Ichinose Takamichi, Nishikawa Masataka, Takano Hirohisa, Sera Nobuyuki, Sadakane Kaori, Mori Ikuko, Yanagisawa Rie, Oda Toshio, Tamura Hiroshi, Hiyoshi Kyoko, Quan Hao, Tomura Shigeo, Shibamoto Takayuki
Department of Health Sciences, Oita University of Nursing and Health Sciences, 2944-9 Megusuno, Notsuharu, Oita 870-1201, Japan.
Environ Toxicol Pharmacol. 2005 Jul;20(1):48-56. doi: 10.1016/j.etap.2004.10.009. Epub 2004 Dec 21.
Asian yellow dust (Kosa) causes adverse respiratory health effects in humans. The objective of this study was to clarify the lung toxicity of Kosa. ICR mice (5 weeks of age) were administered intratracheally with Kosa samples-two samples from Maowusu desert and Shapotou desert, one sample consisted of Shapotou Kosa plus sulfate, and natural Asian dust (NAD) from the atmosphere of Beijing-at doses of 0.05, 0.10 or 0.20mg/mouse at four weekly intervals. The four Kosa samples tested had similar compositions of minerals and concentrations of elements. Instillation of dust particles caused bronchitis and alveolitis in treated mice. The magnitude of inflammation was much greater in NAD-treated mice than in the other particles tested. Increased neutrophils, lymphocytes or eosinophils in bronchoalveolar lavage fluids (BALF) of treated mice were dose dependent. The number of neutrophils in BALF at the 0.2mg level was parallel to the content of β-glucan in each particle. The numbers of lymphocytes and eosinophils in BALF at the 0.2mg level were parallel to the concentration of SO(4)(2-) in each particle. Pro-inflammatory mediators-such as interleukin (IL)-12, tumor necrosis factor-(TNF)-α, keratinocyte chemoattractant (KC), monocyte chemotactic protein (MCP)-l and macrophage inflammatory protein-(MIP)-lα in BALF-were greater in the treated mice. Specifically, NAD considerably increased pro-inflammatory mediators at a 0.2mg dose. The increased amounts of MlP-lα and TNF-α at 0.2mg dose corresponded to the amount of β-glucan in each particle. The amounts of MCP-l or IL-12 corresponded to the concentration of sulfate (SO(4)(2-)) at a 0.2mg dose. These results suggest that inflammatory lung injury was mediated by β-glucan or SO(4)(2-), which was adsorbed into the particles, via the expression of these pro-inflammatory mediators. The results also suggest that the variations in the magnitude of inflammation of the tested Kosa samples depend on the amounts of these toxic materials.
亚洲黄沙(沙尘暴)会对人类呼吸系统健康产生不利影响。本研究的目的是阐明沙尘暴的肺毒性。将5周龄的ICR小鼠每周经气管给予沙尘暴样本——来自毛乌素沙漠和沙坡头沙漠的两个样本、一个由沙坡头沙尘暴加硫酸盐组成的样本,以及来自北京大气的天然亚洲沙尘(NAD),剂量为0.05、0.10或0.20毫克/只小鼠,共进行四周。所测试的四个沙尘暴样本具有相似的矿物质组成和元素浓度。向小鼠滴注沙尘颗粒会导致其发生支气管炎和肺泡炎。NAD处理组小鼠的炎症程度比其他测试颗粒处理组的要严重得多。处理组小鼠支气管肺泡灌洗液(BALF)中中性粒细胞、淋巴细胞或嗜酸性粒细胞数量的增加呈剂量依赖性。在0.2毫克剂量水平时,BALF中中性粒细胞的数量与每个颗粒中β-葡聚糖的含量平行。在0.2毫克剂量水平时,BALF中淋巴细胞和嗜酸性粒细胞的数量与每个颗粒中SO(4)(2-)的浓度平行。处理组小鼠BALF中的促炎介质,如白细胞介素(IL)-12、肿瘤坏死因子-(TNF)-α、角质形成细胞趋化因子(KC)、单核细胞趋化蛋白(MCP)-1和巨噬细胞炎性蛋白-(MIP)-1α含量更高。具体而言,NAD在0.2毫克剂量时会显著增加促炎介质的含量。在0.2毫克剂量时,MIP-1α和TNF-α增加的量与每个颗粒中β-葡聚糖的量相对应。在0.2毫克剂量时,MCP-1或IL-12的量与硫酸盐(SO(4)(2-))的浓度相对应。这些结果表明,炎性肺损伤是由吸附在颗粒上的β-葡聚糖或SO(4)(2-)通过这些促炎介质的表达介导的。结果还表明,所测试的沙尘暴样本炎症程度的差异取决于这些有毒物质的含量。