Zelikoff Judith T, Chen Lung Chi, Cohen Mitchell D, Fang Kaijie, Gordon Terry, Li Yun, Nadziejko Christine, Schlesinger Richard B
New York University School of Medicine, Nelson Institute of Environmental Medicine, Tuxedo, NY 10987, USA.
Inhal Toxicol. 2003 Feb;15(2):131-50. doi: 10.1080/08958370304478.
Respiratory-tract infection, specifically pneumonia, contributes substantially to the increased morbidity and mortality among elderly individuals exposed to airborne particulate matter of <10 microm diameter (PM(10)). These epidemiological findings suggest that PM(10) may act as an immunosuppressive factor that can undermine normal pulmonary antimicrobial defense mechanisms. To investigate whether, and how, compromised pulmonary immunocompetence might contribute to increased mortality, two sets of laboratory studies were performed. The first examined the effects of a single inhalation exposure to concentrated ambient PM(2.5) (CAPS) from New York City air on pulmonary/systemic immunity and on the susceptibility of exposed aged rats to subsequent infection with Streptococcus pneumoniae. The second set of studies determined whether CAPS exposure, at a concentration approximating or somewhat greater than the promulgated 24-h NAAQS of 65 microg/m(3), could exacerbate an ongoing infection. Taken together, results demonstrated that a single exposure of healthy animals to CAPS had little effect on pulmonary immune function or bacterial clearance during subsequent challenge with S. pneumoniae. Alternatively, CAPS exposure of previously infected rats significantly increased bacterial burdens and decreased percentages of lavageable neutrophils and proinflammatory cytokine levels compared to those in infected filtered-air-exposed controls. These studies demonstrate that a single exposure to ambient PM(2.5) compromises a host's ability to handle ongoing pneumococcal infections and support the epidemiological findings of increased pneumonia-related deaths in ambient PM-exposed elderly individuals.
呼吸道感染，特别是肺炎，在暴露于直径小于10微米的空气颗粒物（PM10）的老年人中，极大地导致了发病率和死亡率的增加。这些流行病学研究结果表明，PM10可能作为一种免疫抑制因子，会破坏正常的肺部抗菌防御机制。为了研究肺部免疫能力受损是否以及如何导致死亡率增加，我们进行了两组实验室研究。第一组研究考察了单次吸入暴露于来自纽约市空气中的浓缩环境PM2.5（CAPS）对肺部/全身免疫以及对暴露的老年大鼠随后感染肺炎链球菌易感性的影响。第二组研究确定了在浓度接近或略高于颁布的24小时国家环境空气质量标准65微克/立方米的情况下，CAPS暴露是否会加重正在进行的感染。综合来看，结果表明健康动物单次暴露于CAPS对随后肺炎链球菌攻击期间的肺部免疫功能或细菌清除几乎没有影响。相反，与感染后暴露于过滤空气的对照组相比，先前感染的大鼠暴露于CAPS后，细菌载量显著增加，可冲洗中性粒细胞百分比和促炎细胞因子水平降低。这些研究表明，单次暴露于环境PM2.5会损害宿主应对正在进行的肺炎球菌感染的能力，并支持了在暴露于环境颗粒物的老年人中与肺炎相关死亡增加的流行病学研究结果。
