half – 55 percent – are in poor condition for aquatic life.

“The health of our Nation’s rivers, lakes, bays and coastal waters depends on the vast network of streams where they begin, and this new science shows that America’s streams and rivers are under significant pressure,” said Office of Water Acting Assistant Administrator Nancy Stoner. “We must continue to invest in protecting and restoring our nation’s streams and rivers as they are vital sources of our drinking water, provide many recreational opportunities, and play a critical role in the economy.”

The 2008-2009 National Rivers and Stream Assessment reflects the most recent data available, and is part of EPA’s expanded effort to monitor waterways in the U.S. and gather scientific data on the condition of the Nation’s water resources.

EPA partners, including states and tribes, collected data from approximately 2,000 sites across the country. EPA, state and university scientists analyzed the data to determine the extent to which rivers and streams support aquatic life, how major stressors may be affecting them and how conditions are changing over time.

Findings of the assessment include:

- Nitrogen and phosphorus are at excessive levels. Twenty-seven percent of the nation’s rivers and streams have excessive levels of nitrogen, and 40 percent have high levels of phosphorus. Too much nitrogen and phosphorus in the water—known as nutrient pollution—causes significant increases in algae, which harms water quality, food resources and habitats, and decreases the oxygen that fish and other aquatic life need to survive. Nutrient pollution has impacted many streams, rivers, lakes, bays and coastal waters for the past several decades, resulting in serious environmental and human health issues, and impacting the economy.

- Streams and rivers are at an increased risk due to decreased vegetation cover and increased human disturbance. These conditions can cause streams and rivers to be more vulnerable to flooding, erosion, and pollution. Vegetation along rivers and streams slows the flow of rainwater so it does not erode stream banks, removes pollutants carried by rainwater and helps maintain water temperatures that support healthy streams for aquatic life. Approximately 24 percent of the rivers and streams monitored were rated poor due to the loss of healthy vegetative cover.

- Increased bacteria levels. High bacteria levels were found in nine percent of stream and river miles making those waters potentially unsafe for swimming and other recreation.

- Increased mercury levels. More than 13,000 miles of rivers have fish with mercury levels that may be unsafe for human consumption. For most people, the health risk from mercury by eating fish and shellfish is not a health concern, but some fish and shellfish contain higher levels of mercury that may harm an unborn baby or young child's developing nervous system.

EPA plans to use this new data to inform decision making about addressing critical needs around the country for rivers, streams, and other waterbodies. This comprehensive survey will also help develop improvements to monitoring these rivers and streams across jurisdictional boundaries and enhance the ability of states and tribes to assess and manage water quality to help protect our water, aquatic life, and human health. Results are available for a dozen geographic and ecological regions of the country.

For more stories on pollution, health, chemical exposure and improving your indoor air quality visit or call to speak to an air quality expert about improving the air in your home 1-888-852-8247.

Monday, March 25, 2013

VIDEO: The Right to Breathe, 2011 Documentary: "While we doing this interview 15 people will die..."

Directed by award-winning documentary filmmaker Alexandre Philippe, this powerful 2011 documentary tells the story of the serious health effects of Southern California's air pollution. It's estimated that 15 people die everyday in the region as a direct cause of air pollution related illnesses. A sobering 20 minutes....

Friday, March 22, 2013

Research Casts Sobering Light on Costs of Air Pollution

Two Canadian researchers have published groundbreaking research that estimates the cost of air pollution sources like vehicles and power plants. The paper, by Carleton University PhD student Amanda Pappin and Engineering Prof. Amir Hakami, was published in the Environmental Health Perspectives journal. It provides a sobering look at the health and environmental effects of air pollution.

Adopting a novel approach, the study combined air quality models with epidemiological models to relate the health impacts of air pollution to individual sources. The researchers assigned a dollar value to premature mortality associated with short-term exposure to ozone air pollution (also known as smog). In Canada, that number is $5.7 million Canadian per statistical life, while in the U.S. it is $8.1 million American dollars per statistical life.

“This is the first time we have been able to relate air pollution health impacts to individual sources such as vehicles,” said Hakami. “The novelty of this approach is in its ability to differentiate between the health effects caused by emissions of the same pollutant but at different locations.”

“I think this research is really valuable,” said Pappin. “We now have the ability to identify and preferentially target emission sources, down to the level of a single vehicle, that have the largest impact on human health.”

For instance, the study estimates that in the Greater Montreal and Toronto areas, the cost of driving one average vehicle, in terms of mortality due to ozone exposure, is $770 and $440 per year respectively. In comparison, the health cost of an average vehicle in much of coastal California is $300 to $800 per year.

Pappin and Hakami were able to work with the numbers to estimate how much reductions in emissions in a given city might benefit North American public health. In Atlanta for example, a 10 per cent reduction in emissions of nitrogen oxides leads to savings of about $180,000 in terms of premature mortality per day. These benefits are estimated at $250,000 and $210,000 per day for emissions near Toronto and Montreal, respectively.

The study also sheds some light on how pollution moves across the Canada-U.S. border.

“Our results suggest that there is significant cross-border influence on air pollution mortality by both countries,” said Hakami. “For instance, the U.S. contributes about as much to air pollution mortality in Canada as Canadians do. This truly underlines the importance of transnational efforts and collaborations for reducing air pollution.”

The researchers were also able to provide insight into how much benefit mass-transit systems add to a city by removing vehicles from the road. In Toronto for example, they estimate the benefit of the subway is about $130-million per year. “This is an underestimation of the benefits as it does not include health effects related to particles, long-term effects or climate related benefits,” said Hakami. These results will have local implications in Ottawa once the new light-rail system is implemented.

“The new light-rail system in Ottawa will result in reduced numbers of vehicles on the road, and we can estimate the resultant impact on human health,” said Pappin. “We weren’t able to do that with such level of detail before.”

Hakami cautions that the public’s conception and official costs of pollution may be drastically undervalued.

“The damage that we assign to pollution is probably much lower than it should be,” said Hakami, pointing to permit costs associated with cap and trade systems that regulate nitrogen oxide emitting power plants in the U.S. “Under this system, the permit cost for each ton of nitrogen oxides was under $1,000 in our study year. The damage that we associate with one ton of nitrogen oxides, however, is upwards of $10,000 per year for many power plants in the U.S.”

Hakami and Pappin hope that the research will allow policy-makers to devise more effective policies that account for both the costs and benefits of cutting emissions.

“Using our approach, you can compare the benefits of reducing pollution with the costs very readily,” said Pappin. “This is the first time we’ve been able to have this information available for policy-makers on a source-by-source basis.”

Hakami has some thoughts to share with policy-makers and the public about the way we consider the costs of pollution on human health.

“While reducing emissions from vehicles and power plants is costly, not reducing emissions also costs money. Our research suggests that ignoring pollution will cost much more in the long term.”

For more stories on health, pollution, chemical exposure and improving your indoor air quality visit or call to speak to an air quality expert about improving the air in your home 1-888-852-8247.

Thursday, March 21, 2013

Road traffic pollution as serious as passive smoke in the development of childhood asthma

New research conducted in 10 European cities has estimated that 14% of chronic childhood asthma is due to exposure to traffic pollution near busy roads.

The results are comparable to the burden associated with passive smoking: the World Health Organization estimates that between 4% and 18% of asthma cases in children are linked to passive smoking.

The findings, published in the European Respiratory Journal, come as the European Commission has declared 2013 the 'Year of Air', which highlights the importance of clean air for all and focuses on actions to improve air quality across the EU.

Until now, traffic pollution was assumed to only trigger asthma symptoms and burden estimations did not account for chronic asthma caused by the specific range of toxicants that are found near heavily used roads along which many Europeans live.

The researchers used a method known as population-attributable fractions to assess the impact of near-road traffic pollution. This calculates the proportional reduction in disease or death that would occur if exposure to a risk factor were reduced to a lower level.

The new research used data from existing epidemiological studies which found that children exposed to higher levels of near-road traffic-related pollution also had higher rates of asthma, even when taking into account a range of other relevant factors such as passive smoking or socioeconomic factors.

The researchers aimed to take these findings further and estimate how many asthma cases could be avoided if exposure was removed.

The results found that 14% of asthma cases across the 10 cities could be attributed to near-road traffic pollution. The findings also take into account differences in the health of the overall population in different cities.

Lead author, Dr Laura Perez at the Swiss Tropical and Public Health Institute, said: "Air pollution has previously been seen to trigger symptoms but this is the first time we have estimated the percentage of cases that might not have occurred if Europeans had not been exposed to road traffic pollution. In light of all the existing epidemiological studies showing that road-traffic contributes to the onset of the disease in children, we must consider these results to improve policy making and urban planning."

Wednesday, March 20, 2013

Secure Pesticides and Chemicals during Poison Prevention Week

More than 145,000 reports made each year to poison centers involving pesticides and disinfectants

During National Poison Prevention Week, March 17-23, the U.S. Environmental Protection Agency (EPA) urges parents and caregivers to secure pesticides and other household chemicals in locked cabinets out of children's reach.

“Poison Prevention Week is a time to raise awareness and strengthen prevention efforts to empower parents and caregivers with information about simple steps that can be taken to prevent poisonings," said James Jones, acting assistant administrator for the EPA’s Office of Chemical Safety and Pollution Prevention. “EPA continues to take action to help prevent these risks to children and help ensure that the products on the market are both safe and effective for consumers. Our recent move to ban the sale of 12 D-Con mouse and rat poison products produced by Reckitt Benckiser Inc is a prime example of our commitment."

Each year, approximately 65,000 children ages 5 and younger are accidentally exposed to pesticides, and more than 10,000 of those exposures involve mouse and rat poisons. Recently, EPA took steps that, with the help of Americans who use these products around their homes, could help lower these statistics. Under new EPA safety standards, consumer use mouse and rat poison products must include a protective tamper-resistant bait station. These measures prevent children from accessing the poison.

More than 90 percent of poisonings happen in people’s homes. Parents and caregivers can protect children and loved ones against pesticide exposure.
Poisonings are preventable. Here are some simple tips to prepare and stay safe:
  • Always store pesticides and other household chemical products in a locked cabinet.
  • To protect children and pets from exposure to mouse and rat poison, use products with a tamper-resistant bait station.
  • Go through your home room by room to see where there are potential poisoning hazards and correct accordingly.
  • Use child-resistant packaging properly by closing the container tightly after use.
  • Never transfer pesticides and other household chemical products to containers that may be mistaken for food or drink.
Program the Poison Help Center number, 1-800-222-1222, in your phone.
Poison prevention tips and resources to protect your family:
Room by room checklist for potential poisoning hazards:
List of rat and mouse products that meet the EPA’s safety standards:
More on National Poison Prevention Week:


Tuesday, March 19, 2013

Researchers invent real time secondhand smoke sensor; Soon to be wearable, affordable

Making headway against a major public health threat, Dartmouth College researchers have invented the first ever secondhand tobacco smoke sensor that records data in real time, a new study in the journal Nicotine and Tobacco Research shows.

The researchers expect to soon convert the prototype, which is smaller and lighter than a cellphone, into a wearable, affordable and reusable device that helps to enforce no smoking regulations and sheds light on the pervasiveness of secondhand smoke. The sensor can also detect thirdhand smoke, or nicotine off-gassing from clothing, furniture, car seats and other material.

The device uses polymer films to reliably measure ambient nicotine vapor molecules and a sensor chip to record the real-time data, pinpointing when and where the exposure occurred and even the number of cigarettes smoked. The prototype proved successful in lab tests. Clinical studies will start this summer.

Such a device could help to enforce smoking bans in rental cars, hotel rooms, apartment buildings, restaurants and other places. It also could help convince smokers that smoking in other rooms, out of windows and using air fresheners still exposes children and other nonsmokers to secondhand smoke. The device would be more accurate and less expensive than current secondhand smoke sensors, which provide only an average exposure in a limited area over several days or weeks.

"This is a leap forward in secondhand smoke exposure detection technology," said Chemistry Professor Joseph BelBruno, whose lab conducted the research.

Federal health officials report there is no safe level of exposure to secondhand smoke, which increases the risks of cancer, cardiovascular disease and childhood illness. An estimated 88 million nonsmoking Americans, including 54 percent of children ages 3 years, are exposed to secondhand smoke.

Dartmouth College has a patent pending for this technology.

Monday, March 18, 2013

Chemicals pollutants threaten health in the Arctic

Photo: Danilo Rizzuti
People living in Arctic areas can be more sensitive to pollutants due to their genetics, says researcher Arja Rautio at the Centre for Arctic Medicine in the University of Oulu, Finland. This is unfortunate since the northernmost areas of Europe are receiving more harmful chemical exposure. Scientists believe climate change may be a culprit as air and water mass movements push some of these undesirable chemicals towards the Arctic.

“In real life, people are exposed to lots of chemicals,” says Rautio, who leads studies into the human health effects from contaminants and the influence of climate change in a EU-funded project called ArcRisk, “and I think the people of the north are exposed to higher levels than for example the general population in Europe.”

Many new contaminants like fluorinated and brominated compounds and bisphenol A can act on hormones and so have impacts on human health. But seeing an effect on humans, at the population level, could take ten or even 20 years, especially in the case of cancer, she adds. This is why ArcRisk has established a database containing data on concentration levels and trends of contaminants in humans. The project team analysed frozen blood samples collected in Norway in 1978, 1986, 1995 and 2008 for polychlorinated biphenyls (PCBs), chlorinated pesticides and polybrominated diphenylethers (PBDEs).

The main challenge that project scientists struggle with is to disentangle the effects of contaminant chemicals from what we do in our everyday lives. “We know that dioxins can lead to more diabetes and high blood pressure,” says Rautio, “but there are many other confounding factors. We are changing our diet and many of us are less active and those lifestyle choices can also increase the risk of diseases like diabetes.” The results of the project are due to be presented at a conference of Arctic Frontiers in Tromsø, Norway, in January 2014.

Previous studies have also struggled with disentangling contaminants effects when trying to understand their impact on health. There are uncertainties between the chemicals and direct health impacts because people are exposed to so many chemicals simultaneously, cautions biologist Thomas Zoeller at the University of Massachusetts Amherst, USA. Besides, the human population is genetically variable and may react differently to the chemicals and we don’t even know which of the chemicals affect us.

“Moreover, some of these chemicals reside in the environment – and in the body – for a long time, and this means that they may build up,” says Zoeller. His recently edited a recent World Health Organization report which warned that chronic diseases are increasing worldwide and many are related to hormones. It noted that known hormone-disrupting chemicals are “only the tip of the iceberg” and better tests are needed to catch others.

Health problems induced by these chemicals could be worse than anticipated. Some of the pollutants found in the Arctic by the project scientists like the fluorinated compounds have higher affinities for hormone receptors than even the natural hormones. “We have documented several direct harmful effects of these and other chemicals, especially in seabirds, top predators such as the glaucous and ivory,” says Geir Wing Gabrielsen, an environmental scientist at the Norwegian Polar Institute, who is not part of ArcRisk.

These animal studies already show worrying trends that do not bode well for humans. “When we see these findings in Arctic animals I am very concerned about what we will find with regards to humans, though we ourselves don’t do human studies,” Gabrielsen says. He notes that long periods of warm air are being transported to the Arctic and that the sea currents around places like the Svalbard islands [located midway between Norway and the North Pole] now consist of warmer Atlantic water; they used to consist of polar waters. “Climate change is having an effect and it is resulting in higher levels of contaminants in the environment and [therefore] also in the animals,” Gabrielsen warns.

Rautio concludes that there is a need to clarify the effects so that people—not only in those living in the remote northern areas— can make decisions about their own lives, what to eat, how to avoid exposure to harm.

Source: European Research Media Center,

Friday, March 15, 2013

Study: Unhealthy eating puts women in a bad mood

Taking part in unhealthy eating behaviors may cause women who are concerned about their diet and self-image to experience a worsening of their moods, according to Penn State researchers.

In a study, college-age women who were concerned about their eating behaviors reported that moods worsened after bouts of disordered eating, said Kristin Heron, research associate at the Survey Research Center.

"There was little in the way of mood changes right before the unhealthy eating behaviors," said Heron. "However, negative mood was significantly higher after these behaviors."

According to Heron, who worked with Joshua Smyth, professor of biobehavioral health, Stacey Scott, research associate in the Center for Healthy Aging, and Martin Sliwinski, professor of human development and family studies, people who experience disordered eating patterns may exhibit behaviors such as binge eating, loss of control over eating and food intake restriction.

The researchers, who presented their findings at an American Psychosomatic Society conference in Miami, detected little change in the participants' moods prior to unhealthy eating. While negative mood was worse after disordered eating, a positive mood did not change either before or after any of the behaviors studied by the researchers.

The researchers gathered data from participants in real-life situations. The team gave handheld computers to 131 women who had high levels of unhealthy eating habits and concerns about their body shape and weight, but did not have eating disorders. Several times during the day, the devices would prompt the participants to answer questions about their mood and eating behaviors.

"What we know about mood and eating behaviors comes primarily from studies with eating disorder patients or from laboratory studies," said Heron. "We were interested in studying women in their everyday lives to see whether mood changed before or after they engaged in unhealthy eating and weight control behaviors."

Smyth said that the study could lead to better treatments for women experiencing eating problems.

"This study is unique because it evaluates moods and eating behaviors as they occur in people's daily lives, which can provide a more accurate picture of the relationship between emotions and eating," Smyth said.

"The results from this study can help us to better understand the role mood may play in the development and maintenance of unhealthy eating, and weight-control behaviors, which could be useful for creating more effective treatment programs for people with eating and weight concerns."

For more stories on general health, pollution, chemical exposure and improving your indoor air quality visit or call to speak to an air quality expert about improving the air in your home 1-888-852-8247.

Thursday, March 14, 2013

Mild Winter Produces Early Rise in Tree Pollen in Midwest

The Gottlieb Allergy Count, reported by Joseph Leija, MD, will officially begin Monday, March 18, weeks earlier than the usual April 1 start date. For the past week, Dr.Leija has been monitoring the air daily in preparation.

“Today the tree pollen was moderate, which is high for this time of year, and I can see the many budding treetops from the Gottlieb rooftop where the pollen-catching equipment is located,” said Leija, who has been performing the Gottlieb Allergy Count for more than two decades. “So far, what I am seeing in 2013 is equal to what I saw in 2012, which was a very early and especially bad allergy season.”

Leija, performs the official allergy count for the Midwest on behalf of the National Allergy Bureau, and conducted an initial count for the season on Monay, March 11 at 7 a.m. In 2012, Dr. Leija, an allergist, retired from seeing patients but he continues his public health crusade for improved breathing by performing the Gottlieb Allergy Count. In 2012, Dr. Leija issued four air-quality alerts.

"I believe today’s pollen count may actually be higher and some tree pollen has been washed away by the steady rain last night and today," said Dr. Leija, who, at 6 a.m. and in the rain, climbed the stairs to the roof atop Gottlieb Memorial Hospital, part of Loyola University Health System.

Dr. Joseph Leija, allergist at Loyola’s Gottlieb Memorial Hospital, is solely certified by the National Allergy Bureau to perform the daily official allergy count for the Midwest, usually from April – October. Due to the mild winter season, the practice he founded is seeing a dramatic increase in those suffering from respiratory illness and allergies. Dr. Leija will begin reporting the count two weeks early, on March 18, due to elevated pollen counts.

An octagenerian, Dr. Leija rises before dawn to collect specimens from his pollen catching-machine atop Gottlieb and deliver the count to the public by 7 a.m. The Gottlieb Allergy Count is available in English, Polish and Spanish, through Twitter: at and in English at 1-866-4-POLLEN (476-5536).

Wednesday, March 13, 2013

Dwelling on stressful events can increase inflammation in the body, study finds

Dwelling on negative events can increase levels of inflammation in the body, a new Ohio University study finds.

Researchers discovered that when study participants were asked to ruminate on a stressful incident, their levels of C-reactive protein, a marker of tissue inflammation, rose. The study is the first time to directly measure this effect in the body.

“Much of the past work has looked at this in non-experimental designs. Researchers have asked people to report their tendency to ruminate, and then looked to see if it connected to physiological issues. It’s been correlational for the most part,” said Peggy Zoccola, an assistant professor of psychology at Ohio University.

Zoccola is lead author on the new study, which she will present Friday at the annual meeting of the American Psychosomatic Society in Miami, Fla.

The research team recruited 34 healthy young women to participate in the project. Each woman was asked to give a speech about her candidacy for a job to two interviewers in white laboratory coats, who listened with stone-faced expressions, Zoccola said.

Half of the group was asked to contemplate their performance in the public speaking task, while the other half was asked to think about neutral images and activities, such as sailing ships or grocery store trips.

The researchers drew blood samples that showed that the levels of C-reactive protein were significantly higher in the subjects who were asked to dwell on the speech, Zoccola reported.

For these participants, the levels of the inflammatory marker continued to rise for at least one hour after the speech. During the same time period, the marker returned to starting levels in the subjects who had been asked to focus on other thoughts.

The C-reactive protein is primarily produced by the liver as part of the immune system’s initial inflammatory response. It rises in response to traumas, injuries or infections in the body, Zoccola explained.

C-reative protein is widely used as a clinical marker to determine if a patient has an infection, but also if he or she may be at risk for disease later in life.

“More and more, chronic inflammation is being associated with various disorders and conditions,” Zoccola said. “The immune system plays an important role in various cardiovascular disorders such as heart disease, as well as cancer, dementia and autoimmune diseases.”

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Tuesday, March 12, 2013

Prenatal exposure to pesticide DDT linked to adult high blood pressure

Infant girls exposed to high levels of the pesticide DDT while still inside the womb are three times more likely to develop hypertension when they become adults, according to a new study led by the University of California, Davis.

Previous studies have shown that adults exposed to DDT (dichlorodiplhenyltrichloroethane) are at an increased risk of high blood pressure. But this study, published online March 12 in Environmental Health Perspectives, is the first to link prenatal DDT exposure to hypertension in adults.

Hypertension, or high blood pressure, is a high risk factor for heart disease, which remains the leading cause of death in the United States and worldwide.

"The prenatal period is exquisitely sensitive to environmental disturbance because that's when the tissues are developing," said study lead author Michele La Merrill, an assistant professor in the UC Davis Department of Environmental Toxicology.

The U.S. Environmental Protection Agency banned DDT in this country in 1972 after nearly three decades of use. However, the pesticide is still used for malaria control in other parts of the world, such as India and South Africa. That means children born in those areas could have a higher risk of hypertension as adults.

La Merrill said that traces of DDT, a persistent organic pollutant, also remain in the food system, primarily in fatty animal products.

The study examined concentrations of DDT in blood samples collected from women who had participated in the Child Health and Development Studies, an ongoing project of the nonprofit Public Health Institute. The CHDS recruited women who sought obstetric care through Kaiser Permanente Foundation Health Plan in the San Francisco Bay Area between 1959 and 1967. They also surveyed the adult daughters of those women to learn if they had developed hypertension.

"Evidence from our study shows that women born in the U.S. before DDT was banned have an increased risk of hypertension that might be explained by increased DDT exposure," said La Merrill. "And the children of people in areas where DDT is still used may have an increased risk, as well."
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Monday, March 11, 2013

Sleep loss precedes Alzheimer’s symptoms

Sleep is disrupted in people who likely have early Alzheimer’s disease but do not yet have the memory loss or other cognitive problems characteristic of full-blown disease, researchers at Washington University School of Medicine in St. Louis report March 11 in JAMA Neurology.

The finding confirms earlier observations by some of the same researchers. Those studies showed a link in mice between sleep loss and brain plaques, a hallmark of Alzheimer’s disease. Early evidence tentatively suggests the connection may work in both directions: Alzheimer’s plaques disrupt sleep, and lack of sleep promotes Alzheimer’s plaques.

“This link may provide us with an easily detectable sign of Alzheimer’s pathology,” says senior author David M. Holtzman, MD, the Andrew B. and Gretchen P. Jones Professor and head of Washington University’s Department of Neurology. “As we start to treat people who have markers of early Alzheimer’s, changes in sleep in response to treatments may serve as an indicator of whether the new treatments are succeeding.”

Sleep problems are common in people who have symptomatic Alzheimer’s disease, but scientists recently have begun to suspect that they also may be an indicator of early disease. The new paper is among the first to connect early Alzheimer’s disease and sleep disruption in humans.

For the new study, researchers recruited 145 volunteers from the University’s Charles F. and Joanne Knight Alzheimer’s Disease Research Center. All of the volunteers were 45 to 75 years old and cognitively normal when they enrolled.

As a part of other research at the center, scientists already had analyzed samples of the volunteers’ spinal fluids for markers of Alzheimer’s disease. The samples showed that 32 participants had preclinical Alzheimer’s disease, meaning they were likely to have amyloid plaques present in their brains but were not yet cognitively impaired.

Participants kept daily sleep diaries for two weeks, noting the time they went to bed and got up, the number of naps taken on the previous day, and other sleep-related information.

The researchers tracked the participants’ activity levels using sensors worn on the wrist that detected the wearer’s movements.

“Most people don’t move when they’re asleep, and we developed a way to use the data we collected as a marker for whether a person was asleep or awake,” says first author Yo-El Ju, MD, assistant professor of neurology. “This let us assess sleep efficiency, which is a measure of how much time in bed is spent asleep.”

Participants who had preclinical Alzheimer’s disease had poorer sleep efficiency (80.4 percent) than people without markers of Alzheimer’s (83.7 percent). On average, those with preclinical disease were in bed as long as other participants, but they spent less time asleep. They also napped more often.

“When we looked specifically at the worst sleepers, those with a sleep efficiency lower than 75 percent, they were more than five times more likely to have preclinical Alzheimer’s disease than good sleepers,” Ju says.

Ju and her colleagues are following up with studies in younger participants who have sleep disorders.

“We think this may help us get a better feel for the way this connection flows — does sleep loss drive Alzheimer’s, does Alzheimer’s lead to sleep loss, or is it a combination?” Ju says. “That will help us determine whether we can change the course of disease with pharmaceuticals or other treatments.”

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Friday, March 08, 2013

Maternal obesity increases the risk of frequent wheezing in offspring

A new study concludes that the children of mothers obese before falling pregnant are four times more likely to have frequent wheezing, which is one of the symptoms of asthma, compared to the children of mothers weighing a normal weight.

Researchers from the Centre for Research in Environmental Epidemiology (CREAL) assessed whether obesity in mothers increases the risk of their children having frequent wheezing, a symptom associated with susceptibility to asthma during infancy that manifests as sharp, whistling sounds when breathing.

During an asthma attack, the muscles surrounding the airways tense up and their lining becomes inflamed. The passage of air is then reduced. One of the symptoms is wheezing which as a general rule begins subtly and can then worsen during the night or the first few hours of the day when breathing in cold air or even during exercise.

Published in the 'Paediatric and Perinatal Epidemiology', the study confirms that on average the risk of wheezing during the first 14 months of life is four times greater in the children of mothers with obesity compared to the children of mothers with a normal weight.

"We are basing this on the assumption that obesity in mothers can be a potential intergenerational risk factor for asthma," as explained to SINC by Stefano Guerra, lead author of the study. "Our proposal was to determine whether maternal obesity is associated with a greater risk of early wheezing phenotypes in children."

Therefore, the experts analysed the data of 1,107 pairs of mother and child from a Spanish study on infancy and environment (INMA project). The results confirmed the association between maternal obesity and wheezing regardless of the weight of the child and other factors such as the education of the mother, her age, whether she is a smoker, etc.

"The independent relationship of obesity before pregnancy with the increased risk of frequent wheezing in children adds more evidence to the effects of foetal exposure and its consequences on asthma-related phenotypes," states Guerra, suggesting "possible preventative benefits of loosing excess weight."

The search for the cause of asthma in infants

The experts have spent years searching for the key to asthma in infants as it is an illness that affects more than 300 million people worldwide. Of these, 52% are not diagnosed and 47% do not have a good control over the disease.

According to the latest figures from the Spanish Guide to Handling Asthma (GEMA), although the mortality rate of this illness has reduced since 1960 to 2.22 for every 100,000 (based on data from 2005), prevalence in Spain has increased during the same period.

Thursday, March 07, 2013

Salt identified as autoimmune trigger

Photo: Carlos Porto

For the past few decades, health officials have been reporting increases in the incidence of autoimmune diseases such as multiple sclerosis (MS). Now researchers at Yale School of Medicine, Harvard Medical School and the Broad Institute have identified a prime suspect in the mystery — dietary salt.

In the journal Nature, Yale researchers showed that salt can induce and worsen pathogenic immune system responses in mice and that the response is regulated by genes already implicated in a variety of autoimmune diseases.

In accompanying papers in the same issue of Nature, researchers from Brigham and Women's Hospital and Harvard identified the key molecular pathway involved in the response to salt, and the Broad Institute sketched out the regulatory network of genes that governs this autoimmune response.

"These are not diseases of bad genes alone or diseases caused by the environment, but diseases of a bad interaction between genes and the environment," said David Hafler, the Gilbert H. Glaser Professor of Neurology, professor of immunobiology, chair of the Department of Neurology, and senior author of the Yale paper.

The research was inspired, in part, by an observation that eating at fast-food restaurants tended to trigger an increase in production of inflammatory cells, which are mobilized by the immune system to respond to injury or pathogens but which, in autoimmune diseases, attack healthy tissue. Researchers at Yale and colleagues in Germany led by Dominik Mueller wanted to know whether high salt content in diet might induce the destructive immune system response that is the hallmark of autoimmunity.

They found that adding salt to the diet of mice induced production of a type of T cells previously associated with autoimmune diseases and that mice on salt diets developed a more severe form of an MS animal model, experimental autoimmune encephalomyelitis.

The research at the Broad Institute, Brigham and Women's Hospital, Harvard University, and Yale University expands the understanding of how one type of immune cell — known as a T helper 17 or Th17 cell — develops, and how its growth influences the development of other kinds of cells involved in the immune system. Reconstruction of this molecular circuitry confirmed the surprising role of salt, said the researchers.

"The question we wanted to pursue was: How does this highly pathogenic, pro-inflammatory T cell develop?" said Vijay Kuchroo, a senior scientist at Brigham and Women's Hospital and a Broad Institute associate member. Kuchroo is also the Wasserstrom Professor of Neurology at Harvard Medical School and co-director of the Center for Infection and Immunity at Biomedical Research Institutes. "Once we have a more nuanced understanding of the development of the pathogenic Th17 cells, we may be able to pursue ways to regulate them or their function."

"Humans were genetically selected for conditions in sub-Saharan Africa, where there was no salt," Hafler said. "Today, Western diets all have high salt content and that has led to increase in hypertension and perhaps autoimmune disease as well."

Hafler noted that all test-tube cell biology is performed based on the salt levels found in blood and not in the tissues where immune cell ultimately travel to fight infections. That may have been a reason salt's role in autoimmunity has gone undetected.

"We may have been using the wrong concentrations of salt in our experiments for the past half-century," Hafler said. "Nature did not want immune cells to become turned on in the pipeline, so perhaps blood salt levels are inhibitory."

Patient trials to assess affects of salt on autoimmune diseases are being planned.

"The value in doing an unbiased analysis is that we're able to understand a lot more about the molecular biology at play and put forth a completely novel process," said Aviv Regev, a Broad Institute core member and an associate professor of biology at MIT. Regev is also an Early Career Scientist at Howard Hughes Medical Institute and the director of the Klarman Cell Observatory at the Broad.

Hafler is not waiting with his own patients.

"I already recommend that my patients use a low-salt, low-fat diet," he said

Markus Kleinewietfeld was lead author of the Yale-led study.

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Wednesday, March 06, 2013

Processed meat linked to premature death

In a huge study of half a million men and women, research in Biomed Central's open access journal BMC Medicine demonstrates an association between processed meat and cardiovascular disease and cancer.

One of the difficulties in measuring the effect of eating meat on health is the confounding effect of lifestyle on health. Often vegetarians have healthier lifestyles than the general population, they are less likely to smoke, are less fat, and are more likely to be physically active. Only within a very large study can the consequences of eating meat and processed meat be isolated from other lifestyle choices.

This EPIC (European Prospective Investigation into Cancer and Nutrition) study involved ten countries and 23 centres in Europe and almost half a million people. In general a diet high in processed meat was linked to other unhealthy choices. Men and women who ate the most processed meat ate the fewest fruit and vegetables and were more likely to smoke. Men who ate a lot of meat also tended to have a high alcohol consumption.

A person's risk of premature death (increased risk of all cause mortality) increased with the amount of processed meat eaten. This is also true after correcting for confounding variables, although residual confounding cannot be excluded. However, a small amount of red meat appeared to be beneficial which the researchers suggest is because meat is an important source of nutrients and vitamins.

Prof Sabine Rohrmann, from the University of Zurich, who led this analysis explained, "Risks of dying earlier from cancer and cardiovascular disease also increased with the amount of processed meat eaten. Overall, we estimate that 3% of premature deaths each year could be prevented if people ate less than 20g processed meat per day."

Processed meats include bacon, sausage, hot dogs, sandwich meat, packaged ham, pepperoni and salami.
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Tuesday, March 05, 2013

Study: Bitter flavors may trigger a reaction that could help treat asthma

A team of scientists at the University of Massachusetts Medical School have found that substances which give some foods their bitter flavors can also act to reverse the contraction of airway cells. This reversal, known as bronchodilation, is needed to treat airway obstructive diseases such as asthma and chronic obstructive pulmonary disease. The new findings, which could have significant implications for such treatments, are published in the open access journal PLOS Biology.

The sense of taste is mediated by taste receptor cells bundled in our taste buds. These receptors were thought to only exist in the tongue, but recent discoveries have shown that they are actually expressed in various cell types throughout the body. In particular, bitter taste receptors exist in smooth muscle cells in the airway, acting to relax the cells when exposed to bitter-tasting substances.

A hallmark of an asthma attack is excessive contraction of these smooth muscle cells, which causes narrowing of the airways and breathing difficulties. The fact that bitter substances can relax these smooth muscle cells suggests that they may have the potential to halt asthma attacks, and in fact could even be an improvement over current treatments since the relaxation effects are quite fast. Indeed, experiments in mice suggest that the effects are stronger.

However, the mechanisms through which bitter taste receptor activation leads to cell relaxation were unknown. To help unravel these mechanisms, Dr. Ronghua ZhuGe and his colleagues examined the effect of bitter substances on the contraction of airways and in single isolated cells.

During an asthma attack, membrane channels on smooth muscle cells in the airways are opened, allowing calcium to flow into the cell and causing the cell to contract. This leads to the airways becoming narrower, and making breathing more difficult. Dr. ZhuGe and colleagues determined that bitter substances shut down these calcium channels, allowing bronchodilation.

Bitter taste receptors, like most receptors, span the plasma membrane of the cell. Part of the receptor is outside the cell, able to bind to (and hence "sense") bitter substances outside the cell. When a bitter compound binds to a bitter taste receptor, the receptor releases a G-protein, which then splits into two parts: a G alpha subunit and G beta-gamma dimer. "It is the G beta-gamma dimer that likely acts to close the calcium channels on the plasma membrane," explained Kevin Fogarty, director of the Biomedical Imaging Group in the Program in Molecular Medicine at UMMS, and a co-author of the study. "Once the channels are closed, the calcium level returns to normal and the cell relaxes," he said. "This ends the asthma attack."

"With this new understanding of how bitter substances are able to relax airways, we can focus our attention on studying these receptors and on finding even more potent bitter compounds with the potential to be used therapeutically to end asthma attacks," said Dr. ZhuGe.

Monday, March 04, 2013

Researchers describe first 'functional HIV cure' in an infant

Photo: arxtsamui
A team of researchers from Johns Hopkins Children's Center, the University of Mississippi Medical Center and the University of Massachusetts Medical School describe the first case of a so-called "functional cure" in an HIV-infected infant. The finding, the investigators say, may help pave the way to eliminating HIV infection in children.

Johns Hopkins Children's Center virologist Deborah Persaud, M.D., lead author on the report, and University of Massachusetts Medical School immunologist and professor Katherine Luzuriaga, M.D., headed a team of laboratory investigators. Pediatric HIV specialist Hannah Gay, M.D., associate professor of pediatrics at the University of Mississippi Medical Center provided treatment to the baby.

The infant described in the report underwent remission of HIV infection after receiving antiretroviral therapy (ART) within 30 hours of birth. The investigators say the prompt administration of antiviral treatment likely led to this infant's cure by halting the formation of hard-to-treat viral reservoirs — dormant cells responsible for reigniting the infection in most HIV patients within weeks of stopping therapy.

"Prompt antiviral therapy in newborns that begins within days of exposure may help infants clear the virus and achieve long-term remission without lifelong treatment by preventing such viral hideouts from forming in the first place," Persaud says.

The researchers say they believe this is precisely what happened in the child described in the report. That infant is now deemed "functionally cured," a condition that occurs when a patient achieves and maintains long-term viral remission without lifelong treatment and standard clinical tests fail to detect HIV replication in the blood.

In contrast to a sterilizing cure — a complete eradication of all viral traces from the body — a functional cure occurs when viral presence is so minimal, it remains undetectable by standard clinical tests, yet discernible by ultrasensitive methods.

The child described in the current report was born to an HIV-infected mother and received combination antiretroviral treatment beginning 30 hours after birth. A series of tests showed progressively diminishing viral presence in the infant's blood, until it reached undetectable levels 29 days after birth. The infant remained on antivirals until 18 months of age, at which point the child was lost to follow-up for a while and, the researchers say, stopped treatment. Ten months after discontinuation of treatment, the child underwent repeated standard blood tests, none of which detected HIV presence in the blood. Test for HIV-specific antibodies — the standard clinical indicator of HIV infection — also remained negative throughout.

Currently, high-risk newborns — those born to mothers with poorly controlled infections or whose mothers' HIV status is discovered around the time of delivery — receive a combination of antivirals at prophylactic doses to prevent infection for six weeks and start therapeutic doses if and once infection is diagnosed. But this particular case, the investigators say, may change the current practice because it highlights the curative potential of very early ART.

Specialists say natural viral suppression without treatment is an exceedingly rare phenomenon observed in less than half a percent of HIV-infected adults, known as "elite controllers," whose immune systems are able to rein in viral replication and keep the virus at clinically undetectable levels. HIV experts have long sought a way to help all HIV patients achieve elite-controller status. The new case, the researchers say, may be that long-sought game-changer because it suggests prompt ART in newborns can do just that.

The investigators caution they don't have enough data to recommend change right now to the current practice of treating high-risk infants with prophylactic, rather than therapeutic, doses but the infant's case provides the rationale to start proof-of-principle studies in all high-risk newborns.

"Our next step is to find out if this is a highly unusual response to very early antiretroviral therapy or something we can actually replicate in other high-risk newborns," says Persaud, who is also the scientific chair of the HIV Cure Committee of the International Maternal, Pediatric Adolescent AIDS Clinical (IMPAACT) network, a consortium of researchers and institutions that was critical in spearheading the earliest clinical trials of mother-to-child transmission and early treatment of infants 15 years ago.

A single case of sterilizing cure has been reported so far, the investigators note. It occurred in an HIV-positive man treated with a bone marrow transplant for leukemia. The bone marrow cells came from a donor with a rare genetic mutation of the white blood cells that renders some people resistant to HIV, a benefit that transferred to the recipient. Such a complex treatment approach, however, HIV experts agree, is neither feasible nor practical for the 33 million people worldwide infected with HIV.

"Complete viral eradication on a large scale is our long-term goal but, for now, remains out of reach, and our best chance may come from aggressive, timely and precisely targeted use of antiviral therapies in high-risk newborns as a way to achieve functional cure," says Luzuriaga.

Despite the promise this approach holds for infected newborns, the researchers say preventing mother-to-child transmission remains the primary goal.

"Prevention really is the best cure, and we already have proven strategies that can prevent 98 percent of newborn infections by identifying and treating HIV-positive pregnant women," says Gay, the HIV expert who treated the infant.

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Researchers discover how to shutdown cancer's powerful master protein

The powerful master regulatory transcription factor called Bcl6 is key to the survival of a majority of aggressive lymphomas, which arise from the B-cells of the immune system. The protein has long been considered too complex to target with a drug since it is also crucial to the healthy functioning of many immune cells in the body, not just B cells gone bad.

But now, in the journal Nature Immunology, researchers at Weill Cornell Medical College report that it is possible to shut down Bcl6 in the cancer, known as diffuse large B-cell lymphoma (DLBCL), while not affecting its vital function in T cells and macrophages that are needed to support a healthy immune system.

"The finding comes as a very welcome surprise," says the study's lead investigator, Dr. Ari Melnick, Gebroe Family Professor of Hematology/Oncology and director of the Raymond and Beverly Sackler Center for Biomedical and Physical Sciences at Weill Cornell.

"This means the drugs we have developed against Bcl6 are more likely to be significantly less toxic and safer for patients with this cancer than we realized," says Dr. Melnick, who is also a hematologist-oncologist at NewYork-Presbyterian Hospital/Weill Cornell Medical Center.

If Bcl6 is completely inhibited, patients might suffer from systemic inflammation and atherosclerosis. Weill Cornell researchers conducted this new study to help clarify possible risks, as well as to understand how Bcl6 controls the various aspects of the immune system.

DLBCL is the most common subtype of non-Hodgkin lymphoma -- the seventh most frequently diagnosed cancer -- and many of these patients are resistant to currently available treatments.

"Scientists have been searching for the right answer to treat this difficult lymphoma, which, after initial treatment, can be at high risk of relapse and resistant to current therapies," Dr. Melnick says. "Believing that Bcl6 could not be targeted, some researchers have been testing alternative therapeutic approaches. This study strongly supports the notion of using Bcl6-targeting drugs."

In fact, the findings in this study were inspired from preclinical testing of two Bcl6-targeting agents that Dr. Melnick and his Weill Cornell colleagues have developed to treat DLBCLs. These experimental drugs are RI-BPI, a peptide mimic, and the small molecule agent 79-6.

Dr. Melnick says the discovery that a master regulatory transcription factor can be targeted offers implications beyond just treating DLBCL. Recent studies from Dr. Melnick and others have revealed that Bcl6 plays a key role in the most aggressive forms of acute leukemia, as well as certain solid tumors.

Transcription factors are responsible for either inhibiting or promoting the expression of genes, and master regulatory transcription factors are the equivalent of the CPU of a computer – their actions regulate thousands of genes in different kinds of cells. For example, Bcl6 can control the type of immune cell that develops in the bone marrow -- playing many roles in the development of B cells, T cells, macrophages and other cells -- including a primary and essential role in enabling B-cells to generate specific antibodies against pathogens.

"When cells lose control of Bcl6, lymphomas develop in the immune system. Lymphomas are 'addicted' to Bcl6, and therefore Bcl6 inhibitors powerfully and quickly destroy lymphoma cells," Dr. Melnick says.

The big surprise in the current study is that rather than functioning as a single molecular machine, Bcl6 instead seems to function more like a Swiss Army knife, using different tools to control different cell types. This multi-function paradigm could represent a general model for the functioning of other master regulatory transcription factors.

"In this analogy, the Swiss Army knife, or transcription factor, keeps most of its tools folded, opening only the one it needs in any given cell type," Dr. Melnick says. "For B cells, it might open and use the knife tool; for T cells, the cork screw; for macrophages, the scissors. The amazing thing from a medical standpoint is that this means that you only need to prevent the master regulator from using certain tools to treat cancer. You don't need to eliminate the whole knife," he says. "In fact, we show that taking out the whole knife is harmful since the transcription factor has many other vital functions that other cells in the body need."

Prior to these study results, it was not known that a master regulator could separate its functions so precisely.

"Now we know we can take out a specific tool -- to shut down a specific part of the protein -- that causes the disease we want to treat."

Researchers hope this will be a major benefit to the treatment of DLBCL and perhaps other disorders that are influenced by Bcl6 and other master regulatory transcription factors.


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Friday, March 01, 2013

BPA raises risk for childhood asthma

Children exposed to the plastics chemical bisphenol A had an elevated risk for asthma

Researchers at the Columbia Center for Children's Environmental Health at the Mailman School of Public Health are the first to report an association between early childhood exposure to the chemical bisphenol A (BPA) and an elevated risk for asthma in young children. BPA is a component of some plastics and is found in food can liners and store receipts.

Results appear in the March edition of the Journal of Allergy and Clinical Immunology.

"Asthma prevalence has increased dramatically over the past 30 years, which suggests that some as-yet-undiscovered environmental exposures may be implicated. Our study indicates that one such exposure may be BPA," says lead author Kathleen Donohue, MD, an assistant professor of Medicine at Columbia University College of Physicians and Surgeons and an investigator at the Center for Children's Environmental Health.

Dr. Donohue and her co-investigators followed 568 women enrolled in the Mothers & Newborns study of environmental exposures. BPA exposure was determined by measuring levels of a BPA metabolite in urine samples taken during the third trimester of pregnancy and in the children at ages 3, 5, and 7. Physicians diagnosed asthma at ages 5 to 12 based on asthma symptoms, a pulmonary function test, and medical history. A validated questionnaire was used to evaluate wheeze.

After adjusting for secondhand smoke and other factors known to be associated with asthma, the researchers found that post-natal exposure to BPA was associated with increased risk of wheeze and asthma. BPA exposure during the third trimester of pregnancy was inversely associated with risk of wheeze at age 5. This unexpected finding is in contrast to the results of a previous study, which found that BPA exposure during the second trimester, a critical period for the development of airways and the immune system, was positively linked with risk for asthma.

Increased risk for wheeze and asthma was seen at "fairly routine, low doses of exposure to BPA," says Dr. Donohue. "Like most other scientists studying BPA, we do not see a straightforward linear dose-response relationship."

At all three time points, more than 90% of the children in the study had detectable levels of BPA metabolite in their bodies, a finding that is in line with previous research. This does not mean that they will all develop asthma, cautions Dr. Donohue. "Just as smoking increases the risk of lung cancer but not everyone who smokes gets lung cancer, not every child exposed to BPA will develop asthma."

The biological mechanism behind the BPA-asthma connection is unclear. The current study found no evidence that exposure to BPA increased the risk that the immune system would develop more antibodies to common airborne allergens. "Other possible pathways may include changes to the innate immune system, but this remains an open question," says Dr. Donohue.

The new study builds on existing evidence linking BPA exposure to respiratory symptoms, as well as to obesity, impaired glucose tolerance, and behavioral issues, among a range of health problems. In July, the Food and Drug Administration banned BPA in baby bottles and sippy cups.

"It is very important to have solid epidemiologic research like ours to give the regulators the best possible information on which to base their decisions about the safety of BPA," says senior author Robin Whyatt, DrPH, professor of Environmental Health Sciences and deputy director of the Columbia Center for Children's Environmental Health.

To reduce exposure to BPA, the National Institute of Environmental Health Sciences (NIEHS) recommends avoiding plastic containers numbers 3 and 7, eating less canned food, and, when possible, choosing glass, porcelain, or stainless steel containers, especially for hot food and liquids.