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Environmental exposure in relation to exhaled nitric oxide in newborns: is it all about timing?

Exhaled nitric oxide (eNO) is a marker of eosinophilic airway inflammation. It is increasingly used for the diagnosis and monitoring of asthmatic lung disease in adults as well as children 1, 2 and is believed to be helpful in titrating steroids or in predicting relapse in established asthma 3, 4. Although it is known that eNO is increased in healthy atopics 5, its role during the development of asthmatic airway disease is not understood. Only a few studies have examined whether eNO is already elevated before the occurrence of respiratory symptoms or in children that are prone to developing asthma 6, 7. Data published so far showed an interaction with smoke exposure, suggesting that, at least in high-risk children, eNO may play a role in the very initial phases of recurrent respiratory symptoms 6. It is tempting to speculate that eNO is a pre-existing marker before allergic inflammation of the airways occurs and that children can be “eNO phenotyped” early in life 8, enabling the identification of those with a high risk for later asthma development. However, before this can be done it is necessary to understand the natural course of eNO during the time period of fastest lung development, and the influence of external environmental stimuli on this course with possible long-term consequences 9.

In this issue of the European Respiratory Journal , Gabriele et al. 10 help to understand the issues of smoke exposure, airway symptoms and eNO in healthy infants 10. Gabriele et al. 10 examined the effect of pre- and post-natal smoke exposure and respiratory tract infections on eNO measured at age 4–17 weeks in an unselected birth cohort. They found that compared with unexposed infants, post-natal smoke exposure alone led to an increase in eNO, whereas …