台北市大氣粒狀污染物誘導第六介白素（interleukin-6）及第八介白素（interleukin-8）之體外試驗

Interleukin-6 and Interleukin-8 Induced by Taipei City Air Pollution Particulate Matter in Vitro

江怡靜(Yi-Ching Chiang)

指導教授 ： 林嘉明

國立臺灣大學/公共衛生學院/環境衛生研究所/碩士(2007年)

https://doi.org/10.6342/NTU.2007.02459

摘要

本研究探討以汽機車與柴油引擎排放為主要來源之大氣中的微粒物質與所載多環芳香烴化合物（polynuclear aromatic hydrocarbons, PAHs）其誘導人類支氣管上皮細胞（BEAS-2B cell）釋放細胞激素interleukin-6及interleukin-8的狀況。在交通流量高、中、低的三個分區，各選取兩間國民小學作為空氣採樣地點，以多階衝擊器（MOUDI）採集粒狀物，將其溶劑萃取物暴露於BEAS-2B細胞。觀察大氣粒狀物相關特性對IL-6及IL-8釋放的貢獻度及相關性。結果發現，在田口氏實驗設計下，標準添加PAH的濃度為最重要之變項， IL-8的濃度隨PAH的毒性當量濃度（toxic equivalency factors , TEFs）而增加（p < 0.05）；大氣樣品中，PAH的濃度及樣品是否過濾兩者皆會影響IL-6及IL-8的釋放。在樣品中含較多微粒物質及較低PAH毒性當量濃度（TEQ）時，細胞有可能為維持原穩性（homeostasis），調節外來物的入侵，當PAH毒性當量濃度（TEQ）逐漸增加，其機制可能就進入另外的階段；至於微粒質量此一因素，在本研究中造成細胞分泌細胞激素的影響亦可能存在。認為源自於汽機車為重要污染源之微粒及其所載PAHs有可能誘發呼吸道疾病發生，但因子間作用及生物機制複雜，需要進一步研究。

關鍵字

微粒 ； 多環芳香烴化合物（polynuclear aromatic hydrocarbons, PAHs） ； 第六介白素（interleukin-6） ； 第八介白素（interleukin-8）

並列摘要

This study was intended to look at the induction of the proinflammatory cytokines（interleukin 6 and interleukin 8）while the human bronchial epithelial cells （BEAS-2B cell）were exposed to air pollution particulate matters and their particulate-bond polynuclear aromatic hydrocarbons（PAHs）from vehicles and diesel exhaust. Field samples containing ambient particulate matters were collected using MOUDI impactor in the campus of each two elementary schools at one area where traffic condition was classfied as the heavy, the moderate or the light.
The solvent extracts of the field samples were divided into two parts in which one part was treated with the microsyringe filter. The results demonstrated that BEAS-2B cells produced IL-6 and IL-8 due to exposure to the solvent extract matters with PAHs. Upon the trials of Taguchi 's orthogonal array where the standard PAHs were added to the solvent extract matter, indicated that PAHs concentration in terms of toxic equivalency quantity（TEQ）was the statistically significant variable. The IL-8 concentration increase with increment of TEQ（p < 0.05）. However, the field samples without standard addition of PAHs into the solvent extract matter demonstrated the effect of TEQ and particulate on the induction of IL-6 and IL-8. The cells seemly keep in homeostasis as they exposure to samples with relatively great particulate matter and lower PAH TEQ and then the reaction mode alter and move toward the phase of proinflammation when PAH TEQ rise up to a certain level. In regard to particle mass, its influence on release of cytokines may exist according to parts of implication from this study. This study gives implication that ambient particulate matter with particulate-bond polynuclear aromatic hydrocarbons may induce respiratory diseases that involve in the inflammation of epithelial cells, but mechanism involved needs further study.

並列關鍵字

particulate matter ； polynuclear aromatic hydrocarbons（PAHs） ； interleukin 6 ； interleukin 8

參考文獻

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