Prenatal smoke tied to poorer asthma-drug response

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Studies have shown that children whose mothers smoked during pregnancy may have an increased risk of developing asthma. Now new research suggests they may also get less benefit from the inhaled steroid medications used to prevent asthma attacks.

In a study of more than 1,000 kids between five and 12 years old with mild-to-moderate asthma, researchers found that those who had been exposed to smoke in the womb had less of a response to the inhaled corticosteroid budesonide (Pulmicort) than children with no prenatal exposure to smoking.

Overall, both groups of children improved with the medication. However, children with prenatal smoke exposure had 26 percent less of an improvement in their “airway responsiveness.”

Airway responsiveness refers to a “twitchiness” in the airways that, in people with asthma, can be triggered by small amounts of a normally benign irritant, like pollen or pet dander.

Inhaled steroids are the mainstay of therapy for persistent asthma, helping to prevent attacks of coughing, wheezing and breathlessness. One of the ways doctors measure whether a patient is responding to inhaled steroids is by testing airway responsiveness.

In this study, children with prenatal exposure to maternal smoking had less of an improvement in airway responsiveness after starting budesonide—and some had no improvement at all, said Dr. Benjamin A. Raby of Brigham and Women’s Hospital in Boston, one of the researchers on the study.

The full implications of the difference are not clear. The researchers did not have information on whether children exposed to prenatal smoking actually had higher rates of asthma attacks or hospital visits than other children, despite treatment with inhaled steroids.

But the findings do raise that possibility, Raby told Reuters Health.

He stressed, however, that no one is suggesting children with prenatal tobacco exposure should forgo inhaled steroids. “Inhaled steroids are the first-line therapy for persistent asthma, regardless of whether children had in-utero exposure to smoking or not,” Raby said.

Instead, he explained, the findings offer a potential explanation for why a child with prenatal exposure to smoking may not be responding as well as hoped to inhaled steroids. These children may need a second type of medication—such as oral drugs known as leukotriene modifiers—added to their treatment in order to control their asthma, Raby said.

The study, which was led by Dr. Robyn T. Cohen of Drexel University in Philadelphia, is published in the Journal of Allergy & Clinical Immunology.

The data come from a clinical trial in which 1,041 children with persistent asthma were randomly assigned to use budesonide, another type of inhaled asthma medication called nedocromil or a placebo over four years.

Of those children, 150 had been exposed to smoking in the womb, and 39 of them were given budesonide.

The study is the first to link prenatal smoke exposure with a reduced response to inhaled steroids, which, along with the small number of children exposed, means that further research is needed to replicate the findings, according to Raby.

It is also impossible to definitively say that prenatal tobacco exposure is the lone culprit, the researcher noted. He and his colleagues did account for children’s current exposure to secondhand smoke at home, but teasing out the impact of prenatal exposure by itself is difficult.

The researchers do think it is biologically plausible that prenatal tobacco exposure could affect children’s later response to asthma medication.

Lab research suggests that prenatal exposure to smoke can influence the development of the lung structure or the smooth muscles of the airways, which could affect the body’s later response to asthma medications.

SOURCE: http://link.reuters.com/mer34n Journal of Allergy & Clinical Immunology, online August 5, 2010

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