NITROGEN-DIOXIDE EXPOSURE INVIVO AND HUMAN ALVEOLAR MACROPHAGE INACTIVATION OF INFLUENZA-VIRUS INVITRO
NITROGEN-DIOXIDE EXPOSURE INVIVO AND HUMAN ALVEOLAR MACROPHAGE INACTIVATION OF INFLUENZA-VIRUS INVITRO
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DOI：
10.1016/s0013-9351(89)80033-7
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发表时间：
1989-04-01
影响因子：
8.3
通讯作者：
UTELL, MJ
中科院分区：
文献类型：
--
作者：
FRAMPTON, MW;SMEGLIN, AM;UTELL, MJ
流行病学研究报告说，呼吸道感染和疾病的发病率增加与室内二氧化氮（NO2）水平升高有关。动物暴露研究发现，短暂暴露于峰值水平的NO2比持续低水平暴露产生更大的发病率。为了研究吸入NO2对人肺泡巨噬细胞的影响，正常志愿者在环境室中通过双盲随机化顺序暴露于空气或NO2。具有可比浓度×浓度的两种暴露方案使用时间产物：（a）连续0.60 ppm NO2（n = 9），和（B）背景0.05 ppm NO2，具有三个2.0 ppm的15分钟峰（n = 15）。在两种暴露方案中，吸入NO2均未引起肺功能或气道反应性的显著变化。连续暴露于0.60 ppm NO2后3 1/2小时，通过支气管肺泡灌洗获得的肺泡巨噬细胞在体外抑制流感病毒的效果低于空气暴露后收集的细胞（孵育第2天，1.96 vs 1.25 log 10空斑形成单位，P < 0.07）。9名受试者中有4名解释了观察到的病毒灭活损伤;这4名受试者的细胞显示出NO2与空气相比后白细胞介素-1（IL-1）产生增加，而其余5名受试者在NO2后IL-1产生减少。相反，间歇性峰值暴露并不改变病毒灭活或IL-1产生的速率。这种方法有可能确定污染物对人类呼吸防御机制的影响。
Epidemiologic studies have reported an increased incidence of respiratory infections and illness in association with elevated indoor levels of nitrogen dioxide (NO2). Animal exposure studies have found that brief exposures to peak levels of NO2 produce greater morbidity than continuous lower level exposure. In order to examine the effect of NO2 inhalation on human alveolar macrophages, normal volunteers were exposed sequentially to air or NO2, by double-blind randomization, in an environmental chamber. Two exposure protocols with comparable concentration .times. time products were used: (a) continuous 0.60 ppm NO2 (n = 9), and (b) background 0.05 ppm NO2 with three 15-min peaks of 2.0 ppm (n = 15). Inhalation of NO2 caused no significant changes in pulmonary function or airway reactivity in either exposure protocol. Alveolar macrophages obtained by bronchoalveolar lavage 3 1/2 hr after exposure to continuous 0.60 ppm NO2 tended to inactivate influenza virus in vitro less effectively than cells collected after air exposure (1.96 vs 1.25 log10 plaque-forming units on Day 2 of incubation, P < 0.07). Four of nine subjects accounted for the observed impairment in virus inactivation; cells from these four subjects demonstrated an increase in interleukin-1 (IL-1) production after NO2 vs air, whereas the five remaining subjects decreased IL-1 production after NO2. In contrast, intermittent peak exposure did not alter the rate of viral inactivation or IL-1 production. This methodology has the potential to identify pollutant effects of mechanisms of respiratory defense in humans.