中毒是全球一個重要的公共衛生問題，也是病患到急診就醫常見原因之一。了解中毒的流行病學趨勢及改變，對急診室的醫護人員及公衛人員是非常重要的。我們在台南地區進行了一個為期兩年，以醫院急診就醫中毒病人為主的研究，來評估中毒的流行趨勢。研究期間共收集了1512個中毒個案，平均每一千位急診患者中有4.2人是因中毒而求診。研究中發現，藥物是最主要的中毒物質(49.9%), 其次是農藥類(14.5%)。在南台灣，自殺性中毒常見到使用農藥。在亞太地區的國家中，自殺性中毒也常見到使用含有嘉磷(glyphosate)及界面活性劑 (surfactant)成份的除草劑。市面上大多數嘉磷塞成份的除草劑內含有嘉磷塞異丙胺鹽(isopropylamine salt of glyphosate)、不等量的界面活性劑及水。嘉磷塞類除草劑中毒可能引起嚴重的臨床狀。我們的研究發現 肺水腫、高血鉀及酸血症與嘉磷塞類除草劑中毒預後相關。動物實驗發現，嘉磷塞異丙胺鹽與界面活性劑polyoxyethyleneamine的灌流會影響豬隻心血管功能，導致實驗動物的死亡；但相反的，嘉磷塞本身並不會有此現象。又以老鼠肝細胞為材料，探討嘉磷塞異丙胺鹽及嘉磷塞的細胞致毒性機轉。運用流式細胞儀做粒腺體膜電位測量及細胞凋亡分析，証實磷塞異丙胺鹽及嘉磷塞都可能導致粒腺體膜電位的下降，籍此造成細胞的凋亡。然而，細胞存活分析實驗則發現，在相同的濃度及藥物使用時間下，磷塞異丙胺鹽對細胞的毒性遠大於嘉磷塞本身，引起更多的細胞死亡。兩者之間是否存在協同作用及其二者造成粒腺體膜電位下降的機轉，值得更進一步的探討。

Poisoning is a public health problem worldwide and is one of the most common reasons for attendance at hospital emergency departments (EDs). Knowledge of the epidemiology of poisoning and its changes is important to both emergency physicians and public health practitioners. We conducted a two-year hospital-based study in Tainan area to assess the pattern of poisoning. A total of 1512 poisoning cases were recorded at the EDs during the study period, corresponding to an average of 4.2 poisonings per 1000 ED visits. In the epidemiological study, drugs were the dominant poisoning agents involved (49.9%), followed by pesticides (14.5%). Suicidal attempts with pesticides are common in southern Taiwan, and glyphosate-surfactant herbicide (GlySH) has been frequently used in suicide attempts in many Asia-Pacific countries. Most of the GlySH agents are formulated commercial products containing isopropylamine salt of glyphosate (IPAG), variable amount of a surfactant, and water. GlySH poisoning could cause severe clinical symptoms, and some predictors of fatality were identified, including pulmonary edema, hyperkalemia, and acidosis. Furthermore, in the swine study, we demonstrated that both IPAG and the surfactant, polyoxyethyleneamine (POEA) infusion affected hemodynamics and resulted in death, whereas glyphosate (G) had no similar effects. A study on cultured murine hepatocytes (AML-12) was undertaken to explore the mechanism of cytotoxicity induced by IPAG and G. Flow cytometry analysis demonstrated both IPAG and G could cause collapse of mitochondrial membrane potential, leading to apoptotic death of murine hepatocytes. However, the analysis of cell viability showed IPAG caused more cell death than G in the same concentration and incubation time. Further studies that clarify more precisely the mechanisms of the synergistic effect of G and isopropylamine and collapse of mitochondrial membrane potential are required.

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