www.thelancet.com/respiratory Vol 2 November 2014 873 873

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“It is an important piece of work and furthers our understanding of how people with asthma are more sensitive to viruses, especially the common rhinovirus, and how they react in a more vigorous way, which can trigger asthma attacks.”

“This study may drive the development of new medications to stop or limit the release of IL-25 and certainly supports the current practice that all asthma patients should receive the annual fl u vaccination.”

Dr Samantha Walker, of Asthma UK (London, UK), added: “Years of research underfunding means that asthma still remains a relative mystery and the millions of people with asthma need more studies like this to bring us one step closer to new treatments.”

Sanjay Tanday

the infected cells from the people with asthma showed a greater capacity to express IL-25, with a ten times increase in IL-25 mRNA concentrations compared with the healthy cells (p<0·05).

The researchers then infected 39 people with rhinovirus—of which 28 had asthma—to examine what eff ect this has on IL-25 concentrations in nasal secretions. Up to 10 days after infection with rhinovirus, 17 (61%) of those with asthma had a signifi cant increase in their IL-25 concentrations (p<0·001).

Finally, using mice—whose airways had been sensitised by the allergen RV-OVA—the researchers showed that blocking IL-25 with an antibody decreased the concentrations of these other cytokines (p<0·05).

Dr Richard Russell, of the British Lung Foundation (London, UK), said:

Study identifi es how common cold triggers asthma attacksResearchers have, for the first time, identifi ed how the common cold can bring on life-threatening asthma attacks.

They found that rhinoviruses, the main cause of the common cold, can induce interleukin-25 (IL-25) in lung epithelial cells, which triggers the production of other type-2 cytokines leading to a molecular cascade that drives asthma exacerbations. The findings raise the prospect of developing new drugs that target IL-25, and could prevent people with asthma from getting worse symptoms if they catch a cold.

Janine Beale and colleagues compared bronchial epithelial cells taken from the lungs of ten people with asthma with cells from ten healthy people. The cells were infected with rhinovirus in vitro. After 8 h of exposure to rhinovirus,

Published OnlineOctober 15, 2014http://dx.doi.org/10.1016/S2213-2600(14)70243-7

For the study by Beale and colleagues see Sci Transl Med 2014; 6: 256ra134

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Bisphenol A linked to wheeze and reduced lung function Prenatal exposure to bisphenol A, commonly used in the manufacture of some plastics, appears to be linked with the development of persistent wheeze and reduced lung function in young children, say US researchers.

In a study of 398 infants and their mothers, every ten times increase in maternal urinary bisphenol A concentration was associated with a 14·2% (95% CI –24·5 to –3·9) drop in the predicted forced expiratory volume in 1 s (FEV1) at 4 years of age. But this link seemed to disappear by the age of 5 years, the researchers reported.

From maternal urine samples taken at 16 and 26 weeks of pregnancy, the researchers found a ten times increase in average maternal urinary bisphenol A concentration was linked with a 54·8% increase in the odds of wheezing in their off spring (adjusted odds ratio 1·55, 95% CI 0·91–2·63).

A ten times increase in the 16-week maternal urinary bisphenol A concentration was associated with a 4·27 times increase in the odds of persistent wheeze (adjusted odds ratio 4·27, 95% CI 1·37–13·30).

However, child urinary bisphenol A concentrations, which were taken annually to the age of 5 years, were not associated with FEV1 or wheezing.

Bisphenol A is an endocrine-disrupting chemical that in animal studies has been implicated in impaired lung development.

Study leader Adam Spanier, associate professor of paediatrics at University of Maryland, Baltimore, USA, stressed further studies were needed to clarify the link, as results had been inconsistent and the “window of vulnerability” should be investigated in more depth. But he added: “Maternal exposures to bisphenol A during pregnancy may aff ect a child’s future lung health.”

“Pregnant women and women intending to be pregnant may want to take eff orts to minimise exposure to bisphenol A.”

But he said avoiding bisphenol A was a diffi cult task for the consumer and the best approach would be to remove it from the manufacturing process.

Kian Fan Chung, professor of respiratory medicine at Imperial College London said the study appears to show a time window for the epigenetic effects of bisphenol on asthma development and remodelling, or lung airway development. “It looks like an interesting (perhaps important) observation that goes in the same trend as previous studies, but does not correlate with the recent JACI study where the asthma link was with childhood exposure to bisphenol A.”

Emma Wilkinson

Published OnlineOctober 15, 2014http://dx.doi.org/10.1016/S2213-2600(14)70244-9

For the study by Spanier and colleagues see JAMA Pediatr 2014; published online Oct 6. DOI:10.1001/jamapediatrics.2014.1397

For the JACI study see J Allergy Clin Immunol 2013; 131: 736–42

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