Beta‐2 receptor agonist exposure in the uterus associated with subsequent risk of childhood asthma

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Over the past several decades, the prevalence of childhood asthma has been on the rise, particularly in industrialized countries, including Japan.1 Well‐known environmental risk factors for childhood asthma in early infancy include passive smoking as well as exposure to allergens and antibiotics.3 Some risk factors that occur during the fetal period, such as maternal dietary intake, have also been investigated 7 in efforts to better understand what kinds of exposures in utero may influence subsequent childhood asthma. However, studies focusing on the effect of taking maternal medications during the fetal period on subsequent asthma have been limited.10
Although single long‐acting β2‐agonist therapy can dramatically improve the symptoms of wheezing and dyspnea, several studies have reported that continuous use is associated with further severe exacerbation and even asthma‐related death in both childhood and adulthood.13 Thus, chronic single long‐acting β2‐agonist therapy was flagged as a potential risk for asthmatic patients by the US Food and Drug Administration in 2011.15 To date, no studies have focused on the effect of exposure to B2RA via maternal medication in utero on subsequent risk of childhood asthma. One possible reason for that lack could be the strong influence of genetic factors; that is, identifying independent risk of prenatal B2RA is difficult because most women who use B2RA inhalant drugs are doing so to treat their own asthma. Although asthma is the main reason for use of B2RA inhalants among pregnant women, intravenous B2RA is also occasionally administered as a tocolytic agent for women with preterm labor16; this approach is common in Japan.18 As the use of tocolytic agents may not be associated with the presence of maternal asthma, conducting a study of women administered intravenous B2RA could reveal the risk of intrauterine B2RA exposure.
To that end, we conducted a prospective study on the effect of long‐term maternal B2RA exposure in utero on childhood asthma.

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