Systemic inflammation, endothelial dysfunction, and activation in clinically healthy children exposed to air pollutants
Systemic inflammation, endothelial dysfunction, and activation in clinically healthy children exposed to air pollutants
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DOI：
10.1080/08958370701864797
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发表时间：
2008-01-01
影响因子：
2.1
通讯作者：
Reed, W.
中科院分区：
文献类型：
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作者：
Calderon-Garciduenas, L.;Villarreal-Calderon, R.;Reed, W.
墨西哥城的儿童长期暴露于显著浓度的空气污染物中，并表现出慢性呼吸道炎症。流行病学、对照人类暴露、实验室动物模型和体外/体内研究表明，暴露于颗粒物（PM）后，炎症、内皮功能障碍和内皮损伤介质上调。内皮功能障碍是心血管疾病的重要事件。本研究的重点是调查暴露于包括PM2.5在内的环境空气污染是否会对健康儿童产生全身炎症和内皮损伤。我们测量了52名年龄为8.60.1岁的儿童的内皮活化标志物和炎症介质，这些儿童分别来自墨西哥城（28名）和波洛蒂林（24名），这是一个污染物水平较低的城市。墨西哥城儿童的炎症介质和血管收缩剂显著增加，包括肿瘤坏死因子（TNF）、前列腺素（PG） E2、c反应蛋白、白细胞介素-1和内皮素-1。抗炎反应显著，血管黏附分子-1、细胞间黏附分子-1和-2以及选择因子sE和sL均下调。线性回归结果显示，高暴露儿童TNF - a与24和48 h PM2.5累积水平呈正相关，而7 d PM2.5值与外周血白细胞数量呈负相关。在墨西哥城的儿童中可以看到全身亚临床炎症、内皮素- 1升高和可溶性粘附分子的显著下调。儿童长期暴露在高于标准的细颗粒物中，可能在以后的生活中有患心血管疾病、动脉粥样硬化、中风和其他系统性疾病的风险。
Mexico City children are chronically exposed to significant concentrations of air pollutants and exhibit chronic respiratory-tract inflammation. Epidemiological, controlled human exposures, laboratory-based animal models, and in vitro/in vivo studies have shown that inflammatory, endothelial dysfunction, and endothelial damage mediators are upregulated upon exposure to particulate matter (PM). Endothelial dysfunction is a critical event in cardiovascular disease. The focus of thiswork was to investigate whether exposure to ambient air pollution including PM2.5 produces systemic inflammation and endothelial injury in healthy children. We measuredmarkers of endothelial activation, and inflammatory mediators in 52 children age 8.60.1 yr, residents of Mexico City (n: 28) or of Polotitln (n: 24), a city with lowlevels of pollutants. Mexico City children had significant increases in inflammatory mediators and vasoconstrictors, including tumor necrosis factor (TNF), prostaglandin (PG) E2, C-reactive protein, interleukin-1, and endothelin-1. There was a significant anti-inflammatory response, and a downregulation of vascular adhesion molecule-1, intercellular adhesion molecule-1 and -2, and selectins sE and sL. Results fromlinear regression found TNF a positively associated with 24- and 48-h cumulative levels of PM2.5, while the 7-d PM2.5 value was negatively associated with the numbers of white blood cells in peripheral blood in highly exposed children. Systemic subclinical inflammation, increased endothelin- 1, and significant downregulation of soluble adhesion molecules are seen in Mexico City children. Children chronically exposed to fine PM above the standard could be at risk of developing cardiovascular diseases, atherosclerosis, stroke, and other systemic effects later in life.