Personal exposure to nitrogen dioxide and risk of airflow obstruction in asthmatic children with upper respiratory infection

Citation
Ch. Linaker et al., Personal exposure to nitrogen dioxide and risk of airflow obstruction in asthmatic children with upper respiratory infection, THORAX, 55(11), 2000, pp. 930-933
Citations number
18
Categorie Soggetti
Cardiovascular & Respiratory Systems","da verificare
Journal title
THORAX
ISSN journal
00406376 → ACNP
Volume
55
Issue
11
Year of publication
2000
Pages
930 - 933
Database
ISI
SICI code
0040-6376(200011)55:11<930:PETNDA>2.0.ZU;2-C
Abstract
Background-Several studies have linked air pollution by nitrogen dioxide (N O2) with increased hospital admissions for asthma in children. Exacerbation s of asthma in children are often precipitated by upper respiratory infecti ons. It is therefore possible that NO2 increases the risk of airways obstru ction when asthmatic children develop upper respiratory infections. Methods-To test this hypothesis a sample of 114 asthmatic children aged 7-1 2 years were followed for a total of up to 13 months. Probable upper respir atory infections were identified by consensus review of daily symptom diari es, and episodes of airways obstruction from serial records of peak expirat ory flow (PEF). Personal exposures to NO2 were measured with Palmes tubes t hat were changed weekly. Generalised estimating equations were used to asse ss the relative risk (RR) of an asthmatic exacerbation starting within seve n days of an upper respiratory infection according to estimated NO2 exposur e during the one week period from two days before to four days after the on set of the infection. Results-The children were followed for an average of 34 weeks during which 318 upper respiratory infections and 224 episodes of reduced PEF were diagn osed. PEF episodes were much more likely to occur in the seven days followi ng the onset of an upper respiratory infection than at other times. Estimat ed exposures to NO2 at the time of infections were generally low (geometric mean 10.6 mug/m(3)). Compared with exposures of less than or equal to8 mug /m(3), exposures of >28 mug/m(3) were associated with a RR of 1.9 (95% conf idence interval 1.1 to 3.4) for the development of an asthmatic episode wit hin seven days of an infection. Conclusions-The findings give some support to the hypothesis that NO2 incre ases the risk of asthmatic exacerbations following respiratory infections, even at relatively low levels of exposure. Further studies in populations w ith higher exposures would be useful.