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年度	113	專案性質	實驗性質
專案類別	研究專案	研究主題	調查
申請機構	國立清華大學	申請系所	分析與環境科學研究所
專案主持人	周秀專	職等/職稱	教授兼所長
專案中文名稱	建立水質監測與預警數據庫： 底泥生殖毒性與生物累積性在評析新興污染物環境流佈的應用
中文關鍵字	河川底泥,新興汙染物,人類細胞株,生殖毒性,生物累積性,環境流佈
專案英文名稱	Establishing a water quality monitoring and early warning database: Application of sediment reproductive toxicity and bioaccumulation to evaluate the environmental distribution of emerging pollutants
英文關鍵字	River sediment, emerging pollutants, human cell lines, reproductive toxicity, bioaccumulation, environmental distribution
執行金額	810,000元
執行期間	2024/11/1 至 2025/11/30
計畫中文摘要	底泥能長期累積水體中之污染物，特別是重金屬與有機污染物，能反映河川污染趨勢並對生態與人體健康造成潛在威脅。因此，定期進行底泥監測與毒性評估對於掌握污染源及水質變化至關重要。本研究以新竹地區頭前溪流域為核心，針對鹿寮坑溪（工業廢水區）、油羅溪馬胎段（家庭污水區）、竹東中興河道（綜合污染區）及湳雅、隆恩堰取水口等具有代表性的河段進行底泥採樣，分別於枯水期與豐水期進行重金屬與有機污染物分析，並結合人類卵巢細胞株（A2780）進行生物毒性與細胞反應機制評估，以探討底泥污染對生殖健康之潛在風險。 研究結果顯示： 1. 各採樣點中以鹿寮坑溪與竹東中興河道污染最為嚴重，推測與工業廢水排放及生活污水輸入有關。主要重金屬污染物為鎳（Ni）、銅（Cu）、鋅（Zn）、鉛（Pb）、鉻（Cr）與砷（As），而鎘（Cd）與汞（Hg）多數未檢出。 2. 依污染因子（CFi）與污染負荷指數（PLI）評估結果，污染程度依序為工業廢水區 > 綜合污染區 > 家庭污水區 > 取水口。豐水期污染物濃度普遍高於枯水期，顯示降雨引起的再懸浮效應與水文擾動會提升污染風險。 3. 底泥及萃取液分析顯示部分樣點檢測到多環芳香烴（PAHs）與塑化劑（DEHP），其中萘（naphthalene）與DEHP濃度已接近環境部底泥規範下限值，應列為優先監測污染物。 4. 細胞毒性分析顯示，底泥萃取液暴露可顯著降低A2780細胞存活率，並造成活性氧（ROS）累積、粒線體膜電位（MMP）下降與細胞凋亡。其機制涉及抗氧化路徑蛋白（Nrf2、Keap1、HO-1）及凋亡相關蛋白（Bax、Bcl-2）之表現變化，顯示氧化壓力為主要致毒途徑。 5. 雌激素相關蛋白（ERα、ERβ、FSHR、CYP19A1）表現受到污染物影響，顯示底泥污染可能干擾生殖相關荷爾蒙途徑，增加生殖毒性風險。 6. 進一步建立之細胞馴化模型顯示，長期低濃度暴露後細胞對污染物產生耐受性，顯示底泥中污染物具生物累積與潛在適應性效應。此平台可用於長期監測污染物之慢性毒性趨勢。 7. 綜合而言，本研究證實CFi與PLI可有效辨識污染熱點，細胞模式亦能靈敏反映污染物之生物效應，為底泥監測與健康風險評估提供重要依據。建議未來應加強對DEHP及PAHs等有機污染物之長期追蹤，並強化底泥清淤與源頭控管策略，以降低對生態及人類健康的潛在危害。
計畫英文摘要	Sediments can act as long-term reservoirs for aquatic pollutants, particularly heavy metals and organic contaminants, reflecting river pollution trends and posing potential threats to both ecosystems and human health. Therefore, regular sediment monitoring and toxicity assessment are crucial for identifying pollution sources and understanding water quality variations. This study focused on the Touqian River basin in Hsinchu, Taiwan, with top sediment samples collected from representative sections — including Luliaokeng stream (industrial wastewater zone), Youluo River Matai section (domestic sewage zone), Zhudong Zhongxing River (mixed pollution zone), and the Nanya and Longen Weir water intake sites. Sampling was conducted during both dry and wet seasons to analyze heavy metals and organic pollutants. Additionally, human ovarian cells (A2780) were used to evaluate cytotoxicity and cellular response mechanisms, aiming to elucidate the potential reproductive risks associated with sediment contamination. Research results: Among the sampling sites, Luliaokeng stream and Zhudong Zhongxing River exhibited the highest contamination levels, likely influenced by industrial effluents and domestic wastewater inputs. Major heavy metals detected included nickel (Ni), copper (Cu), zinc (Zn), lead (Pb), chromium (Cr), and arsenic (As), whereas cadmium (Cd) and mercury (Hg) were mostly undetected. Based on the Contamination Factor (CFi) and Pollution Load Index (PLI), the overall pollution level followed the order: industrial wastewater zone (I) > mixed pollution zone (I+D) > domestic sewage zone (D) > water intake site (W). Pollutant concentrations were generally higher during the wet season, suggesting that resuspension and hydrological disturbance induced by rainfall may increase contamination risks. Sediment and extract analyses detected the presence of polycyclic aromatic hydrocarbons (PAHs) and plasticizer DEHP at several sites, with naphthalene and DEHP concentrations approaching the lower regulatory limits set by the Ministry of Environment, indicating the need for priority monitoring of these pollutants. Cytotoxicity assays revealed that sediment extracts significantly reduced A2780 cell viability, induced reactive oxygen species (ROS) accumulation, decreased mitochondrial membrane potential (MMP), and triggered apoptosis. Mechanistically, these effects were associated with altered expression of antioxidant pathway proteins (Nrf2, Keap1, HO-1) and apoptosis-related proteins (Bax, Bcl-2), indicating oxidative stress as the primary toxic pathway. Expression of estrogen-related proteins (ERα, ERβ, FSHR, CYP19A1) was also affected, suggesting that sediment pollutants may disrupt reproductive hormone signaling and increase reproductive toxicity risks. Furthermore, an established cell adaptation model demonstrated that prolonged exposure to low pollutant concentrations induced cellular tolerance, implying potential bioaccumulation and adaptive effects of sediment contaminants. This platform provides a useful tool for long-term monitoring of chronic toxicity trends. In conclusion, this study confirmed that CFi and PLI effectively identify pollution hotspots, while the cell-based model sensitively reflects the biological effects of sediment pollutants. Together, they offer valuable references for sediment monitoring and health risk assessment. Future work should focus on long-term tracking of organic pollutants such as DEHP and PAHs and strengthening sediment dredging and source control strategies to mitigate potential ecological and human health hazards.