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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 林嘉明 | |
| dc.contributor.author | Yi-Ching Chiang | en |
| dc.contributor.author | 江怡靜 | zh_TW |
| dc.date.accessioned | 2021-06-13T00:13:47Z | - |
| dc.date.available | 2008-08-08 | |
| dc.date.copyright | 2007-08-08 | |
| dc.date.issued | 2007 | |
| dc.date.submitted | 2007-07-27 | |
| dc.identifier.citation | 1. 台北市衛生局健康網. www.healthcity.net.tw, 2006.
2. Hsieh, K.H., Shen, J.J., Prevalence of childhood asthma in Taipei, Taiwan, and other Asian Pacific countries. Journal of Asthma, 1988. 25(2): 73-82. 3. Marks, G.B., Environmental factors and gene-environment interactions in the aetiology of asthma. Clinical & Experimental Pharmacology & Physiology, 2006. 33(3): 285-289. 4. Ober, C., Perspectives on the past decade of asthma genetics. Journal of Allergy & Clinical Immunology, 2005. 116(2): 274-278. 5. Yang, I.A., Savarimuthu, S., Kim, S.T., Holloway, J.W., Bell, S.C., Fong, K.M., Gene-environmental interaction in asthma. Current Opinion in Allergy & Clinical Immunology, 2007. 7(1): 75-82. 6. Takizawa, H., Diesel exhaust particles and their effect on induced cytokine expression in human bronchial epithelial cells. Current Opinion in Allergy and Clinical Immunology, 2004. 4: 355-359. 7. Pope, C.A., 3rd, Dockery, D.W., Spengler, J.D., Raizenne, M.E., Respiratory health and PM10 pollution. A daily time series analysis. American Review of Respiratory Disease, 1991. 144(3 Pt 1): 668-674. 8. Schwartz, J., Slater, D., Larson, T.V., Pierson, W.E., Koenig, J.Q., Particulate air pollution and hospital emergency room visits for asthma in Seattle. American Review of Respiratory Disease, 1993. 147(4): 826-831. 9. Hiura, T.S., Slater, D., Larson, T.V., Pierson, W.E., Koenig, J.Q., Chemicals in diesel exhaust particles generate reactive oxygen radicals and induce apoptosis in macrophages. Journal of Immunology, 1999. 163(10): 5582-5591. 10. Li, N., Wang M., Oberley, T.D., Sempf, J.M., Nel, A.E., Comparison of the pro-oxidative and proinflammatory effects of organic diesel exhaust particle chemicals in bronchial epithelial cells and macrophages. Journal of Immunology, 2002. 169(8): 4531-4541. 11. Li, N., Hao M., Phalen, R.F., Hinds, W.C., Nel, A.E., Particulate air pollutants and asthma. A paradigm for the role of oxidative stress in PM-induced adverse health effects. Clinical Immunology, 2003. 109: 250-265. 12. Takenaka, H., Airway epithelial cells as regulators of airway inflammation. International Journal of Molecular Medicine, 1998. 1: 367-378. 13. Message, S.D., Johnston, S.L., Host defense function of the airway epithelium in health and disease: clinical background. Journal of Leukocyte Biology, 2004. 75(1): 5-17. 14. Ohtoshi, T., Takizawa, H., Okazaki, H., Kawasaki, S., Takeuchi, N., Ohta, K., Ito, K., Diesel exhaust particles stimulate human airway epithelial cells to produce cytokines relevant to airway inflammation in vitro. Journal of Allergy & Clinical Immunology, 1998. 101(6 Pt 1): 778-785. 15. Brunekreef, B., Holgate, S.T., Air pollution and health. The Lancet, 2002. 360: 1233-1242. 16. Dockery, D.W., Pope, C.A. 3rd., Xu, X., Spengler, J.D., Ware, J.H., Fay, M.E., Ferris, B.G. Jr., Speizer, F.E., An association between air pollution and mortality in six U.S. cities. New England Journal of Medicine, 1993. 329(24): 1753-1759. 17. Bates, D.V., Health indices of the adverse effects of air pollution: the question of coherence. Enviromental Research, 1992. 59(2): 336-349. 18. Schwartz, J., Air pollution and admissions for cardiovascular disease in Tucson. Epidemiology, 1997. 8: 371-377. 19. Hetland, R.B., Cassee, F.R., Refsnes, M. Schwarze, P.E., Lag. M., Boere, A.J., Dybing. E., Release of inflammatory cytokines, cell toxicity and apoptosis in epithelial lung cells after exposure to ambient air particles of different size fractions. Toxicology in Vitro, 2004. 18: 203-212. 20. Guo, Y.L., Lin, Y.C., Sung, F.C., Huang, S.L., Ko, Y.C., Lai, J.S., Su, H.J., Shaw, C.K., Lin, R.S., Dockery, D.W., Climate,traffic-related air pollutants, and asthma prevalence in middle-school children in Taiwan. Environmental Health Perspectives, 1999. 107,12: 1001-1006. 21. Dockery, D.W., Speizer, F.E., Stram, D.O., Ware, J.H., Spengler, J.D., Ferris, B.G. Jr., Effects of inhalable particles on respiratory health of children. American Review of Respiratory Disease, 1989. 139(3): 587-594. 22. Dockery, D.W., Cunningham, J., Damokosh, A.I., Neas, L.M., Spengler, J.D., Koutrakis, P., Ware, J.H., Raizenne, M., Speizer, F.E., Health effects of acid aerosols on North American children: respiratory symptoms. Environmental Health Perspectives, 1996. 104(5): 500-505. 23. Driscoll, K.E., Carter, J.M., Hassenbein D.G., Howard B., Cytokines and particle-induced inflammatory cell recruitment. Environmental Health Perspectives, 1997. 105: 1159-1164. 24. Van Eeden, S.F., Yeung, A., Quinlam, K., Hogg, JC., Systemic Response to Ambient Particulate Matter Relevance to Chronic Obstructive Pulmonary Disease. Proceedings of the American Thoracic Society, 2005. 2: 61-67. 25. Suwa, T., Hogg, J.C., English, D., Van Eeden, S.F., Interleukin-6 induces demargination of intravascular neutrophils and shortens their transit in marrow. American Journal of Physiology - Heart & Circulatory Physiology, 2000. 279: H2954-H2960. 26. Gabay, C., Kushner, I., Acute-phase proteins and other systemic responses to inflammation. New England Journal of Medicine, 1999. 340: 448-454. 27. Jansen, J.H., Kluin-Nelemans, J.C., Van Damme, J., Wientjens, G.J., Willemze, R., Fibbe, W.E., Interleukin 6 is a permissive factor for monocytic colony formation by human hematopoietic progenitor cells. Journal of Experimental Medicine, 1992. 175: 1151-1154. 28. Terashima, T., English, D., Hogg, J.C., Van Eeden, S.F., The release of polymorphonuclear leukocyte from the bone marrow by interleukin 8. Blood, 1998. 92: 1062-1069. 29. Suwa, T., Hogg, J.C., Klut, M.E., Hards, J., Van Eeden, S.F., Interleukin-6 changes deformability of neutrophils and induces their sequestration in the lung. American Journal of Respiratory & Critical Care Medicine, 2001. 163: 970-976. 30. Van Eeden, S.F., Kitagawa, Y., Sato, Y., Hogg, J.C., Polymorphonuclear leukocytes released from the bone marrow and acute lung injury. Chest, 1999. 116: S43-S46. 31. Peters, A., Dockery, D.W., Muller, J.E., Mittleman, M.A., Increased particulate air pollution and the triggering of myocardial infarction. Circulation, 2001. 103: 2810-2815. 32. Seaton, A., MacNee, W., Donaldson K., Godden D., Particulate air pollution and acute health effects. Lancet, 1995. 345: 176-178. 33. Li, N., Kim, S., Wang, M., Froines, J., Sioutas, C., Nel, A., Use of a stratified oxidative stress model to study the biological effects of ambient concentrated and diesel exhaust particulate matter. Inhalation Toxicology, 2002. 14: 459-486. 34. Soukup, J.M., Becker, S., Human alveolar macrophage responses to air pollution particulates are associated with insoluble components of coarse material, including particulate endotoxin. Toxicology and Applied Pharmacology, 2001. 171: p. 20-26. 35. Lippmann, M., Frampton, M., Schwartz, J., Dockery, D., Schlesinger, R., Koutrakis, P., Froines, J., Nel, A., Finkelstein, J., Godleski, J., Kaufman, J., Koenig, J., Larson, T., Luchtel, D., Liu, L.J., Oberdorster, G., Peters, A., Sarnat, J., Sioutas, C., Suh, H., Sullivan, J., Utell, M., Wichmann, E., Zelikoff, J., The U.S. Environmental Protection Agency particulate matter health effects research centers program: A midcourse report of status, progress, and plans. Environmental Health Perspectives, 2003. 111: 1074-1092. 36. Nel, A.E., Diaz-Sanchez, D., Li, N., The role of particulate pollutants in pulmonary inflammation and asthma: Evidence for the involvement of organic chemicals and oxidative stress. Current Opinion in Pulmonary Medicine, 2001. 7: 20-26. 37. Prestera, T., Talalay, P., Alam. J., Ahn, YI., Lee, P.J., Choi, A.M., Parallel induction of heme oxygenase-1 and chemoprotective phase 2 enzymes by electrophiles and antioxidants : Regulation by upstream antioxidant-responsive elements (ARE). Molecular Medicine, 1995. 1: 827-837. 38. Takizawa, H., Ohtoshi, T., Kawasaki, S., Kohyama, T., Desaki, M., Kasama, T., Kobayashi, K., Nakahara, K., Yamamoto, K., Matsushima, K., Kudoh, S., Diesel exhaust particles induce NF-k B activation in human bronchial epithelial cells in vitro: Importance in cytokine transcription. Journal of Immunology, 1999. 162: 4705-4711. 39. Hiura, T.S., Kaszubowski, M.P., Li, N., Nel, A.E., Chemicals in diesel exhaust particles generate reactive oxygen radicals and apoptosis in macrophages. Journal of Immunology, 1999. 163: 5582-5590. 40. Hiura, T.S., Li, N., Kaplan, R., Horwitz, M., Seagrave, J.C., Nel, A.E., The role of a mitochondrial pathway in the induction of apoptosis by chemicals extracted from DEP. Journal of Immunology, 2000. 165: 2703-2711. 41. Li, N., Sioutas, C., Cho, A., Schmitz, D., Misra, C., Sempf, J., Wang, M., Oberley, T., Froines, J., Nel, A., Ultrafine particulate pollutants induce oxidative stress and mitochondrial damage. Environmental Health Perspectives, 2003. 111: 455-460. 42. Whitekus, M.J., Li, N., Zhang, M., Wang, M., Horwitz, M.A., Nelson, S.K., Horwitz, L.D., Brechun, N., Diaz-Sanchez, D., Nel, A.E., Thiol antioxidants inhibit the adjuvant effects of aerosolized diesel exhaust particles in a murine model for ovalbumin sensitization. Journal of Immunology, 2002. 168: 2560-2567. 43. Madden, M.C., Richards, J.H., Dailey, L.A., Hatch, G.E., Ghio, A.J., Effect of ozone on diesel exhaust particle toxicity in rat lung, Toxicology & Applied Pharmacology, 2000. 168: 140-148. 44. Held, H.D., Uhlig, S., Mechanisms of endotoxin-induced airway and pulmonary vascular hyperreactivity in mice. American Journal of Respiratory & Critical Care Medicine, 2000. 162: 1547-1552. 45. Osornio-Vargas, Á.R., et al., Proinflammatory and cytotoxic effects of Mexico City air pollution particulate matter in vitro are dependent on particle size and composition. Environmental Health Perspectives, 2003. 111(10): 1289-1296. 46. Fang, G.C., Chang, K.F., Lu, C., Bai, H., Estimation of PAHs dry deposition and BaP toxic equivalency factors (TEFs) study at urban, industry park and rural sampling sites in central Taiwan, Taichung. Chemosphere, 2004. 55: 787-796. 47. Becher, R., Hetland, R.B., Refsnes, M., Dahl, J.E., Dahlman, H.J., Schwarze, P.E., Rat lung inflammatory responses after in vivo and in vitro exposure to various stone particles. Inhalation Toxicology, 2001. 13: 789-805. 48. Vanhée, D., Gosset, P., Boitelle, A., Wallaert, B., Tonnel, A.B., Cytokines and cytokine network in silicosis and coal workers' pneumoconiosis, European Respiratory Journal, 1995. 8: 834-842. | |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/28603 | - |
| dc.description.abstract | 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。 | zh_TW |
| dc.description.abstract | 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. | en |
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| dc.description.tableofcontents | 誌 謝 i
摘 要 ii Abstract iii 目 錄 v 表目錄 viii 圖目錄 x 第一章 緒論 1 一、 背景 1 二、 研究目的 2 三、 研究架構 3 第二章 文獻回顧 4 一、 空氣污染對易感受族群健康之危害 4 二、 呼吸道系統的免疫機制 6 三、 微粒物質粗細的影響 7 四、 微粒物質表面負載化學物質的種類 8 五、 氧化壓力 9 六、 微生物的內毒素 12 第三章 材料與方法 13 一、 採樣策略及對象 13 二、 材料 14 三、 方法 - 細胞暴露試驗 16 3.1 細胞之繼代培養 17 3.2 細胞密度測試 19 3.3 接種（seeding） 20 3.4 細胞暴露 21 3.5 ELISA 分析 22 第四章 結果 26 一、 Dimethyl sulfoxide（DMSO）的量影響BEAS-2B分泌 interleukin-8 26 二、 BEAS-2B細胞分泌interleukin-8隨PAHs標準添加而變化 26 三、 BEAS-2B細胞暴露於校園粒狀物溶劑萃取且經過濾所得物時， interleukin-8的變化 27 四、 BEAS-2B細胞暴露於校園粒狀物溶劑萃取且未經過濾物時的 interleukin-8的變化 27 五、 比較粒狀物萃取物過濾與未過濾以及PAH之毒性當量濃度 （TEQ）對BEAS-2B細胞分泌interleukin-8 的影響 28 六、 Dimethyl sulfoxide（DMSO）的量影響BEAS-2B分泌 interleukin-6 29 七、 BEAS-2B細胞分泌interleukin-6隨PAHs標準添加而變化 30 八、 BEAS-2B細胞暴露於校園粒狀物溶劑萃取且經過濾所得物時， interleukin-6的變化 30 九、 BEAS-2B細胞暴露於校園粒狀物溶劑萃取且未經過濾物時的 interleukin-6的變化 31 十、 比較粒狀物萃取物過濾與未過濾以及PAH之毒性當量濃度 （TEQ）對BEAS-2B細胞分泌interleukin-6的影響 32 十一、 細胞存活率的探討 33 第五章 討論 34 一、 控制變項對細胞激素表現的影響 34 二、 探討微粒的影響 34 三、 機制的探討 35 四、 細胞分泌之細胞激素與存活率的關係 36 五、 細胞分泌之細胞激素與質量的關係 37 六、 研究限制與建議 37 參考文獻 39 表目錄 表一. BEAS-2B 細胞株之詳細資料 45 表二. 細胞毒性試驗之田口氏實驗設計所用的變項與級數 46 表三. 暴露不同濃度 dimethyl sulfoxide（DMSO）下，BEAS-2B細胞分泌interleukin-8之試驗結果 47 表四. Interleukin -8濃度（pg/mL）變化與dimethyl sulfoxide濃度 （mg/mL）間關係的迴歸分析 49 表五. 粒狀物萃取物暴露BEAS-2B的interleukin-8濃度的分析結果 50 表六. 影響BEAS-2B細胞分泌interleukin-8的因子之變異數分析 51 表七. Interleukin 8（pg/mL）與 PAH濃度（μg/mL）的線性迴歸關係 52 表八. Proposed toxic equivalency factors (TEFs) for individual PAHs [46] 53 表九. 國民小學校園粒狀物萃取物經過濾後暴露BEAS-2B的 interleukin-8濃度的分析結果 54 表十. 國民小學校園粒狀物萃取物經過濾後暴露於BEAS-2B的 interleukin-8分析結果 55 表十一. 國民小學校園粒狀物萃取物未過濾樣品暴露BEAS-2B的 interleukin-8濃度的分析結果 56 表十二. 國民小學粒狀物萃取物未過濾樣品暴露於BEAS-2B的 interleukin-8分析結果 57 表十三. 國民小學校園粒狀物萃取物經過濾後暴露BEAS-2B的 interleukin-8濃度的分析結果 58 表十四. 國民小學校園粒狀物萃取物未過濾樣品暴露BEAS-2B的 interleukin-8濃度的分析結果 59 表十五. 雙因子分析（過濾狀況及PAH之TEQ濃度） 60 表十六. Interleukin -6濃度（pg/mL）變化與dimethyl sulfoxide濃度 （mg/mL）間關係的迴歸分析 61 表十七. 粒狀物萃取物暴露BEAS-2B的interleukin-6濃度的分析結果 62 表十八. 影響BEAS-2B細胞分泌Interleukin-6的因子之變異數分析 63 表十九. Interleukin 6（pg/mL）與 PAH濃度（μg/mL）的線性迴歸關係 64 表二十. 國民小學校園粒狀物萃取物經過濾後暴露BEAS-2B的 interleukin-6濃度的分析結果 65 表二十一. 國民小學校園粒狀物萃取物經過濾後暴露於BEAS-2B的interleukin-6分析結果 66 表二十二. 國民小學校園粒狀物萃取物未過濾樣品暴露BEAS-2B的interleukin-6濃度的分析結果 67 表二十三. 國民小學粒狀物萃取物未過濾樣品暴露於BEAS-2B的 interleukin-6 分析結果 68 表二十四. 國民小學校園粒狀物萃取物經過濾後暴露BEAS-2B的 interleukin-6 濃度的分析結果 69 表二十五. 國民小學校園粒狀物萃取物未過濾樣品暴露BEAS-2B的 interleukin-6濃度的分析結果 70 表二十六. 雙因子分析（過濾狀況及PAH之TEQ濃度） 71 圖目錄 圖一. Interleukin-8濃度變化與dimethyl sulfoxide（DMSO）濃度的關係 73 圖二. Interleukin-8濃度與PAHs標準添加的關係 74 圖三. 比較BEAS-2B細胞暴露於PAHs標準添加時之interleukin-8濃度(dimethyl sulfoxide, DMSO濃度在每組試驗別內是相等的,但組別 之間的DMSO是循序增加,分別為2.75 mg/mL, 5.5 mg/mL, 8.25 mg/mL) 75 圖四. 暴露於”過濾”與”未過濾”之學校粒狀物萃取物的PAHs毒性當量濃度 與BEAS-2B細胞分泌之interleukin-8的關係 76 圖五. 暴露於國小校園粒狀物萃取物”過濾”及”未過濾”樣品之BEAS-2B細胞分泌interleukin-8濃度（校正細胞存活率後）與PAHs毒性當量濃度關係之散佈圖 77 圖六. Interleukin-6濃度變化與dimethyl sulfoxide（DMSO）濃度的關係 78 圖七. Interleukin-6濃度與PAHs標準添加的關係 79 圖八. 比較BEAS-2B細胞暴露於PAHs標準添加時之interleukin-6濃度(dimethyl sulfoxide, DMSO濃度在每組試驗別內是相等的,但組別 之間的DMSO是循序增加,分別為2.75 mg/mL, 5.5 mg/mL, 8.25 mg/mL) 80 圖九. 暴露於”過濾”與”未過濾”之學校粒狀物萃取物的PAHs毒性當量濃度 與BEAS-2B細胞分泌之interleukin-6的關係 81 圖十. 暴露於國小校園粒狀物萃取物”過濾”及”未過濾”樣品之BEAS-2B細胞分泌interleukin-6濃度（校正細胞存活率後）與PAHs毒性當量濃度關係之散佈圖 82 圖十一. 在田口氏設計下, PAHs毒性當量濃度（TEQ）及細胞存活率的關係 83 圖十二. 暴露於國小校園粒狀物萃取物”過濾”及”未過濾”樣品之 BEAS-2B細胞存活率與PAHs毒性當量濃度關係之散佈圖 84 圖十三. 未過濾樣品，單位質量粒狀物的PAHs毒性當量濃度 （toxic equivalency quantity of PAHs, TEQ）與interleukin-8的關係 85 圖十四. 未過濾樣品，單位質量粒狀物的PAHs毒性當量濃度 （toxic equivalency quantity of PAHs, TEQ）與interleukin-6的關係 86 | |
| dc.language.iso | zh-TW | |
| dc.subject | 第八介白素（interleukin-8） | zh_TW |
| dc.subject | 微粒 | zh_TW |
| dc.subject | 多環芳香烴化合物（polynuclear aromatic hydrocarbons | zh_TW |
| dc.subject | PAHs） | zh_TW |
| dc.subject | 第六介白素（interleukin-6） | zh_TW |
| dc.subject | interleukin 6 | en |
| dc.subject | interleukin 8 | en |
| dc.subject | particulate matter | en |
| dc.subject | polynuclear aromatic hydrocarbons（PAHs） | en |
| dc.title | 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 | zh_TW |
| dc.title | Interleukin-6 and Interleukin-8 Induced by Taipei City Air Pollution Particulate Matter in Vitro | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 95-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 鄭尊仁,謝玲玲 | |
| dc.subject.keyword | 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）, | zh_TW |
| dc.subject.keyword | particulate matter,polynuclear aromatic hydrocarbons（PAHs）,interleukin 6,interleukin 8, | en |
| dc.relation.page | 86 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2007-07-28 | |
| dc.contributor.author-college | 公共衛生學院 | zh_TW |
| dc.contributor.author-dept | 環境衛生研究所 | zh_TW |
| 顯示於系所單位： | 環境衛生研究所 | |
文件中的檔案：
| 檔案 | 大小 | 格式 | |
|---|---|---|---|
| ntu-96-1.pdf 未授權公開取用 | 529.53 kB | Adobe PDF |
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