A randomized cross-over study of inhalation of diesel exhaust, hematological indices, and endothelial markers in humans.
A randomized cross-over study of inhalation of diesel exhaust, hematological indices, and endothelial markers in humans.
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DOI：
10.1186/1743-8977-10-7
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发表时间：
2013-03-26
影响因子：
10
通讯作者：
Kaufman JD
中科院分区：
文献类型：
--
作者：
Krishnan RM;Sullivan JH;Carlsten C;Wilkerson HW;Beyer RP;Bammler T;Farin F;Peretz A;Kaufman JD
暴露于交通相关空气污染（TRAP）被认为是急性心血管事件的触发因素。柴油机尾气排放是造成TRAP的主要原因之一。我们使用专门的设施评估了DE吸入对人类循环血细胞群、血液学指标和全身炎症细胞因子的影响。在一项按顺序平衡的随机双盲交叉研究中，17名代谢综合征（MetS）受试者和15名健康受试者在不同日期吸入过滤空气（FA）或DE暴露2小时，洗脱期至少为2周。我们收集了暴露前、暴露开始后7小时和22小时的血液，并测量了全血细胞计数和分类。我们进行了多重细胞因子测定，以测量全身炎症细胞因子和内皮粘附分子的变化（n=15）。配对分析比较了DE和FA暴露对从暴露前到后续时间点变化的影响。与FA暴露[0.5%（95% CI：-0.09至1.0%）; p=0.008]相比，DE后7小时观察到红细胞压积显著增加[1.4%（95% CI：0.9至1.9%）]。DE后7小时的血红蛋白水平[0.3 gm/dL（95% CI：0.2 - 0.5 gm/dL）]与FA暴露[0.2 gm/dL（95% CI：0 - 0.3 gm/dL）]相比无显著性增加; p=0.06。此外，在健康受试者中，DE暴露后22小时血小板计数增加，但在MetS受试者中未增加[DE：16.6（95% CI：10.2至23）千个血小板/mL vs [FA：3.4（95% CI：-9.5至16.3）千个血小板/mL]; p=0.04。未观察到对WBC、中性粒细胞、淋巴细胞或红细胞的DE效应。使用多重测定，暴露开始后7小时，基质金属蛋白酶-9、白细胞介素（IL）-1 β、6和10出现小的边界显著增加，而暴露后22小时，E-选择素、细胞间粘附分子-1、血管细胞粘附分子-1和髓过氧化物酶出现显著增加。我们的研究结果表明，短期DE暴露导致血液浓缩和血小板增多，这是急性心血管事件的重要决定因素。多重测定显示暴露后IL-1β和IL-6立即无显著增加，随后是髓过氧化物酶和内皮活化分子。在更大的人群中进行进一步的特异性测定将提高我们对急性暴露于TRAP后全身炎症机制的理解。研究是在2004年至2006年期间进行的，在预期登记之前。
Exposure to traffic-related air pollution (TRAP) is considered a trigger for acute cardiovascular events. Diesel Exhaust (DE) is a major contributor to TRAP in the world. We evaluated the effect of DE inhalation on circulating blood cell populations, hematological indices, and systemic inflammatory cytokines in humans using a specialized facility. In a randomized double-blind crossover study balanced to order, 17 metabolic syndrome (MetS) and 15 healthy subjects inhaled filtered air (FA) or DE exposure in two-hour sessions on different days with a minimum 2-week washout period. We collected blood pre-exposure, 7, and 22 hours after exposure initiation and measured the complete blood count and differential. We performed multiplex cytokine assay to measure the changes in the systemic inflammatory cytokines, and endothelial adhesion molecules (n=15). A paired analysis compared the effect of DE and FA exposures for the change from pre-exposure to the subsequent time points. A significant increase in the hematocrit was noted 7 hrs after DE [1.4% (95% CI: 0.9 to 1.9%)] compared to FA exposure [0.5% (95% CI: -0.09 to 1.0%); p=0.008. The hemoglobin levels increased non-significantly at 7 hrs post DE [0.3 gm/dL (95% CI: 0.2 to 0.5 gm/dL)] versus FA exposure [0.2 gm/dL (95% CI: 0 to 0.3 gm/dL)]; p=0.06. Furthermore, the platelet count increased 22 hrs after DE exposure in healthy, but not in MetS subjects [DE: 16.6 (95% CI: 10.2 to 23) thousand platelets/mL versus [FA: 3.4 (95% CI: -9.5 to 16.3) thousand platelets/mL)]; p=0.04. No DE effect was observed for WBC, neutrophils, lymphocytes or erythrocytes. Using the multiplex assay, small borderline significant increases in matrix metalloproteinase-9, interleukins (IL)-1beta, 6 and 10 occurred 7 hrs post exposure initiation, whereas E-selectin, intercellular adhesion molecule-1, and vascular cell adhesion molecule -1, and myeloperoxidase 22 hrs post exposure. Our results suggest that short-term DE exposure results in hemoconcentration and thrombocytosis, which are important determinants of acute cardiovascular events. Multiplex assay showed a non-significant increase in IL-1β and IL-6 immediately post exposure followed by myeloperoxidase and endothelial activation molecules. Further specific assays in a larger population will improve our understanding of the systemic inflammatory mechanisms following acute exposure to TRAP. Study was conducted between 2004 to 2006, prior to expectation for registration.
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影响因子：
2.2
作者：
Dossus, Laure;Becker, Susen;Rinaldi, Sabina
通讯作者：
Rinaldi, Sabina
影响因子：
2.1
作者：
Carlsten C;Kaufman JD;Trenga CA;Allen J;Peretz A;Sullivan JH
通讯作者：
Sullivan JH
影响因子：
10
作者：
Barath S;Mills NL;Lundbäck M;Törnqvist H;Lucking AJ;Langrish JP;Söderberg S;Boman C;Westerholm R;Löndahl J;Donaldson K;Mudway IS;Sandström T;Newby DE;Blomberg A
通讯作者：
Blomberg A
影响因子：
4.8
作者：
GAGNON, DR;ZHANG, TJ;KANNEL, WB
通讯作者：
KANNEL, WB
影响因子：
10.4
作者：
Delfino, Ralph J.;Staimer, Norbert;Sioutas, Constantinos
通讯作者：
Sioutas, Constantinos