Rusznak C, Devalia J L, Davies R J
Department of Asthma and Allergic Respiratory Diseases, St Bartholomew's School of Medicine, London, UK.
Thorax. 1996 Nov;51(11):1105-8. doi: 10.1136/thx.51.11.1105.
Recent studies have suggested that air pollutants resulting from vehicle exhaust emissions and burning of fossil fuels, either in combination or individually, may enhance the airway response of asthmatic subjects to inhaled allergen. It was hypothesised that the airway response to inhaled allergen after exposure to a combination of 400 ppb nitrogen dioxide (NO2) and 200 ppb sulphur dioxide (SO2) is increased 24-48 hours after exposure.
Thirteen mild atopic asthmatic volunteers were exposed for six hours to a single exposure of air and three exposures of the combination of 400 ppb NO2 + 200 ppb SO2 in randomised order, and then challenged with increasing concentrations of Dermatophagoides pteronyssinus allergen either immediately after exposure to air, or immediately, 24 hours or 48 hours after exposure to the combination of the two pollutants, until a 20% fall in forced expiratory volume in one second (FEV1) was recorded.
Exposure to 400 ppb NO2 + 200 ppb SO2 significantly decreased the dose of D pteronyssinus allergen required to produce a 20% fall in FEV1 (PD20FEV1) at all times after exposure when compared with air. The mean percentage changes in allergen PD20FEV1 immediately, 24 hours, and 48 hours after exposure to 400 ppb NO2 + 200 ppb SO2 were -37% (95% confidence intervals (CI) -50 to -23), -63% (CI -75 to -51), and -49% (CI -75 to -28.8), respectively, when compared with the PD20FEV1 after air exposure and were significant at all time points studied. The allergen PD20FEV1 at 24 hours after exposure to the combination of the two pollutants was also found to be significantly lower when compared with that immediately after exposure to the two pollutants.
These results demonstrate that exposure to a combination of NO2 and SO2, at concentrations which can be encountered during episodes of increased outdoor and indoor air pollution, enhances the airway response to inhaled allergen in asthmatic subjects. This effect persists over a period of 24-48 hours and is maximal 24 hours after exposure to these air pollutants.
近期研究表明,车辆尾气排放和化石燃料燃烧产生的空气污染物,无论是单独还是混合存在,都可能增强哮喘患者气道对吸入性过敏原的反应。研究假设,暴露于400 ppb二氧化氮(NO₂)和200 ppb二氧化硫(SO₂)的混合物后,气道对吸入性过敏原的反应在暴露后24 - 48小时会增强。
13名轻度特应性哮喘志愿者按随机顺序,分别单次暴露于空气6小时,以及暴露于400 ppb NO₂ + 200 ppb SO₂的混合物3次,每次6小时。然后,在暴露于空气后立即,或在暴露于两种污染物的混合物后立即、24小时或48小时,用浓度递增的屋尘螨过敏原进行激发试验,直至记录到一秒用力呼气量(FEV₁)下降20%。
与暴露于空气相比,暴露于400 ppb NO₂ + 200 ppb SO₂后,在所有时间点,产生FEV₁下降20%所需的屋尘螨过敏原剂量(PD₂₀FEV₁)均显著降低。与暴露于空气后的PD₂₀FEV₁相比,暴露于400 ppb NO₂ + 200 ppb SO₂后立即、24小时和48小时,过敏原PD₂₀FEV₁的平均百分比变化分别为-37%(95%置信区间(CI)-50至-23)、-63%(CI -75至-51)和-49%(CI -75至-28.8),在所有研究时间点均具有统计学意义。与暴露于两种污染物后立即相比,暴露于两种污染物的混合物后24小时的过敏原PD₂₀FEV₁也显著降低。
这些结果表明,暴露于室外和室内空气污染加重期间可能出现的浓度水平的NO₂和SO₂混合物,会增强哮喘患者气道对吸入性过敏原的反应。这种效应在24 - 48小时内持续存在,且在暴露于这些空气污染物后24小时达到最大。