Gong Henry, Sioutas Constantinos, Linn William S
Los Amigos Research and Education Institute, 51 Medical Science Bldg, 7601 East Imperial Hwy, Downey, CA 90242, USA.
Res Rep Health Eff Inst. 2003 Dec(118):1-36; discussion 37-47.
Epidemiologic studies report health effects associated with exposure to ambient particulate matter (PM), but underlying biologic mechanisms remain unclear. We evaluated pulmonary and systemic effects in twelve healthy human adult and twelve asthmatic volunteers exposed once for 2 hours in a whole-body chamber to approximately 200 microg/m3 concentrated ambient particles (CAPs) in the fine (< 2.5 microm) size range and once to filtered air. Neither healthy nor asthmatic subjects showed significant changes in symptoms, spirometry, or routine hematologic measurements attributable to CAPs exposure compared with filtered air. Both groups showed CAPs-related (1) decreases of columnar cells in induced sputum after exposure, (2) increases in certain blood mediators of inflammation (ie, soluble intercellular adhesion molecule 1 [ICAM-1] and interleukin [IL] 6 [marginally significant in asthmatic subjects only]), and (3) parasympathetic stimulation of heart rate variability (HRV). In the asthmatic group, systolic blood pressure modestly increased during filtered air exposure and decreased during CAPs exposure, whereas the pattern was reversed in the healthy group. In summary, this study measured a large number and wide range of biologic endpoints on a relatively small number of healthy and asthmatic volunteers and found few biologic endpoints that responded to CAPs and filtered air exposures with significantly different values. However, observed changes in some mediators of inflammation in blood and changes in HRV were consistent with PM-related effects reported from epidemiologic studies. They suggest that exposure to concentrated PM 2.5 pm or smaller in aerodynamic diameter (PM2.5) tends to elicit more systemic than pulmonary effects. This investigation is one of the first to apply concentrator-exposure technology in a high-risk group (subjects with asthma). Further studies of responses to CAPs that involve other biologic endpoints, other PM size modes, and subjects with other risk factors are needed.
流行病学研究报告了与暴露于环境颗粒物（PM）相关的健康影响，但其潜在的生物学机制仍不清楚。我们评估了12名健康成年志愿者和12名哮喘志愿者的肺部和全身影响，这些志愿者在全身舱中分别暴露于约200微克/立方米的细颗粒（<2.5微米）范围内的浓缩环境颗粒物（CAPs）2小时一次，以及过滤空气一次。与过滤空气相比，健康受试者和哮喘受试者均未显示出因暴露于CAPs而导致的症状、肺功能或常规血液学测量的显著变化。两组均显示出与CAPs相关的变化：（1）暴露后诱导痰中柱状细胞减少；（2）某些血液炎症介质增加（即可溶性细胞间粘附分子1 [ICAM-1]和白细胞介素[IL] 6 [仅在哮喘受试者中略有统计学意义]）；（3）心率变异性（HRV）的副交感神经刺激。在哮喘组中，收缩压在暴露于过滤空气期间适度升高，而在暴露于CAPs期间降低，而在健康组中则相反。总之，本研究对相对较少数量的健康和哮喘志愿者测量了大量且广泛的生物学终点，发现很少有生物学终点对CAPs和过滤空气暴露有显著不同的反应值。然而，观察到的血液中一些炎症介质的变化和HRV的变化与流行病学研究报告的与PM相关的影响一致。这些结果表明，暴露于空气动力学直径为2.5微米或更小的浓缩颗粒物（PM2.5）往往会引发更多的全身影响而非肺部影响。本研究是首批将浓缩器暴露技术应用于高危人群（哮喘患者）的研究之一。需要进一步研究涉及其他生物学终点、其他PM粒径模式以及具有其他风险因素的受试者对CAPs的反应。
