Linaker C H, Coggon D, Holgate S T, Clough J, Josephs L, Chauhan A J, Inskip H M
MRC Environmental Epidemiology Unit, University of Southampton, Southampton General Hospital, Southampton SO16 6YD, UK.
Thorax. 2000 Nov;55(11):930-3. doi: 10.1136/thorax.55.11.930.
Several studies have linked air pollution by nitrogen dioxide (NO(2)) with increased hospital admissions for asthma in children. Exacerbations of asthma in children are often precipitated by upper respiratory infections. It is therefore possible that NO(2) increases the risk of airways obstruction when asthmatic children develop upper respiratory infections.
To test this hypothesis a sample of 114 asthmatic children aged 7-12 years were followed for a total of up to 13 months. Probable upper respiratory infections were identified by consensus review of daily symptom diaries, and episodes of airways obstruction from serial records of peak expiratory flow (PEF). Personal exposures to NO(2) were measured with Palmes tubes that were changed weekly. Generalised estimating equations were used to assess the relative risk (RR) of an asthmatic exacerbation starting within seven days of an upper respiratory infection according to estimated NO(2) exposure during the one week period from two days before to four days after the onset of the infection.
The children were followed for an average of 34 weeks during which 318 upper respiratory infections and 224 episodes of reduced PEF were diagnosed. PEF episodes were much more likely to occur in the seven days following the onset of an upper respiratory infection than at other times. Estimated exposures to NO(2) at the time of infections were generally low (geometric mean 10.6 microg/m(3)). Compared with exposures of < or = 8 microg/m(3), exposures of >28 microg/m(3) were associated with a RR of 1.9 (95% confidence interval 1.1 to 3.4) for the development of an asthmatic episode within seven days of an infection.
The findings give some support to the hypothesis that NO(2) increases the risk of asthmatic exacerbations following respiratory infections, even at relatively low levels of exposure. Further studies in populations with higher exposures would be useful.
多项研究已将二氧化氮(NO₂)造成的空气污染与儿童哮喘住院人数增加联系起来。儿童哮喘发作常常由上呼吸道感染诱发。因此,当哮喘儿童患上呼吸道感染时,NO₂有可能增加气道阻塞的风险。
为验证这一假设,对114名7至12岁的哮喘儿童进行了为期长达13个月的跟踪研究。通过对每日症状日记的一致性审查确定可能的上呼吸道感染,并根据呼气峰值流速(PEF)的连续记录确定气道阻塞发作情况。使用每周更换一次的帕尔姆斯管测量个人对NO₂的暴露情况。采用广义估计方程,根据感染发作前两日至发作后四日这一周期间估计的NO₂暴露量,评估上呼吸道感染后七日内开始出现哮喘发作的相对风险(RR)。
对这些儿童平均跟踪了34周,在此期间诊断出318次上呼吸道感染和224次PEF降低发作。与其他时间相比,上呼吸道感染发作后七日内PEF发作的可能性要大得多。感染时估计的NO₂暴露量一般较低(几何平均数为10.6微克/立方米)。与暴露量≤8微克/立方米相比,暴露量>28微克/立方米与感染后七日内出现哮喘发作的RR为1.9(95%置信区间1.1至3.4)相关。
这些发现为以下假设提供了一定支持,即即使在相对低的暴露水平下,NO₂也会增加呼吸道感染后哮喘发作的风险。对暴露水平较高人群进行进一步研究将很有帮助。