Bad air causes rise in allergies, study shows

Allergies and asthma are on the rise - and researchers
blame pollution, second-hand smoke and other factors.

Pollution among the factors causing more allergies among children - and figures are set to rise

Three-quarters of parents with at least one child under the age of three report that the child has allergies, a study shows - and researchers warn the figure will grow.

Some 58 per cent of the youngsters had eczema or a skin allergy, 32 per cent had rhinitis or hay fever and 25 per cent airway allergies such as asthma.

Some of the children suffered more than one type of allergy.

The findings of the survey by the Allergy Association, commissioned by the University of Hong Kong, were based on interviews with 511 parents.

Only 30 per cent of the children were believed to have inherited the condition from their parents - meaning the rest might be down to factors such as pollution, exposure to second-hand smoke, Cesarean delivery or not being breastfed exclusively in their first six months.

"We have seen many more allergy cases in this generation than the last," said Dr Marco Ho Hok-kung, chairman of the association.

"I believe the number is only going to rise in the future, in keeping with the global trend. It is vital to understand the risk of allergies and take preventive measures."

Allergies could affect the long-term growth of infants, said Ho. Some research suggests that infants who develop an allergy before the age of two have a 24 per cent increased risk of developing emotional problems later in life.

Families with children suffering from allergies often have to devote a lot of effort to preventing exposure to allergens such as peanuts, milk or seafood in meals and dust mites at home.

According to the World Health Organisation, 40 to 50 per cent of children across the globe are bothered by one or more types of allergy.

Ho said if either parent had an allergy, there was a 30 per cent chance of their child inheriting it. This increased to 50 per cent if both parents were sufferers. And in general, every child has 5 to 15 per cent chance of developing an allergy even if neither parent has the condition.

Paediatrician Dr Alfred Tam Yat-cheung said risks could be attributed to environmental factors such as pollution and exposure to second-hand smoke. They could be reduced by giving birth naturally and feeding the babies only breast milk in their first six months, he said.

Source: South China Morning Post

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Study sheds light on asthma and respiratory viruses

Researchers try to find out why people with asthma have
more difficulty when contracting a respiratory virus.

People with asthma often have a hard time dealing with respiratory viruses such as the flu or the common cold, and researchers have struggled to explain why.

In a new study that compared people with and without asthma, the answer is becoming clearer. The researchers found no difference in the key immune response to viruses in the lungs and breathing passages.

The work, at Washington University School of Medicine in St. Louis, suggests that a fundamental antiviral defense mechanism is intact in asthma.

This means that another aspect of the immune system must explain the difficulty people with asthma have when they encounter respiratory viruses.

Among researchers who study asthma, there is debate over why patients with this common breathing disorder might have more trouble dealing with airway viruses than people without asthma.

The debate has centered on the role of proteins called interferons, which are released by cells lining the airways and are so named because they "interfere" with an invading virus.

"One school of thought says there is a defect in interferon production — that patients with asthma don't produce enough interferon," said senior author Michael J. Holtzman, MD, the Selma and Herman Seldin Professor of Medicine. "But we couldn't find any significant differences between the two groups. In fact, we were struck by how similar they were."

Holtzman and his colleagues looked at two common airway viruses — influenza A and respiratory syncytial virus (RSV) — and the interferon response they triggered in airway cells sampled from 11 patients with mild to severe asthma and seven control participants without asthma.

Though the study's sample size was small, the researchers performed an elaborate analysis that took into consideration the downstream events triggered by interferon release.

"Even though we showed both groups made similar amounts of interferon, we recognized that there might be a difference in effectiveness, a difference in how well it triggered downstream events necessary to fighting the virus," Holtzman said.

To find out whether the same amount of interferon might be less effective in patients with asthma, the investigators compared the genes activated by interferon in both groups of patients.

"The products of these genes are very effective in their antiviral action," Holtzman said. "But on the other side, the virus has a lot of ways of getting around them. So it's a battlefield. Who will win out? The interferon-stimulated genes or the viral genes?"

Holtzman and his colleagues showed that even in this downstream activation of genes, asthma patients and those without the condition were remarkably similar.

They also measured similar amounts of virus living in the cells at various points of time during the study, indicating that the battles against the viruses progressed similarly in both groups.

"Whatever is causing asthmatics and non-asthmatics to experience differences in how well they recover from these respiratory infections — why patients with asthma are more likely to end up in the hospital, for example — this interferon mechanism is not the deciding factor based on what we've seen so far," Holtzman said.

Given the complexity of the immune system, there are many other possible culprits to investigate. Holtzman and his colleagues are continuing to research these possibilities in similar studies with larger sample sizes and in studies looking at different aspects of the immune system.

One likely possibility that the group has proposed is that viruses have a special means to induce inflammatory airway disease, and the susceptibility to this process may be an essential feature of asthma and related lung diseases such as chronic obstructive pulmonary disease.

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Asthma drugs suppress children's growth say researchers

Corticosteroid drugs that are given by inhalers to children with asthma may suppress their growth, evidence suggests.

Two new systematic reviews published in The Cochrane Library focus on the effects of inhaled corticosteroid drugs (ICS) on growth rates.

The authors found children’s growth slowed in the first year of treatment, although the effects were minimized by using lower doses.

Inhaled corticosteroids are prescribed as first-line treatments for adults and children with persistent asthma.

They are the most effective drugs for controlling asthma and clearly reduce asthma deaths, hospital visits and the number and severity of exacerbations, and improve quality of life.

Yet, their potential effect on the growth of children is a source of worry for parents and doctors.

Worldwide, seven ICS drugs are currently available: beclomethasone, budesonide, ciclesonide, flunisolide, fluticasone, mometasone and triamcinolone.

Ciclesonide, fluticasone and mometasone are newer and supposedly safer drugs.

The first systematic review focused on 25 trials involving 8,471 children up to 18 years old with mild to moderate persistent asthma.

These trials tested all available inhaled corticosteroids except triamcinolone and showed that, as a group, they suppressed growth rates when compared to placebos or non-steroidal drugs. 14 of the trials, involving 5,717 children, reported growth over a year.

The average growth rate, which was around 6-9 cm per year in control groups, was reduced by about 0.5 cm in treatment groups.

The researchers found that growth suppression varied across studies, and so they looked at the relationship between a variety of factors and their effects on growth. Some of the variation could be explained by the drugs used, although since this was an indirect comparison the authors say more evidence is needed.

“Conclusions about the superiority of one drug over another should be confirmed by further trials that directly compare the drugs,” said Zhang.

More long-term trials and trials comparing different doses are also needed, particularly in children with more severe asthma requiring higher doses of inhaled corticosteroids, the researchers conclude.

“Only 14% of the trials we looked at monitored growth in a systematic way for over a year. This is a matter of major concern given the importance of this topic,” said Francine Ducharme, one of the authors of both reviews and senior author of the second review, based at the Department of Paediatrics at the University of Montreal in Montreal, Canada.

“We recommend that the minimal effective dose be used in children with asthma until further data on doses becomes available. Growth should be carefully documented in all children treated with inhaled corticosteroids, as well in all future trials testing inhaled corticosteroids in children.”

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Study: Breathing in smoke at home impairs child’s response to asthma treatment

Children exposed to cigarette smoke at home have lower levels of an enzyme that helps them respond to asthma treatment, a study has found.

Passive smoking is known to worsen asthma symptoms in children and impair their response to inhaled steroid treatment, but how this effect occurs was not known.

Researchers at Imperial College London found that children with severe asthma with a parent who smokes at home have lower levels of the enzyme HDAC2 compared with those whose parents don’t smoke. HDAC2 is required for steroids to exert their beneficial anti-inflammatory effects in asthma.

Professor Peter Barnes FRS, from the National Heart and Lung Institute at Imperial College London, said: “The mechanism we’ve identified makes children less sensitive to inhaled steroid treatment, so they suffer more symptoms and might have to take higher doses of steroids, which may lead to side effects.

“These findings underline the importance of legislation aimed at protecting children from being exposed to cigarette smoke. Restricting smoking in cars is a positive step, but the same should be applied in homes.”

The findings are reported in the journal Chest.

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Heavy kids exposed to air pollution have triple the risk for asthma

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Obese children exposed to high levels of air pollutants were nearly three times as likely to have asthma, compared with non-obese children and lower levels of pollution exposure, report researchers at Columbia University Medical Center (CUMC).

Rates of childhood obesity and asthma have both increased dramatically in the past 30 years. The percentage of American children who are obese has increased from 7% in 1980 to 20% in 2008. Childhood asthma is up from 4% in 1980 to 10% in 2009. Rates are higher among urban minority populations.
The researchers followed 311 children in predominantly Dominican and African-American neighborhoods of New York City. They monitored indoor air in each child's home for two weeks at age 5 or 6, to measure exposure to a family of air pollutants, polycyclic aromatic hydrocarbons (PAH). The child's height and weight were measured and respiratory questionnaires were administered. In all, 20% were found to have asthma and 20% were categorized as obese based on body mass index.

The researchers found that high PAH exposure was associated with asthma only among obese children. In particular, the association was with the alkylated forms of PAH, which are emitted by vehicles and by cigarette smoke, cooking, incense, burning candles, and various other indoor air pollution sources. A two- to three-fold increase in asthma risk was seen among obese children exposed to high levels of the PAH chemicals 1-methylphenanthrene and 9-methylphenanthrene. Exposure to PAH or obesity alone did not predict asthma.

"Our results suggest that obesity may magnify the effects of these air pollutants, putting children at greater risk for having asthma," says lead author Kyung Hwa Jung, PhD, associate research scientist in the Department of Medicine at Columbia University College of Physicians and Surgeons.

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Number of asthmatics with cat allergies has doubled

It's estimated that 60 to 85 percent of people with asthma have at least one allergy, and it seems may of those people have one thing in common - cats.

A new study has revealed that the number of people with asthma that are also allergic to cats has more than doubled over an 18 year period.

“From 1976 to 1994, positive allergy skin tests in people with asthma have increased significantly,” said Leonard Bielory, MD, ACAAI fellow and study author. “Not only have we found the number of asthma sufferers allergic to cats has more than doubled, but those with asthma are also 32 percent more likely to be allergic to cats than those without asthma.”

The study also found those with asthma are more likely to be allergic to several environmental triggers  including ragweed, ryegrass and alternaria fungus.

“This study helps us better understand common trends in allergy and asthma, which can lead to improved diagnosis and treatment,” said allergist James Sublett, M.D., chair of the ACAAI Indoor Environment Committee. “While it is unknown exactly why there has been an increase in asthma and allergy sufferers, it is thought a number of environmental factors can be responsible.”

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PVC flooring linked to asthma in children

A new study has found that Children exposed to PVC flooring are more likely to develop asthma during the following 10 year period.

There are also indications that PVC flooring in the parents’ bedrooms were actually more strongly associated with the new cases of asthma when compared with child's own bedroom. This could be an indication that the children were exposed in the womb as well.

Soft polyvinyl chloride (PVC) includes phthalates that normally are released to the surrounding environment. Phthalates is a group of chemicals with suspected endocrine disrupting properties that may impact on several chronic diseases/disorders such as asthma and allergy. The current study was aimed to investigate if PVC-flooring in the home of children in the age of 1-5 years was associated with the development of asthma in 5-year and 10-year follow-up investigations.

The Dampness in Buildings and Health (DBH) study started in the year of 2000 with a questionnaire to the parents of more than 14,000 children (1-5 years of age) in Värmland, Sweden, with responses from almost 11,000 children corresponding to a response rate of 79%. In this baseline questionnaire we screened for health in the family, lifestyles, building characteristics, etc. In 2005 we made a first 5 year follow up study and 2010 we made a second 10 year follow up, i.e., the data for the current study. The major interest in the follow up studies was to identify children that had developed asthma and other allergic diseases during the period after the baseline investigation.

Children who had PVC floorings in the bedroom were more likely to develop doctor diagnosed asthma during the following 10 years period when compared with children living without such flooring material. The risk was in several cases more than doubled. Furthermore, there were indications that PVC flooring in the parents’ bedrooms were stronger associated with the new cases of doctor diagnosed asthma when compared with child's bedroom. This could be an indication that prenatal exposure is of importance.

The scientists previously found that PVC flooring material is a source for phthalates found in indoor air, specifically in household dust. This exposure can be associated with eczema and asthma in children.

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Protein explains increased asthma severity in children exposed to traffic pollution

A new study shows that exposure to diesel exhaust particles from traffic pollution leads to increased asthma severity in children. Moreover, the study finds that this is due to increased blood levels of IL-17A, a protein associated with several chronic inflammatory diseases, in children with high diesel exposure.

The study by researchers at Cincinnati Children's Hospital Medical Center is published online in the Journal of Allergy and Clinical Immunology.

The research, conducted in mice and in humans, showed that neutralizing IL-17A prevented airway inflammation. Neutralization of IL-17A "may be a useful potential therapeutic strategy to counteract the asthma-promoting effects of traffic-related air pollution, especially in highly exposed, severe allergic asthmatics," says Gurjit Khurana Hershey, MD, PhD, director of asthma research at Cincinnati Children's and senior author of the study.

Dr. Hershey and her colleagues studied 235 children and teens with asthma. The researchers plotted each person's primary address and estimated their diesel exposure attributable to traffic based on where they lived. The researchers also studied mice exposed to diesel particles and dust mites, a common household allergen.

In children with asthma, diesel exposure was associated with more frequent asthma symptoms and increased IL-17A blood levels. Similarly, exposure to both diesel and dust mites resulted in more severe asthma in mice compared to dust mite exposure alone. When IL-17A was neutralized in mice, it alleviated airway inflammation induced by diesel exposure.

"Blocking IL-17A may be a useful strategy to counteract the effects of traffic-related air pollution, especially in highly exposed allergic asthmatic children," says Dr. Hershey.
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Children with allergy, asthma, milk intolerance may be at higher risk for ADHD

The number of children being diagnosed with attention-deficit disorder (ADHD), allergy and asthma is increasing in the United States. And according to a new study, there might be a link between the growth of these three conditions.

The study, published in the August issue of Annals of Allergy, Asthma & Immunology, the scientific journal of the American College of Allergy, Asthma and Immunology (ACAAI), found there is an increased risk of ADHD in boys that have a history of allergy or asthma.

"ADHD, a chronic mental health disorder, is most commonly found in males, while asthma is also more common in young boys than girls," said Eelko Hak, lead study author. "We found there is an increased risk of ADHD in boys with a history of asthma and an even stronger risk associated with milk intolerance."

Researchers in the Netherlands and Boston studied 884 boys with ADHD and 3,536 boys without the disorder. Of the children with ADHD, 34 percent had asthma and 35 percent had an allergic disorder. The study suggests medications used to treat these conditions may be associated with an increased ADHD risk.

"Further research is needed to understand why there appears to be an increased risk of developing ADHD in children with allergy and asthma," said Gailen Marshall, MD, editor-in-chief of Annals of Allergy, Asthma & Immunology. "Medications for these conditions far outweigh the risks, and can be life-saving in some conditions. Treatment should not be stopped, unless advised by a board-certified allergist."

According to the ACAAI, allergy and asthma often run in families. If both parents have an allergy a child has a 75 percent chance of being allergic. If neither parent has allergy, the chance of a child developing an allergy is only 10 to 15 percent. Allergists also know allergies and asthma are linked. An estimated 60 to 80 percent of children with asthma also have an allergy. While the cause of ADHD is unknown, this disorder is also thought to run in families.
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Great-grandma's cigarette habit could be the cause of child's asthma

Photo: freedigitalphotos.net

With some 300 million people around the world living with asthma, a study by Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center (LA BioMed) found for the first time that maternal smoking can cause the third generation of offspring to suffer from the chronic lung disease.

The study, published online by the American Journal of Physiology - Lung Cellular and Molecular Physiology, reported that maternal nicotine exposure during pregnancy is linked to asthma in the third generation in disease models. This is known as a "transgenerational" linkage because the third generation was never directly exposed to nicotine or smoking. Previous research had found nicotine exposure was linked to asthma in the second generation, or was a "multigenerational" cause of asthma.

"Even though there are multiple causes for childhood asthma, research linking this serious chronic condition to maternal nicotine exposure during pregnancy for up to three generations should give mothers-to-be even more reasons to reconsider smoking," said Virender K. Rehan, MD, an LA BioMed lead researcher and the corresponding author of the study. "Eliminating the use of tobacco during pregnancy could help halt the rise in childhood asthma and ensure healthier children for generations to come."

Worldwide, approximately 250 million women smoke daily, and the number of people living with asthma is expected to grow by about a third by 2025, reaching approximately 400 million. Twelve percent of women in the U.S. continue to smoke during pregnancy, resulting in the birth of at least 400,000 smoke-exposed infants per year in the U.S. alone.

In previous studies, the researchers have concluded that the cause of the second generation's asthma was epigenetic modification (an environmental factor causing a genetic change). Nicotine was affecting both the lung cells and the sex cells in ways that caused the lungs that developed from those cells to develop abnormally, causing asthma. The current study "paves the way for determining the epigenetic mechanisms" behind smoking and the transmission of asthma to future generations, the researchers concluded.

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Inflammatory on and off switch identified for allergic asthma and COPD

Japanese researchers have made a new step toward understanding why—and how to stop—runaway inflammation for both chronic obstructive pulmonary disorder (COPD) and allergic asthma.

In a new report appearing in the August 2013 issue of The FASEB Journal scientists show that two receptors of an inflammatory molecule, called "leukotriene B4," play opposing roles in turning inflammation on and off for allergic asthma and COPD. The first receptor, called "BLT1," promotes inflammation, while the second receptor, called "BLT2," has a potential to weaken inflammation during an allergic reaction. This discovery also is important because until now, BLT2 was believed to increase inflammatory reaction.

"Leukotriene B4 levels are elevated in the airways of the patients with asthma and COPD, and the opposite role of BLT1 and BLT2 in allergic inflammation implies that drug development should target BLT1 and BLT2 differently," said Hiromasa Inoue, M.D., study author from the Department of Pulmonary Medicine at the Graduate School of Medical and Dental Sciences at Kagoshima University in Kagoshima, Japan. "We hope that better anti-asthma drugs or anti-COPD drugs will be produced in the future to treat millions of patients who suffer from severe asthma and COPD."

To make this discovery, scientists compared the allergic reactions in BLT2-gene deleted mice to those in normal mice. Then an allergic asthma reaction was provoked by inhalation of allergens. BLT2-gene deleted mice showed more inflammatory cells in the lung compared to normal mice. Without the BLT2 gene, lung allergic inflammation was stronger than that of normal mice. The production of interleukin-13, an important mediator of allergic inflammation from T lymphocytes, was increased in the group without the BLT2 gene. Results suggest that targeting these two receptors differently and/or separately could achieve vastly different outcomes. Conventional anti-leukotriene B4 drugs block both of the pathways induced by BLT1 and BLT2. By manipulating the specific target, it may be possible to develop more effective anti-leukotriene B4 drugs.

"This is one case where BLT isn't a sandwich! Distinguishing between BLT1 and BLT2 is an important step forward to developing more effective drugs for lung inflammation," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "Understanding the specific roles of these and other receptors allow researchers to identify new drug targets, which in turn can lead to new and more effective drugs."

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Researchers find enzyme that could hold the key for asthma sufferers

An enzyme known for its role in heart disease may well be a promising target to treat asthma. Researchers from the University of Iowa have found that the enzyme, called CaMKII, is linked to the harmful effects of oxidation in the respiratory tract, triggering asthmatic symptoms. The finding could lead to the development of a drug that would target the CaMKII enzyme, the researchers say.

Asthma affects billions of people worldwide. In the United States, 8.5 percent of the population has asthma, which causes 3,000 deaths and more than $56 billion annually in medical and lost work costs, according to the federal Centers for Disease Control and Prevention. Despite its toll on health and productivity, treatment options remain confined to steroids, which have harmful, even life-threatening, side effects for those with severe cases.

Current treatments don’t work well, noted Mark Anderson, professor and chair in internal medicine at the UI and a co-corresponding author on the paper, published July 24 in the journal Science Translational Medicine.

“It’s a kind of an epidemic without a clear, therapeutic option," Anderson says. "The take-home message is that inhibiting CaMKII appears to be an effective anti-oxidant strategy for treating allergic asthma."

Anderson and co-corresponding author Isabella Grumbach knew from previous work that the CaMKII enzyme played a role in the oxidation of heart muscle cells, which can lead to heart disease and heart attacks. The scientists surmised the same enzyme may affect oxidation in the respiratory system as well.

The team first tested the enzyme in airway muscle cells, but to little effect. They then tried to block the enzyme in the airway lining (epithelial) cells. They noticed that mice with the blocked enzyme had less oxidized CaMKII, no airway muscle constriction and no asthma symptoms. Similarly, mice without the blocked enzyme showed high “oxidative stress,” meaning lots of oxidized enzymes in the epithelial cells, a constricted airway and asthma symptoms.

“[The study] suggests that these airway lining cells are really important for asthma, and they’re important because of the oxidative properties of CaMKII,” says Anderson, whose primary appointment is in the Carver College of Medicine. “This is completely new and could meet a hunger for new asthma treatments. Here may be a new pathway to treat asthma.”

"Ten years ago, not much was known about what CaMKII does outside of nerve cells and muscle cells in the heart," says Grumbach, associate professor in internal medicine at the UI. "My lab has worked on investigating its function mainly in blood vessels with the long-term goal to use blockers of CaMKII to treat common diseases. We are constantly finding that CaMKII is interesting and important."

The researchers also took tissue samples from the airways of patients with asthma. True to their hypothesis, they found more oxidized enzymes in those patients than in healthy individuals. Taking a step further, the team found that mild asthma patients who inhaled an allergen had a spike in oxidized CaMKII in the epithelial cells just a day later.

“We have this very compelling association,” Anderson says, adding that more studies in patients are needed to validate the approach.

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Scientists: Early exposure to traffic pollution may be the cause of childhood #asthma

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A research team led by scientists at the University of California, San Francisco has found that exposure in infancy to nitrogen dioxide (NO2), a component of motor vehicle air pollution, is strongly linked with later development of childhood asthma among African Americans and Latinos.

The researchers said their findings indicate that air pollution might, in fact, be a cause of the disease, and they called for a tightening of U.S government standards for annual exposure to NO2.

The study is reported online currently in the American Journal of Respiratory and Critical Care Medicine ahead of print publication.

In the study, the largest to date of air pollution exposure and asthma risk in minority children in the United States, the team found that for every five parts per billion increase in NO2 exposure during the first year of life, there was a 17 percent increase in the risk of developing asthma later in life.

The study involved 3,343 Latino and 977 African American participants.

"Many previous studies have shown an obvious link between traffic-related pollution and childhood asthma, but this has never been thoroughly looked at before in an all-minority population," said lead author Katherine K. Nishimura, MPH, a graduate student in the laboratory of senior author Esteban G. Burchard, MD, MPH, a UCSF professor of bioengineering and therapeutic sciences and medicine and director of the UCSF Center for Genes, Environment & Health.

Minorities tend to live in areas of higher air pollution and have a higher risk of developing asthma, the researchers said.

What made the current study different from previous research, said Nishimura, was that the scientists looked retrospectively at the study participants' exposure to air pollution in early childhood, before they developed asthma. Children who developed asthma before this exposure period were excluded.

"Any participant with asthma in this study was exposed to air pollution in infancy, before they developed the disease, which is a step in the right direction in inferring causality," said Nishimura.

"This work adds to the growing body of evidence that traffic-related pollutants may be causally related to childhood asthma," said Burchard.

Study co-author John R. Balmes, MD, of UC San Francisco and UC Berkeley, pointed out that a previous study of children living in southern California showed that living and attending school close to major roadways was associated with an increased risk of new-onset asthma. "Together with our findings, this makes for strong evidence that reducing children's exposure to traffic emissions can prevent some cases of asthma," said Balmes.

One immediate implication of the study, said Burchard, is that the national standard for NO2 set by the Environmental Protection Agency (EPA) is "too lax by far." He noted that the current EPA annual standard is 53 parts per billion (ppb), while the study subjects were exposed, on average, to 19 ppb during the first year of life.

"Children growing up in southern California have been shown to have reduced growth of lung function when annual NO2 levels exceed the current national annual standard," added Balmes.

The participants, who were 8 to 21 years old and had no other lung diseases or chronic illnesses, were recruited from study centers in Chicago, New York City, Houston, the San Francisco Bay Area, and Puerto Rico. To adjust for instances when study participants moved residences, air pollution exposure for all subjects was assessed by using the residential histories from birth through time of recruitment. The researchers based their air pollution exposure estimates on EPA annual measurements.

"The geographic diversity of the study population strengthens the results, because the effects we see are consistent across a wide range of urban environments and conditions," said Nishimura. While the study was not designed to investigate how air pollution might cause childhood asthma, said Nishimura, the investigators are looking at two possible causes.

The first is that NO2 can interact with a number of other pollutants to create reactive oxygen species — chemically reactive molecules containing oxygen — which can, in turn, damage developing lungs. Immune systems that develop under such conditions, she said, could be "trained" to respond to pollutants as triggers that could later induce asthma.

Another possible explanation, said Nishimura, is that pollutants can potentially cause a genetic predisposition to asthma by altering methylation patterns in DNA. Methylation is a chemical change that alters gene expression without affecting the underlying structure of the DNA itself.

"It has been shown that changes in methylation, which can be affected by pollution, tobacco smoke and even stress, can be inherited across multiple generations," said Burchard. "Our group is currently investigating methylation as the possible outcome of exposures to a number of pollutants."

Burchard cautioned that air pollution is "not the entire story," noting that despite its low air pollution levels, Puerto Rico has the highest asthma prevalence and morbidity in the United States. "This is intriguing, and leaves us more work to do," he said.

Smoke exposure puts infants with family history of asthma/allergies at higher risk for severe infection

More evidence has surfaced that supports the war on smoking, especially if smokers have an infant in their household. A study published today in the June issue of Annals of Allergy, Asthma & Immunology, the scientific journal of the American College of Allergy, Asthma and Immunology (ACAAI), found that infants with a family history of allergic disease with lower respiratory tract infections, who are exposed to secondhand smoke are at risk for longer hospital stays.

An estimated 20 to 30 percent of otherwise healthy infants develop lower respiratory infections, such as bronchiolitis, annually. Of these, three percent are hospitalized.

"Respiratory infections in infants are common, but if the infant has a family history of respiratory issues such as asthma, they are at higher risk for infection and hospitalization," said allergist Meghan Lemke, MD, ACAAI member and lead study author. "Our research found that infants with a family history of allergic disease who are also exposed to secondhand smoke had a 23 percent longer hospital stay than those without secondhand smoke exposure."

Researchers examined 451 mothers and infants enrolled in a study focusing on childhood asthma and atopic disease outcomes associated with viral respiratory infections. In this group, 57 percent of infants were exposed to secondhand smoke. While 36 percent had a mother with atopic disease and an allergy, and 68 percent had an immediate relative with an allergic disease.

"Infants that are hospitalized for bronchiolitis have up to a 30 percent chance of developing persistent wheezing or asthma within the first decade of life," said allergist James Sublett, MD, chair of the ACAAI Indoor Environment Committee. "Secondhand smoke is extremely harmful to children with asthma and other respiratory illnesses, and has been shown to contribute to uncontrolled asthma."

According to the Centers for Disease Control and Prevention (CDC), secondhand smoke contains more than 7,000 chemicals, hundreds of which are toxic and 70 that can cause cancer.

"Secondhand smoke can trigger asthma attacks in small children, which can be life-threatening," said Dr. Sublett. "It is critical that parents and other family members never smoke around children, young or old, especially inside of the home and car where smoke can linger."

Seven million American children have asthma, a disease that is a leading cause of missed school days and 456,000 hospitalizations in the United States annually. Asthmatics under the care of a board-certified allergist have a 60 to 89 percent reduction in hospitalizations.

Unique omega-3 supplement effective at reducing exercise-induced asthma symptoms

An Indiana University study has found that a unique omega-3 supplement derived from the New Zealand green-lipped mussel significantly improved lung function and reduced airway inflammation in asthmatics who experience exercise-induced bronchoconstriction, also called exercise-induced asthma.

Timothy Mickleborough, professor in the IU School of Public Health-Bloomington, said his findings are similar to his studies involving fish oil but required a much smaller dosage of the supplement. His new study, appearing online in the journal Respiratory Medicine, found a 59 percent improvement in lung function after an airway challenge, and a reduction in airway inflammation, asthma symptoms and use of emergency medication.

"Not only does it reduce symptoms, which will make you feel better, but it potentially could improve athletic performance," Mickleborough said. "Any time you can reduce medication is good."

In exercise-induced asthma, vigorous exercise triggers an acute narrowing of the airway afterward, making breathing difficult. Other symptoms include coughing, tightening of the chest and excessive fatigue. About 90 percent of people with asthma have this condition, which also is found in an estimated 10 percent or more of elite athletes and as much as 10 percent of the general population without asthma.

Mickleborough's study used Lyprinol/Omega XL, which contains PCSO-524, a patented extract of stabilized lipids from the New Zealand green-lipped mussel, combined with olive oil and vitamin E. PCSO-524 includes the five main lipid classes: sterol esters, sterols, polar lipids, triglycerides and free fatty acids, including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).

Previous studies involving PCSO-524 have found it to be effective in treating osteoarthritis, rheumatoid arthritis and inflammatory bowel disease. Mickleborough's study is the first to show that it is effective in reducing the airway inflammation experienced by asthmatic study participants diagnosed with exercise-induced asthma.

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Exposure to traffic pollution increases asthma severity in pregnant women

Air pollutants from traffic are associated with increased asthma severity levels in pregnant asthmatic women, according to a new study.

"Air pollution is a known trigger for asthma symptoms," said lead author Janneane Gent, PhD, Research Scientist in Epidemiology (Environmental Health) at the Yale School of Public Health.

 "In our study, exposures were assessed using a sophisticated air pollution modeling system (Community Multiscale Air Quality, CMAQ) that permits community-level estimates (i.e., close to where the subject resides) instead of assigning regional measurements made at Environmental Protection Agency (EPA) central site monitors to all subjects. Using community-level estimates, we found that exposure to nitrogen dioxide at levels much lower than the current EPA standard was associated with increased risk of asthma morbidity."

The results of the study will be presented at the ATS 2013 International Conference.

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Exposure to nitrogen dioxide, fine particulate matter, and the elemental carbon content of fine particulate matter were estimated using the CMAQ modeling system. Analyses of the relationship between exposure to traffic-related pollutants and asthma severity were adjusted for a number of possible confounding factors, including month of pregnancy, pre-pregnancy body mass index, demographics, health, household exposures and season.

Mean community-level predicted concentrations for nitrogen dioxide, elemental carbon and fine particulate matter were 23.7 parts per billion (ppb), 0.67 micrograms (one-millionth of a gram) per cubic meter of air (g/m3) and 11.1 g/m3, respectively.

Each 10 ppb increase in community-level nitrogen dioxide was associated with an increased risk of wheeze, with an odds ratio (the odds that an outcome will occur after a particular exposure, compared to the odds of the outcome occurring in the absence of that exposure) of 1.27. Each 10 ppb increase in nitrogen dioxide was also associated with a higher asthma severity score (odds ratio 1.31). Similarly, each 0.5 g/m3 increase in elemental carbon was associated with an increased risk of wheeze (odds ratio 1.30) and higher asthma severity score (odds ratio 1.32).

Exposure to fine particulate matter did not significantly increase asthma morbidity or asthma severity score.

"Exposure to air pollution from traffic is known to have a number of deleterious effects on human health," said Dr. Gent. "Our study suggests that exposures to community-level concentrations of traffic-related pollutants are associated with increased asthma morbidity, and that these pollutant concentrations are likely to be lower than those measured at EPA central monitoring sites."

"Dustless" school chalk found to trigger allergy symptoms and asthma in those with milk allergy

Photo:  Anusorn P Nachol/freedigtalphotos.net

Many of today’s school teachers opt for dustless chalk to keep hands and classrooms clean. But according to a study published in the May issue of Annals of Allergy, Asthma & Immunology, the scientific journal of the American College of Allergy, Asthma and Immunology (ACAAI), this choice in chalk may cause allergy and asthma symptoms in students that have a milk allergy.

Casein, a milk protein, is often used in low-powder chalk. When milk allergic children inhale chalk particles containing casein, life-threatening asthma attacks and other respiratory issues can occur.

“Chalks that are labeled as being anti-dust or dustless still release small particles into the air,” said Carlos H. Larramendi, MD, lead study author. “Our research has found when the particles are inhaled by children with milk allergy, coughing, wheezing and shortness of breath can occur. Inhalation can also cause nasal congestion, sneezing and a runny nose.”

Milk allergy affects an estimated 300,000 children in the United States, according to the ACAAI. Although it has been believed the majority of children will outgrow milk allergy by age three, recent studies contradict this theory, showing school aged children are still affected. However, 80 percent of children with milk allergy will likely outgrow it by age 16.

“Chalk isn’t the only item in a school setting that can be troublesome to milk allergic students,” said James Sublett, MD, chair of the ACAAI Indoor Environment Committee. “Milk proteins can also be found in glue, paper, ink, and in other children’s lunches.”

Even in the wake of whiteboards, overhead projectors and tablets, chalk is a classroom staple that likely won’t become extinct anytime soon. Parents with milk allergic children should ask to have their child seated in the back of the classroom where they are less likely to inhale chalk dust, advises Sublett.

“Teachers should be informed about foods and other triggers that might cause health problems for children,” said Sublett. “A plan for dealing with allergy and asthma emergencies should also be shared with teachers, coaches and the school nurse. Children should also carry allergist prescribed epinephrine, inhalers or other life-saving medications.”

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Have Asthma? You Likely Have an Allergy as Well

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

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

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

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

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

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

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

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

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

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.