六種農藥對環境底棲指標生物—搖蚊—之毒性效應

Abstract

農藥施用後，會藉由淋洗或地表逕流的方式進入水域環境，這些農藥可能藉由吸附或重力作用沉積於底泥當中，底泥匯集了多種的毒物，使得底棲生物長期暴露到毒物，受到較大的風險。為了評估農藥對於底棲生態之影響，選擇搖蚊作為試驗生物，其具有較短的生命週期、易在實驗室馴養及環境重要性等特點，適合作為環境毒理評估的底棲指標生物。而藉由建立臺灣本土搖蚊之毒理系統，可評估農藥對當地環境之影響，試驗藥劑則挑選河川中較常檢出、臺灣用量較高或對搖蚊較高毒性之農藥，如氟大滅、施得圃、大滅松、待克利、丁基拉草及達有龍，以搖蚊死亡率、羽化率、雌雄比及羽化時間作為試驗終點觀察藥劑對搖蚊全生命週期之影響，且藉由抗氧化酵素測定進一步探討搖蚊的氧化逆境。 由48小時搖蚊急毒性的結果，農藥對搖蚊毒性大小依序為氟大滅>施得圃>大滅松>待克利>丁基拉草>達有龍，半數致死劑量 (Median lethal concentration, LC50) 按毒性大小分別為0.101, 0.853, 0.917, 1.474, 2.227及2.302 mg L-1，前三者依水生物急毒性分類屬於劇毒，後三者則為中等毒。根據搖蚊慢毒性試驗之試驗結果顯示，氟大滅和待克利在羽化率評估有較低的最低可觀察影響濃度 (Lowest observed effect concentration, LOEC)，分別為12.5及50 μg L-1；施得圃與達有龍在發育速率有較明顯抑制的效果，LOEC值分別為 50及150 μg L-1。六種藥劑之LOEC值皆高出環境濃度一個數量級以上，這代表環境的農藥殘留濃度尚不足以對搖蚊族群造成影響。 於抗氧化酵素測試，在施得圃和大滅松的暴露中皆可觀察到超氧化物岐化? (Superoxide dismutase, SOD) 及過氧化物? (Catalase, CAT) 活性的上升，達有龍則造成CAT活性上升。與施得圃與大滅松的結果相反，待克利會抑制SOD及CAT活性，這導致超氧自由基無法被有效分解，造成氧化逆境。於脂質過氧化 (Lipid peroxidation, LPO) 的測試得知氟大滅、大滅松、施得圃、丁基拉草及待克利在低於LC50濃度下皆會產生過量的丙二醛 (Malondialdehyde, MDA)，代表藥劑的暴露可能已造成氧化損傷，進而造成搖蚊發育遲緩，甚至死亡的情形。 綜合上述，搖蚊C. crassiforceps於多種試驗終點都具有敏感，為合適的指標生物，由研究結果得知六種農藥於急性和慢性評估中對於搖蚊皆不會造成風險。

After pesticide application, the pesticides may flow into the groundwater by leaching or runoff, and these pesticides may be deposited in the sediment by gravity or adsorption. The sediment collects a variety of toxic substances, putting benthic organisms at greater risk. In order to evaluate the effects of pesticides on benthic ecology, chironomid were selected as the test organisms. Chironomid has a relatively short life cycle, is easily domesticated in the laboratory, and has environmental importance, making it a suitable indicator organism for environmental toxicological assessment. By establishing the toxicological system of chironomid in Taiwan, the impact of pesticides on the local environment can be evaluated. The pesticides that are more frequently detected in rivers and have higher usage in Taiwan or are more toxic to chironomid were selected, such as flubendiamide, pendimethalin, dimethoate, difenoconazole, butachlor, and diuron. In addition, antioxidant enzyme assays were used to further investigate the oxidative stress of chironomid. The 48-hour acute toxicity results showed that the toxicity of the six pesticides was in the order of flubendiamide > pendimethalin > dimethoate > difenoconazole > butachlor > diuron, with LC50s of 0. 01, 0.853, 0.917, 1.474, 2.227, and 2.302 mg L-1. The first three pesticides were classified as high toxicity, while the last three were moderate toxicity. According to the chronic toxicity test, the emergence rate had lower lowest observed effect concentration (LOEC) of 12.5, 62.5, and 50 μg L-1, exposure to flubendiamide and difenoconazole, respectively. In contrast, the development rate had more significant inhibitory effects with LOEC of 50 and 150 μg L-1, exposure to pendimethalin and diuron, respectively. The LOEC for all six pesticides was more than one order of magnitude higher than the environmental concentration, which means that the environmental pesticide residues were not sufficient to affect the chironomid population. In the antioxidant enzyme test, the activity of superoxide dismutase (SOD) and catalase (CAT) can be observed in the exposure of pendimethalin and dimethoate, while diuron only caused the increase in CAT activity. However, it was found that the SOD and CAT activities were inhibited by difenoconazole, which accumulated superoxide radicals and caused oxidative stress. In the lipid peroxidation test, it was found that flubendiamide, dimethoate, pendimethalin, butachlor, and difenoconazole caused the excessive accumulation of malondialdehyde at concentrations below LC50, representing that the exposure to pesticides may have caused oxidative damage, which also caused retarded development and even death of chironomid. Overall, chironomid has the sensitivity for many endpoints and was a suitable ecological benthic indicator species. In the result, the acute and chronic assessments revealed that six pesticides posed no risk for chironomid.