Acetamiprid啶虫脒-FAO标准

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啶虫脒乳油标准

啶虫脒乳油标准
啶虫脒乳油是一种广泛应用于农业、卫生及家庭领域的杀虫剂，具有优异的杀虫性能和较低的毒性。

本文将对啶虫脒乳油的标准进行详细介绍，以期为消费者和从业者提供有益的参考。

一、啶虫脒乳油简介
啶虫脒乳油是一种有机氮类杀虫剂，具有触杀和胃毒作用。

其主要通过干扰昆虫神经系统，导致昆虫死亡。

啶虫脒乳油对多种农作物的害虫具有较好的防治效果，如棉花、小麦、玉米等。

二、啶虫脒乳油的标准分类
根据我国相关规定，啶虫脒乳油产品可分为两类：一类是农用啶虫脒乳油，另一类是卫生用啶虫脒乳油。

两类产品在用途、使用方法和剂量上有所不同，需根据实际需求选择合适的产品。

三、啶虫脒乳油的应用领域
1.农业领域：啶虫脒乳油在农业上主要用于防治棉花、小麦、玉米等作物的害虫，如棉铃虫、小麦蚜虫、玉米螟等。

2.卫生领域：啶虫脒乳油在卫生领域可用于防治蚊子、苍蝇、蟑螂等卫生害虫。

3.家庭领域：啶虫脒乳油在家庭中可用于防治衣柜、衣物等物品上的跳蚤、蛀虫等。

四、啶虫脒乳油的注意事项
1.遵守使用剂量：使用啶虫脒乳油时，应严格按照说明书要求的剂量进行
喷洒，避免过量使用。

2.注意安全防护：在使用过程中，应佩戴防护手套、口罩等防护用品，避免直接接触皮肤和眼睛。

3.储存条件：啶虫脒乳油应存放在阴凉、干燥、远离火源的地方，避免儿童接触。

4.避免食物接触：喷洒啶虫脒乳油后，需等待一段时间方可进食或处理食物。

五、总结
啶虫脒乳油作为一种高效、低毒的杀虫剂，在农业、卫生和家庭领域具有广泛的应用。

Q_HTH022-202022.5%氯氟·啶虫脒可湿性粉剂

最终抽样量不少于 200g。 4.2 鉴别试验
高效液相色谱法──本鉴别试验可与高效氯氟氰菊酯、啶虫脒质量分数的测定同时进行。在相同的色谱操作条件下，试样溶液某一色谱峰的保留时间与标样溶液中高效氯氟氰菊酯、啶虫脒色谱峰的保留时间，其相对差值应在 1.5%以内。 4.3 高效氯氟氰菊酯质量分数的测定 4.3.1 方法提要
1
1—啶虫脒图 3 标样高效液相色谱图
4.4.5 测定步骤 4.4.5.1 标样溶液的配制
1—啶虫脒图 4 试样高效液相色谱图
7
Q/HTH-022 -2020
备案号：
称取啶虫脒标样约 0.1g（准确至 0.0002g），置于 50mL 容量瓶中，用甲醇稀释至刻度，
超声波振荡 10min 使试样溶解，冷却至刻度，摇匀。用移液管精确吸出 5.0mL 上述溶液于 50 mL 容量瓶中，用甲醇定容至刻度，摇匀，备用。 4.4.5.2 试样溶液的配制
3. 要求
3.1 外观：组成均匀的疏松粉末，不应有团块。
3.2 22.5%氯氟·啶虫脒可湿性粉剂应符合表 1 要求。
表 1 22.5%氯氟·啶虫脒可湿性粉剂控制项目指标
项
目
高效氯氟氰菊酯质量分数，%
啶虫脒质量分数，%
高效氯氟氰菊酯悬浮率，%
≥
啶虫脒悬浮率，%
≥
水分，%
≤
pH 值范围
润湿时间，s
≤
为了贯彻对到期标准进行重新备案的精神，结合目前本公司产品生产的实际情况。同时，为了规范标准化管理，特此对 22.5%氯氟·啶虫脒可湿性粉剂进行了重新修订。
本标准与原标准不同是：对标准年代号作了修改。本标准自 2020 年 1 月 16 日起实施。本标准由杭州泰丰化工有限公司提出。本标准起草单位：杭州泰丰化工有限公司。本标准主要起草人：李书华、谭建林。本标准于 2008 年 8 月 25 日首次发布，本次为第四次修订。

欧盟修订啶虫脒等农药的最大残留限量

欧盟修订啶虫脒等农药的最大残留限量
佚名
【期刊名称】《化学分析计量》
【年(卷),期】2008(17)5
【摘要】据设在国家质检总局的中国WTO／SPS国家通报咨询中心消息，欧盟不久前发出通报告知欧盟成员国及向欧盟出口相关产品的第三国，欧盟委员会制定指令草案，修订有关啶虫脒（acetamiprid）、茚虫威（indoxacarb）、二甲戊乐灵（pendimethalin）、吡蚜酮（pymethrozine）、肟菌酯（trifloxystrobin）等农药的最大残留限量，涉及到某些植物源性产品，包括水果和蔬菜。

【总页数】1页(P9-9)
【关键词】欧盟成员国;最大残留限量;啶虫脒;农药;修订;国家质检总局;植物源性产品;欧盟委员会
【正文语种】中文
【中图分类】TQ453.299;TS207.53
【相关文献】
1.欧盟修订啶虫脒等农药最大残留限量 [J],
2.加拿大拟修订烯禾啶、二噻虫胺和啶酰菌胺的最大残留限量 [J],
3.植物源性食品葡萄和大蒜中啶虫脒最大残留限量的评估转化 [J], 马磊;冯格格;王猛强;陈颖;李艾琳;高丽萍;佘永新
4.欧盟修订氰虫酰胺、啶虫脒等20种农药残留限量 [J],
5.欧盟拟修订苹果中农药氟啶胺的最大残留限量 [J],
因版权原因，仅展示原文概要，查看原文内容请购买。

国内外毛豆农药残留限量标准比对分析

63国内外毛豆农药残留限量标准比对分析张利真1 汪滨1 张明1* 周坤超2 于立梅1 李菁1（1.中国标准化研究院；2.衢州华友钴新材料有限公司）摘　要：以毛豆、蚕豆为主的豆类蔬菜是我国出口速冻蔬菜的主要品种，在国际贸易中占有主导地位[1]，而农药最高残留限量是农产品国际贸易中最被关注的问题。

因此，选取毛豆作为研究对象，对比分析我国与国际食品法典委员会（CAC ）、欧盟、日本、韩国、美国等5个国家地区或组织的毛豆农药残留限量标准，并分析了我国毛豆农残限量标准存在的问题，提出修订我国毛豆农残限量标准的建议。

关键词：毛豆，标准，农药残留，比对DOI编码：10.3969/j.issn.1674-5698.2021.06.012Comparative Analysis of Pesticide Residue LimitStandards in Green Soybean at Home and Abroad ZHANG Li-zhen 1 WANG Bin 1 ZHANG Ming 1* ZHOU Kun-chao 2 YU Li-mei 1 LI Jing 1（1.China National Institute of Standardization; 2. Quzhou Huayou Cobalt New Material Co., Ltd.）Abstract: Legume vegetables, mainly green soybeans and broad beans, are the main varieties of quick-frozen vegetables exported from China, occupying a leading position in the international trade. Therefore, this paper selects green soybean as the research object, makes a comparative analysis on the pesticide residue limit standards of Chinese and other five countries, regions or organizations including Codex Alimentarius Commission, the European Union, Japan, South Korea, the United States, and analyzes the problems existing in China's green soybean pesticide residue limit standard, and puts forward the suggestion of revising the pesticide residue limit standard in China.Keywords: green soybean, standard, pesticide residue, comparison基金项目：本文是国家重点研发计划“中国标准适用性技术研究（二期）”（项目编号：2017YFF0209500）的研究成果。

啶虫脒——精选推荐

啶⾍脒基本信息中⽂通⽤名：啶⾍脒中⽂其他名：莫⽐朗商品名称：⽐⾍清、⼄⾍脒、⼒杀死、蚜克净、乐百农、赛特⽣、农家盼等⼏⼗种名字。

英⽂通⽤名：acetamiprid英⽂其他名：Mospilan分⼦式：C10H11ClN4分⼦量：222.68化学名称：E-N'-[(6-氯-3-吡啶基)甲基]-N^(2)-氰基-N'-甲基⼄酰胺化学结构式：啶⾍脒化学结构式CA登记号：135410-20-7农药类别：吡啶类杀⾍剂理化性质浅黄⾊结晶粉，⽐重1.330，熔点98～101℃，蒸⽓压<1×10^(－8)mmHg。

(25℃)，⽔中溶解度约4g/L，可溶于⼤多数极性有机溶剂。

丙酮>200，⼄醇 >200，⼆氯甲烷>200，⼰烷0.00654(均在25℃g/L)。

在中性或偏酸性介质中稳定，常温下稳定。

毒性　⼤⿏急性⼝服LD50：雄217mg/kg，雌146 mg/kg；⼩⿏：雄198mg/kg，雌184 mg/kg；⼤⿏急性经⽪LD50：雄、雌>2000mg/kg。

对⼈畜低毒，每⽇允许摄⼊量0.017mg/kg/day(公司)。

环境⽔⽣⽣物：LC50(96h)>100mg/kg(鲤鱼)蜜蜂：LD50=1µg天敌：LD50鹑180mg/kg；蚕:在0.03ppm时对蚕⽆副作⽤；蚯蚓LC50(7天)10mg/kg.⽔⼟保持：半衰期1.1～2.1天(⼟),420天(25℃,pH9),21天(河⽔)作⽤特点啶⾍脒属硝基亚甲基杂环类化合物，是⼀种新型杀⾍剂，作⽤于昆⾍神经系统突触部位的烟碱⼄酰胆碱受体，⼲扰昆⾍神经系统的刺激传导，引起神经系统通路阻塞，造成神经递质⼄酰胆碱在突触部位的积累，从⽽导致昆⾍⿇痹，最终死亡。

天达药业植保公司开发的3%啶⾍脒乳油，具有触杀、胃毒和较强的渗透作⽤，杀⾍速效，⽤量少、活性⾼、杀⾍谱⼴、持效期长达20天左右，对环境相容性好等。

5%啶虫脒微乳剂企业标准

Q/XZF 西安市植丰农药厂企业标准Q/XZF25-20185%啶虫脒微乳剂2018-02-20发布2018-02-26实施西安市植丰农药厂发布Q/XZF25-2018前言本标准由西安市植丰农药厂提出。

本标准由西安市植丰农药厂起草。

本标准主要起草人：穆亚伯韩喻霍军辉1.本标准按GB/T1.1-2009的要求编排；2.规范性引用文件进行了查新，在标准中引用了最新现行国、行标；3.产品所选项目及相关参数均参照相关国、行标规定。

IQ/XZF25-20185%啶虫脒微乳剂该产品中各有效成分的其他名称，结构式和基本物化参数如下：ISO通用名称：acetamiprid；商品名称：N1-25，莫比朗；CIPAC数字代号：649化学名称：（E)-N-[(6氯吡啶）-3-基-N-腈基-N-甲基乙酰胺]；结构式：CH3CNC NCH2NCH3NCl分子式：C10H11C1N4；相对分子质量：222.68（按照2003国际相对原子质量计）；生物活性：杀虫；熔点：101-103.2℃；蒸汽压（25℃）：＜1.33×10-6pa溶解度（g/1，25℃）：水中4.2，易溶于丙酮、甲醇、乙醇、二氯甲烷、氯仿、乙腈；稳定性：常温贮存稳定性2年；1范围本标准规定了5%啶虫脒微乳剂的要求，试验方法、检验规则及标志、标签、包装和贮运；本标准适用于由符合标准的啶虫脒原药、水与适宜的助剂加工制成的5%啶虫脒微乳剂。

2规范性引用文件下列文件对于本标准的应用是必不可少的，凡是注日期的引用文件，仅注日期的版本使用于本标准。

凡是不注日期的引用标准，其最新版本适用本标准。

GB/T601化学试剂标准滴定溶液的制备GB/T603化学制剂实验方法中所用制剂及制品的制备GB/T1601农药PH值测定方法GB/T1603农药乳液稳定性测定方法GB/T1604商品农药验收规则GB/T1605商品农药采样方法GB3796农药包装通则GB4838农药乳油包装GB/T8170数值修约规则与极限数值的表示和判定GB/T19136农药热贮稳定性测定方法GB/T19137农药低温稳定性测定方法GB/T28135农药酸（碱）度测定方法GB/T28137农药持久起泡性测定方法3要求3.1组成与外观：本品应由符合标准的啶虫脒原药、水和适宜的助剂制成，应为透明或半透明均相液体，Q/XZF25-2018无可悬浮物和沉淀；3.2产品技术指标应符合表1要求。

啶虫脒知识

【通用名称】啶虫脒（Acetamiprid）【化学名称】E-N-［（6-氯-3-吡啶基）］-N-(2)-氰基-N-甲基乙酰胺【结构式】【分子式】C10H11ClN4【分子量】222.68【理化性质】外观为白色晶体，熔点为101.0～103.3℃，蒸汽压>1.33×10-6帕(25℃)。

25℃时在水中的溶解度4200毫升/升，能溶于丙酮、甲醇、乙醇、二氯甲烷、氯仿、乙腈、四氢呋喃等。

在PH=7的水中稳定，PH=9时，于45℃逐渐水解，在日光下稳定【毒性】大鼠急性口服LD50：雄217mg/kg，雌146 mg/kg；小鼠：雄198mg/kg，雌184 mg/kg；大鼠急性经皮LD50：雄、雌>2000mg/kg【防治对象】主要用于防治柑桔、苹果、黄瓜等作物上蚜虫。

【制剂】3%EC，20%SP啶虫脒是我公司最近开发的超高效广谱内吸收性新型杀虫剂，与吡虫啉属同一系列，但它的杀虫谱比吡虫啉更广主要对黄瓜、苹果、柑桔、烟草上的蚜虫具有较好的防治效果。

该产品有较强的触杀和渗透作用，杀虫迅速且持效期长。

作用机智独特，能防治对现有药剂抗性的蚜虫。

本品具有强内吸性，故可以作为种子处理剂，防治地下害虫。

性能特点:§本品是新一代烟碱超高效新型杀虫剂，对害虫具有胃毒、触杀外在还具有较强的内吸性和强渗作用，因而能稳定的发挥其强大的速效性和20多天以上的持效力。

§本品为可溶性粉剂，是目前世界上先进的剂型。

入水后迅速分散。

§本品与世界上独一无二的VA助剂结合后，增强其在作物表面附着力、延展力和超强渗透力，施药后有效成分能快速穿透叶片及虫体，真正达到"正面打药，隔叶死虫"。

特别针对各种作物上的蚜虫、蓟马、稻飞虱、粉虱、蝽蟓、叶蝉、康氏粉蚧等效果显著。

啶虫脒分类：杀虫剂质量指标：通用名：啶虫脒规格：3%乳油、5%乳油、20%可溶性浓剂、20%可溶性粉剂、95%原药化学名称：N-[（6-氯吡啶）-3-基]-N2-腈基-N1-甲基乙酰胺分子式：C10H11N4CL生物活性：杀虫、杀螨其它说明：使用说明：本品是一种新型广谱且具有一定杀螨活性的杀虫剂，其作用方式为土壤和枝叶的系统杀虫剂。

气相色谱法对毒死、啶虫脒和噻嗪酮的定量分析

气相色谱法对毒死、啶虫脒和噻嗪酮的定量分析摘要:采用气相色谱法用SUBTM-5型毛细管柱，以双甲脒为内标物，NPD检测器对毒死蜱､啶虫脒和噻嗪酮3种农药制剂进行了同时定量分析。

结果表明，毒死蜱的线性回归方程为y=1.570 486x+0.546 76(r=0.998 2)，有效成分含量为32.58%;啶虫脒的线性回归方程为y=0.544 916x+0.859 651(r=0.998 9)，有效成分含量为45.62%;噻嗪酮的线性回归方程为y=0.743 658x+1.243 762(r=0.999 7)，有效成分含量为27.83%。

关键词:气相色谱;毒死蜱;噻嗪酮;啶虫脒;定量分析气相色谱法由于具有分离效能高､分析速度快､选择性好等优点而被广泛应用于环境样品中的污染物分析､药品质量检验､天然产物成分分析､食品中农药残留量测定､工业产品质量监控等领域[1]。

据FAO和WHO报道，欧盟对进口水果提出最高残留限量要求的农药为124种，美国对农产品提出最高残留限量要求的农药多达300余种，其目的都在于最大限度控制滥用农药[2]。

现今，用GC分析农药残留的方法比较成熟，被广泛认同。

随着新型气相色谱仪器､检测器､数据分析方法的出现，气相色谱的应用领域也必将越来越广阔。

毒死蜱属含杂环的有机磷农药，商品名称为乐斯本，是广谱性杀虫，杀螨剂，在世界范围内广泛应用。

其在中性和弱酸性介质中水解缓慢，有效期可达数月[3]。

噻嗪酮属噻二嗪类昆虫生长调节剂，商品名有优乐得，稻虱灵等。

该药剂兼具触杀和胃毒作用，对飞虱，叶蝉，粉虱有特效[4]。

啶虫脒属氯代烟碱类杀虫剂，又名莫比朗､吡虫清，兼具触杀和胃毒作用，并具有卓越的内吸活性，对现有有机磷､氨基甲酸酯类具有较强抗性的害虫有特效[5]。

FBT075-2009 番茄及其制品中啶虫脒检测方法-气相色谱法

FB番茄及其制品中啶虫脒残留量检测方法-气相色谱法Determination of acetamiprid in tomato and processed products- gas chromatography新疆出入境检验检疫局技术中心发布FB/T 075—2009II前言本非标方法的附录A为资料性附录。

本非标方法由新疆出入境检验检疫局技术中心食品实验室提出。

本非标方法由新疆出入境检验检疫局技术中心归口。

本非标方法起草单位：新疆出入境检验检疫局技术中心食品实验室。

本非标方法主要起草人：李锋格、姚伟琴、朱慧萍、李欣、李炎、胡建民、沈梦圆。

FB/T 075—2009 番茄及其制品中啶虫脒残留量检测方法-气相色谱法1 范围本非标方法规定了番茄及其制品中啶虫脒气相色谱测定方法。

本非标方法适用于番茄及其制品中啶虫脒残留量的测定。

2 规范性引用文件下列文件中的条款通过本标准的引用而成为本标准的条款。

凡是注日期的引用文件，其随后所有的修改单（不包括勘误的内容）或修订版均不适用于本标准，然而，鼓励根据本标准达成协议的各方研究是否可使用这些文件的最新版本。

凡是不注日期的引用文件，其最新版本适用于本标准。

GB/T 6682 分析实验室用水规格和试验方法SN/T 0001 出口商品中农药、兽药残留量及生物毒素检验方法标准编写的基本规定3 原理番茄及其制品经乙腈提取，盐析，氟罗里硅土固相萃取小柱，用配有微池电子捕获检测器的气相色谱仪检测，外标法定量。

4 试剂及材料除非另有说明，所有试剂均为分析纯，水为GB/T6682规定的一级水。

4.1 乙腈：色谱纯。

4.2 丙酮：色谱纯。

4.3 正己烷：色谱纯。

4.4 氯化钠：650℃灼烧4h，冷却后贮于密闭容器中。

4.5 丙酮-正己烷溶液（10+90，V+V）：准确量取100mL丙酮和900mL正己烷，混合后备用。

4.6 丙酮-正己烷溶液（40+60，V+V）：准确量取400mL丙酮和600mL正己烷，混合后备用。

fao农药产品标准

fao农药产品标准一、产品质量要求FAO农药产品标准对产品质量有严格的要求，包括以下方面：1. 有效性：产品应具有所需的病虫害防治效果，且对作物和环境无害。

2. 化学成分：产品应符合规定的化学成分含量和比例。

3. 物理性质：产品的外观、颜色、粒度、密度、粘度等物理性质应符合要求。

4. 稳定性：产品应具有足够的稳定性，以保证在贮存和使用过程中有效成分的含量不会降低。

5. 安全性：产品应无毒或低毒，对使用者、作物和环境安全。

6. 使用方法：产品应具有明确的使用方法，包括适用作物、使用剂量、使用次数、使用时间等。

7. 标签和说明书：产品的标签和说明书应清晰明了，包括产品名称、化学成分、使用方法、注意事项等信息。

二、产品安全性评估FAO农药产品标准要求对产品进行安全性评估，以确定产品对人类健康和环境的安全性。

评估内容包括以下方面：1. 急性毒性：评估产品对人类和动物的急性毒性，以确定产品的安全使用范围。

2. 慢性毒性：评估产品对人类和动物的慢性毒性，以确定产品长期使用的安全性。

3. 致畸性：评估产品对人类和动物的致畸性，以确定产品对孕妇和胎儿的安全性。

4. 致突变性：评估产品对人类和动物的致突变性，以确定产品对遗传物质的安全性。

5. 环境安全性：评估产品对土壤、水体和生态系统的安全性，以确定产品对环境的安全性。

三、产品稳定性评估FAO农药产品标准要求对产品的稳定性进行评估，以确定产品在贮存和使用过程中的稳定性。

评估内容包括以下方面：1. 外观稳定性：评估产品在贮存和使用过程中的外观变化，如颜色、粒度等。

2. 化学稳定性：评估产品在贮存和使用过程中有效成分含量的变化，以确定产品的有效期。

3. 物理稳定性：评估产品在贮存和使用过程中物理性质的变化，如粘度、密度等。

四、产品使用方法及注意事项FAO农药产品标准要求提供明确的产品使用方法和注意事项，以确保产品的有效性和安全性。

使用方法应包括适用作物、使用剂量、使用次数、使用时间等，注意事项应包括贮存方法、安全穿戴防护用品等。

柑橘国家标准

喹硫磷（quinalphos）
0.5
0.5*
氯氟氰菊酯和高效氯氟氰菊酯
0.2
0.2
乐果（dimethoate）
2（乐果与氧乐果之和，以乐果表示）
2*
氯氰菊酯和高效氯氰菊酯
1
1
联苯菊酯（bifenthrin）
lathion）
2
2
硫线磷（cadusafos）
0.005
0.005
0.5
0.5
亚胺硫磷（phosmet）
5
5
毒死蜱（chlorpyrifos）
1
1
亚胺唑（imibenconazole）
1*
1*
多菌灵（carbendazim）
5（全果）
5
烟碱（nicotine）
0.2
0.2
噁唑菌酮（famoxadone）
1
1
乙螨唑（etoxazole）
0.5
0.5
氟苯脲（teflubenzuron）
1
1
炔螨特（propargite）
5
5
苯丁锡（fenbutatin oxide）
1
1
噻螨酮（hexythiazox）
0.5
0.5
苯菌灵（benomyl）
5**
5*
噻嗪酮（buprofezin）
0.5
0.5
苯硫威（fenothiocarb）
5
0.5
三氯杀螨醇（dicofol）
1
1
苯螨特（benzoximate）
柑橘农药中文名原标准现标准农药中文名原标准现标准氯钠mcpasodium0101嘧菌酯azoxystrobin阿维菌素abamectin002002灭多威methomyl百草枯paraquat0202苯丁锡fenbutatinoxide噻螨酮hexythiazox0505苯菌灵benomyl噻嗪酮buprofezin0505苯硫威fenothiocarb苯螨特benzoximate0303三唑磷triazophos02果0202三唑酮triadimefon丙炔氟草胺flumioxazin005005杀铃脲triflumuron002005丙溴磷profenofos0202杀螟丹cartap草甘膦glyphosate0505杀扑磷methidathion双甲脒amitraz0505春雷霉素kasugamycin0101水胺硫磷isocarbophos002002哒螨灵pyridaben四螨嗪clofentezine0505代森联metriam肟菌酯trifloxystrobin0505代森锰锌mancozeb单甲脒和单甲脒盐酸盐0505烯啶虫胺nitenpyram0505稻丰散phenthoate丁醚脲diafenthiuron0202溴氰菊酯deltamethrin005005啶虫脒acetamiprid0505亚胺硫磷phosmet烟碱nicotine0202噁唑菌酮famoxadone乙螨唑etoxazole0505氟苯脲teflubenzuron0505抑霉唑imazalil氟虫脲flufenoxuron0505唑螨酯fenpyroximate0202氟啶脲chlorfluazuron0505螺虫乙酯spirotetramat螺螨酯spirodiclofen0505喹硫磷quinalphos05050202乐果dimethoate2乐果与氧乐果之和以乐果表示联苯菊酯bifenthrin005005马拉硫磷malathion硫线磷cadusafos00050005氧乐果omethoate002glufosinateammonium05腈菌唑myclobutanil联苯肼酯bifenazate07氯噻啉imidaclothiz02噻菌灵thiabendazole10噻唑锌zincthiazole05双胍三辛烷基苯磺酸盐

啶虫脒生产工艺规程试行版

咤虫豚生产工艺规程（试行）***L主题内容与适用范围 (2)2.术语 (2)3.产品概况 (2)3.1产品名称 (2)3.2理化性质 (2)3.3毒性 (3)3.4防治对象 (3)3.5产品规格 (3)3.6执行标准 (3)4、原料及中间体性质 (3)1.1甲苯 (3)1.2一甲胺 (3)1.3溶齐IJ B (4)1.4氟基乙脂 (4)1.5盐酸 (4)1.6催化剂C (4)1.72-氯-5-氯甲基口比咤（CCMP） (4)1.8N-甲基-（6-氯毗咤3基）甲胺（简称节胺或中I ） (5)5.化学反应、生产原理及生产工艺技术条件 (5)5.1化学反应 (5)5.2生产工艺技术条件 (5)6.操作规程 (6)6.1胺化工段 (6)6.2、酯化工段 (7)6.3注意事项 (8)7、安全规程 (9)7.1通胺岗位 (9)7.2合成岗位 (9)7.3脱溶岗位 (9)7.4萃取岗位 (10)7.5岗位应急处理 (10)8生产设备一览表 (11)附录A:溶媒、母液回收再利用及废水处理 (12)咤虫眯生产工艺规程(试行)1.主题内容与适用范围主题内容：本标准规定了***有限公司咤虫眯原药生产所用原料、产品的质量要求、生产原理、工艺技术条件和安全生产注意事项。

适用范围：本规程适用于指导本企业咤虫眯生产工序的操作、控制和验收。

2.术语二氯一一反应所需的原料CCMP即2-氯-5-氯甲基毗咤甲苯一一胺化反应所用溶剂溶剂B——酯化反应所用溶剂催化剂C一一酯化反应所用有机碱催化剂3.产品概况3.1产品名称中文名称：咤虫睬英文名称:acetamiprid化学名称:N-(N-氟基.乙亚胺基卜N-甲基2氯毗咤-5.甲胺CAS RN.: 135410-20-7分子式：C IO H II CIN4分子量：222.683.2理化性质外观为白色晶体，熔点为IOLO~103.3°C,蒸汽压＞1.33x10-6帕(25℃)。

25℃时在水中的溶解度4200毫克/升，能溶于丙酮、甲醇、乙醇、二氯甲烷、氯仿、乙懵、四氢吠喃等。

菊花中啶虫脒的残留降解规律

櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄櫄［１０］ＯｙａｉｚｕＭ．Ｓｔｕｄｉｅｓｏｎｐｒｏｄｕｃｔｓｏｆｂｒｏｗｎｉｎｇｒｅａｃｔｉｏｎ：ａｎｔｉｏｘｉｄａｔｉｖｅａｃｔｉｖｉｔｉｅｓｏｆｐｒｏｄｕｃｔｓｏｆｂｒｏｗｎｉｎｇｒｅａｃｔｉｏｎｐｒｅｐａｒｅｄｆｒｏｍｇｌｕｃｏｓｅａｍｉｎｅ［Ｊ］．ＪａｐａｎｅｓｅＪｏｕｒｎａｌｏｆＮｕｔｒｉｔｉｏｎ，１９８６，４４：３０７－３１５．［１１］ＪｉｎＭ，ＣａｉＹＸ，ＬｉＪＲ，ｅｔａｌ．１，１０－ｐｈｅｎａｎｔｈｒｏｌｉｎｅ－Ｆｅ２＋ｏｘｉｄａｔｉｖｅａｓｓａｙｏｆｈｙｄｒｏｘｙｒａｄｉｃａｌｐｒｏｄｕｃｅｄｂｙＨ２Ｏ２／Ｆｅ２＋［Ｊ］．ＰｒｏｇｒｅｓｓＢｉｏｃｈｅｍｉｓｔｒｙ＆Ｂｉｏｐｈｙｓｉｃｓ，１９９６，２３（６）：５５３－５５５．［１２］ＤｕａｎＸＷ，ＪｉａｎｇＹＭ，ＳｕＸＧ，ｅｔａｌ．Ａｎｔｉｏｘｉｄａｎｔｐｒｏｐｅｒｔｉｅｓｏｆａｎｔｈｏｃｙａｎｉｎｓｅｘｔｒａｃｔｅｄｆｒｏｍｌｉｔｃｈｉ（ＬｉｔｃｈｉｃｈｉｎｅｎｅｓｉｓＳｏｎｎ．）ｆｒｕｉｔｐｅｒｉｃａｒｐｔｉｓｓｕｅｓｉｎｒｅｌａｔｉｏｎｔｏｔｈｅｉｒｒｏｌｅｉｎｔｈｅｐｅｒｉｃａｒｐｂｒｏｗｎｉｎｇ［Ｊ］．ＦｏｏｄＣｈｅｍｉｓｔｒｙ，２００７，１０１（４）：１３６５－１３７１．［１３］ＭａｎｉｖａｓａｇａｎＰ，ＶｅｎｋａｔｅｓａｎＪ，ＳｅｎｔｈｉｌｋｕｍａｒＫ，ｅｔａｌ．ＩｓｏｌａｔｉｏｎａｎｄｃｈａｒａｃｔｅｒｉｚａｔｉｏｎｏｆｂｉｏｌｏｇｉｃａｌｌｙａｃｔｉｖｅｍｅｌａｎｉｎｆｒｏｍＡｃｔｉｎｏａｌｌｏｔｅｉｃｈｕｓｓｐ．ＭＡ－３２［Ｊ］．ＩｎｔｅｒｎａｔｉｏｎａｌＪｏｕｒｎａｌｏｆＢｉｏｌｏｇｉｃａｌＭａｃｒｏｍｏｌｅｃｕｌｅｓ，２０１３，５８：２６３－２７４．［１４］周巾英，欧阳玲花，王　丽，等．白藜芦醇清除ＤＰＰＨ自由基反应的动力学［Ｊ］．食品工业，２０２０，４１（６）：２２２－２２６．［１５］余　佳，王　生，许文琦，等．葛仙米藻胆蛋白粗提物、藻蓝蛋白和藻红蛋白的体外抗氧化活性比较研究［Ｊ］．食品研究与开发，２０１９，４０（２３）：１０４－１０８．［１６］ＬｉｕＦ，ＮｇＴＢ．Ａｎｔｉｏｘｉｄａｔｉｖｅａｎｄｆｒｅｅｒａｄｉｃａｌｓｃａｖｅｎｇｉｎｇａｃｔｉｖｉｔｉｅｓｏｆｓｅｌｅｃｔｅｄｍｅｄｉｃｉｎａｌｈｅｒｂｓ［Ｊ］．ＬｉｆｅＳｃｉｅｎｃｅ，２０００，６６（８）：７２５－７３５．　［１７］刘占才，牛俊英．超氧阴离子自由基对生物体的作用机理研究［Ｊ］．焦作教育学院学报（综合版），２００２，１８（４）：４８－５１．［１８］ＬｉＪＷ，ＬｉｕＹＦ，ＦａｎＬＰ，ｅｔａｌ．ＡｎｔｉｏｘｉｄａｎｔａｃｔｉｖｉｔｉｅｓｏｆｐｏｌｙｓａｃｃｈａｒｉｄｅｓｆｒｏｍｔｈｅｆｒｕｉｔｉｎｇｂｏｄｉｅｓｏｆＺｉｚｙｐｈｕｓｊｕｊｕｂａｃｖ．Ｊｉｎｓｉｘｉａｏｚａｏ［Ｊ］．ＣａｒｂｏｈｙｄｒａｔｅＰｏｌｙｍｅｒｓ，２０１１，８４（１）：３９０－３９４．［１９］熊双丽，卢　飞，史敏娟，等．ＤＰＰＨ自由基清除活性评价方法在抗氧化剂筛选中的研究进展［Ｊ］．食品工业科技，２０１２，３３（８）：３８０－３８３．卢　飞，郑尊涛，张江兆，等．菊花中啶虫脒的残留降解规律［Ｊ］．江苏农业科学，２０２１，４９（６）：１５５－１５９．ｄｏｉ：１０．１５８８９／ｊ．ｉｓｓｎ．１００２－１３０２．２０２１．０６．０２７菊花中啶虫脒的残留降解规律卢　飞１，３，４，郑尊涛２，张江兆１，３，４，沈　燕１，２，３［１．江苏省食品质量安全重点实验室－省部共建国家重点实验室培育基地，江苏南京２１００１４；２．农业农村部农药检定所，北京１０００００；３．农业农村部农产品质量安全风险评估实验室（南京），江苏南京２１００１４；４．农业农村部农产品质量安全控制技术与标准重点实验室，江苏南京２１００１４］摘要：通过食用液相－质谱联用方法研究河南安阳、江苏盐城、贵州贵阳、广东广州、浙江杭州及湖北湘潭等６地菊花啶虫脒的残留降解规律，为菊花病虫害防治以及菊花中的啶虫脒残留分析提供参考。

新生大鼠啶虫脒亚慢性暴露致成年后神经系统毒性的研究

生态毒理学报Asian Journal of Ecotoxicology第18卷第2期2023年4月V ol.18,No.2Apr.2023㊀㊀基金项目:国家自然科学基金资助项目(81160338);宁夏科技重点研发项目(2020BEG03048);宁夏自然科学基金资助项目(2020AAC03176)㊀㊀第一作者:李姝霖(1996 ),女,硕士研究生,研究方向为神经退行性变的环境机制,E -mail:****************㊀㊀*通信作者(Corresponding author ),E -mail:****************DOI:10.7524/AJE.1673-5897.20220914005李姝霖,曹持,王文成,等.新生大鼠啶虫脒亚慢性暴露致成年后神经系统毒性的研究[J].生态毒理学报,2023,18(2):327-337Li S L,Cao C,Wang W C,et al.Sub -chronic exposure to acetamiprid in neonatal rats leads to neurotoxicity in adulthood [J].Asian Journal of Ecotoxi -cology,2023,18(2):327-337(in Chinese)新生大鼠啶虫脒亚慢性暴露致成年后神经系统毒性的研究李姝霖1,曹持1,2,王文成3,马瑞1,4,邓倩1,张亚文1,于春洋1,田建英1,*1.宁夏医科大学基础医学院,银川7500042.宁夏医科大学总医院,银川7500043.宁夏回族自治区人民医院,银川7500024.银川市第一人民医院,银川750004收稿日期:2022-09-14㊀㊀录用日期:2022-12-24摘要:观察新生大鼠啶虫脒(acetamiprid,ACE)慢暴露对成年后神经行为㊁大脑皮质与海马的影响㊂选择出生一周的雄性Spra -gue -Dawley (SD)大鼠18只,随机分为对照组(Control)㊁ACE -15组(15mg ㊃kg -1㊃d -1)㊁ACE -40组(40mg ㊃kg -1㊃d -1),每组6只㊂ACE 暴露组灌胃干预9周,期间每周检测体质量㊂采用开放旷场实验(OFT)㊁Morris 水迷宫(MWM)检测大鼠行为学变化;采用试剂盒检测大脑皮质和海马组织中丙二醛(MDA)和超氧化物歧化酶(SOD)水平;采用Western Blot 法检测白细胞介素IL -1β㊁IL -10蛋白表达量;采用苏木精-伊红(H&E)染色法检测大脑皮质和海马组织病理学改变;采用Nissl 染色法检测大脑海马DG ㊁CA3区神经元变化㊂OFT 结果显示,与对照组相比,ACE 暴露组大鼠在中央区运动距离和时间均减少㊂MWM 结果显示,定位巡航期间,暴露组逃逸潜伏期时间增加,目标象限停留时间减少㊂空间探索期间,ACE -40组跨平台次数减少,目标象限内游泳速度降低㊂暴露组大鼠脑皮质和海马组织中MDA 浓度增高;暴露组大鼠脑皮质SOD 活性降低,海马组织SOD 活性增高㊂Western Blot 结果显示,与对照组相比,暴露组大鼠皮质和海马组织中IL -1β表达量增高;IL -10表达量降低㊂H&E 结果显示,ACE -40组海马DG ㊁CA3区神经元出现排列紊乱㊁层数减少和轮廓模糊㊂Nissl 染色结果显示,暴露组大鼠海马DG ㊁CA3区神经元数量减少,尼氏小体减少㊂以上结果表明,新生大鼠ACE 亚慢性暴露能够导致成年后神经行为变化,可能与脑皮质和海马组织的氧化应激与炎症有关㊂关键词:啶虫脒;SD 大鼠;亚慢性暴露;神经行为;神经毒性文章编号:1673-5897(2023)2-327-11㊀㊀中图分类号:X171.5㊀㊀文献标识码:ASub-chronic Exposure to Acetamiprid in Neonatal Rats Leads to Neurotox-icity in AdulthoodLi Shulin 1,Cao Chi 1,2,Wang Wencheng 3,Ma Rui 1,4,Deng Qian 1,Zhang Yawen 1,Yu Chunyang 1,Tian Jianying 1,*1.School of Basic Medical Sciences,Ningxia Medical University,Yinchuan 750004,China2.General Hospital of Ningxia Medical University,Yinchuan 750004,China3.People s Hospital of Ningxia Hui Autonomous Region,Yinchuan 750002,China4.The First People s Hospital of Yinchuan,Yinchuan 750004,China328㊀生态毒理学报第18卷Received14September2022㊀㊀accepted24December2022Abstract:To observe the effects of sub-chronic exposure to acetamiprid(ACE)in neonatal rats on neurobehavior, cerebral cortex,and hippocampus in adulthood.18one-week-old male Sprague-Dawley(SD)rats were randomly divided into control group,ACE-15group(15mg㊃kg-1㊃d-1)and ACE-40group(40mg㊃kg-1㊃d-1),with6rats in each group(n=6).The ACE-exposed groups were given gavage intervention for9weeks,during which body weight was measured weekly.Open field test(OFT)and Morris water maze(MWM)were used for neurobehavioral assessment in SD rats;malondialdehyde(MDA)and superoxide dismutase(SOD)levels in cerebral cortex and hip-pocampus were detected by ELISA kits;IL-1βand IL-10expression were detected by Western Blot;hematoxylin and eosin(H&E)staining was used to detect histopathological changes in cerebral cortex and hippocampus;Nissl staining was used to detect neuronal changes in the DG and CA3regions of the hippocampus.The OFT results showed that the movement distance and duration of movement in the central zone were reduced in the ACE-ex-posed groups rats compared to the control group.The MWM results showed that the escape latency was increased and the target quadrant residence was decreased in the ACE-exposed group compared with the control group;the target crossing was decreased and the swimming speed in the target quadrant was decreased in the ACE-40group. The MDA level was increased in the cerebral cortex and hippocampus,whereas the SOD content was decreased in the cerebral cortex but increased in the hippocampus in ACE-exposed groups.Higher expression of IL-1βand low-er expression of IL-10in the cerebral cortex and hippocampus were also detected in ACE-exposed groups in con-trast to the control rats.Disorders of neuronal arrangement,reduced cell layers,and reduced Nissl bodies in the DG and CA3regions of the hippocampus were observed in ACE-exposed rats.The above results suggest that sub-chro-nic exposure to ACE in neonatal rats can lead to neurobehavioral changes in adulthood,which may be related to oxidative stress and inflammation in the cerebral cortex and hippocampus.Keywords:acetamiprid;SD rats;sub-chronic exposure;neurobehavior;neurotoxicity㊀㊀20世纪70年代,科研人员在烟碱的基础上开发出了新烟碱类杀虫剂,因其低毒㊁高效等特性,被广泛使用[1]㊂新烟碱类杀虫剂能够通过激活昆虫体内的神经元使其发生去极化,使昆虫因神经系统过度兴奋而死亡[2]㊂新烟碱类杀虫剂的作用时间较长,降解缓慢,可在环境残留1d~19a不等[3],且可以被植物根部吸收存在于植物各个部位,不能通过剥皮和水洗去除,能够在食物中长期残留,因此在蔬菜[4]㊁土壤[5]和地下水[6]等非靶标植物和动物体内均能被检出[7]㊂目前,啶虫脒(ACE)作为氯代新烟碱型杀虫剂被广泛使用㊂有研究发现[8],通过对水生环境监测得到的美国德克萨斯州高平原Playa湿地中的ACE,浓度高达225μg㊃L-1㊂尽管新烟碱类杀虫剂的环境残留剂量较低,但近些年来环境介质中新烟碱类杀虫剂的环境残留剂量正在呈逐年上升趋势,这应当引起我们足够的重视㊂根据联合国粮食及农业组织(Food and Agriculture Organization of the United Nations,FAO)标准[9],结合长达2年的大鼠毒性和致癌性实验,设立ACE人群每日允许摄入量为0~0.07mg㊃kg-1㊂还有研究发现[10],长期接触使用新烟碱类杀虫剂的人员可以在尿液中检出其代谢产物㊂Wang等[11]根据上海市儿童尿液中新烟碱含量,推测出新烟碱最大暴露剂量为10.61μg㊃kg-1㊂近期相关研究显示[12],ACE暴露1h后在小鼠大脑中检测到ACE及其代谢物㊂另有研究表明[13],ACE能够在肠道中被完全吸收并且可以通过血脑屏障,长期接触后能够以剂量依赖的方式在体内累积,在不同脑区蓄积,对哺乳动物神经系统可能具有危害[14]㊂出生后10d左右为大鼠脑发育突发期[15],此时大脑发育未完全,容易受到环境和药物暴露后的副作用影响㊂研究表明[16],口服ACE(5mg㊃kg-1)可以显著降低新生小鼠的神经干细胞增殖基因(C1DU)㊁神经元数目,并增加了小胶质细胞的产生,表明新生小鼠海马区神经发生受损㊂然而对于新生期大鼠ACE亚慢性暴露是否会影响其成年后神经行为变化尚不清楚[17]㊂因此,本研究拟通过ACE对新生大鼠亚慢性暴露,观察其对成年后神经行为㊁大脑皮质和海马组织的影响㊂第2期李姝霖等:新生大鼠啶虫脒亚慢性暴露致成年后神经系统毒性的研究329㊀1㊀材料与方法(Materials and methods)1.1㊀实验动物及分组选择出生7d的雄性SD大鼠18只,体质量为(35ʃ5)g,由宁夏医科大学实验动物中心提供,实验动物质量许可证SCXK(宁)2020-0001㊂待母鼠适应性饲养1周后,随机分为3组(每组6只),出生20d 断奶后分笼,每笼3只㊂分别设对照组(Control)㊁ACE-15组(15mg㊃kg-1)和ACE-40组(40mg㊃kg-1)㊂每天每只大鼠经口灌胃一次,对照组给予等量玉米油溶剂,连续灌胃9周㊂实验期间大鼠自由饮水㊁摄食,饲养环境温度18~22ħ,湿度40%~70%,每日12h光照12h黑暗㊂1.2㊀主要试剂与仪器啶虫脒(纯度99%,中国北京伊塔生物科技有限公司),SOD测定试剂盒(A001-2-2,中国南京建成生物工程研究所),MDA测定试剂盒(A003-1-2,中国南京建成生物工程研究所),BCA蛋白测定试剂盒(KGP903,中国江苏凯基生物技术股份有限公司),Nissl染色试剂盒(G1430,中国北京索莱宝科技有限公司),兔抗多克隆抗体IL-10(DF6894,美国Af-finity Biosciences公司),兔抗多克隆抗体IL-1β(AF5103,美国Affinity Biosciences公司),β-actin (DF13469,美国Affinity Biosciences公司),辣根酶标记山羊抗兔IgG(ZB-2301,北京中山金桥生物技术有限公司),垂直式蛋白电泳仪(Amersham,Ima-ger600,美国Bio-Rad公司),ECL发光法成像系统(Power Pac Basic,美国Thermo Fisher Scientific公司),图像采集系统显微镜(BX51TF,日本Olympus 公司)㊂1.3㊀实验方法1.3.1㊀大鼠行为学检测开放旷场(OFT)实验在长100cmˑ宽100cmˑ高40cm的无盖方形箱子中进行,将底部平均分为25个方格(5ˑ5),中间9个方格(3ˑ3)定义为中央区㊂应用SMART3.0软件记录10min内大鼠的运动轨迹㊁距离及时间等参数㊂Morris水迷宫(MWM)实验在直径为1.2m的圆形水池进行㊂将水池平均分为4个象限,平台放置于第3象限㊂定位航行期:前4天,每天将大鼠分别从4个不同象限面向池壁放入水中,应用SMART 3.0软件记录大鼠在1min内找到平台的时间(逃逸潜伏期)㊂若超过1min未能找到平台,则引导大鼠到平台上适应30s㊂空间探索期:第5天撤去平台,将大鼠从第3象限面向池壁放入水中,应用SMART 3.0软件记录大鼠在1min内跨平台次数和目标象限游泳速度㊂1.3.2㊀大鼠大脑皮质和海马组织MDA浓度㊁SOD 活性测定㊀㊀使用七氟烷将大鼠麻醉后,迅速剪开胸腹腔,充分暴露心脏,使用注射器经右心耳采集血液,收集于2mL离心管中,静置离心(3600r㊃min-1,10min),取上层清液,按照试剂盒说明书及计算公式,测定大鼠大脑皮质和海马组织中MDA浓度㊁SOD活性㊂1.3.3㊀Western Blot检测大鼠大脑皮质和海马组织中IL-10㊁IL-1β的蛋白表达量㊀㊀按照说明书步骤提取大鼠大脑皮质和海马组织蛋白并进行蛋白定量,蛋白上样量为40μg㊂经质量分数为8%~15%SDS PAGE凝胶电泳分离蛋白,转移蛋白至PVDF膜上,5%脱脂奶粉室温封闭2h㊂用TBST液漂洗3次,每次10min;4ʎC冰箱一抗(1ʒ2000)孵育过夜,TBST液漂洗3次,每次10min;室温下二抗(1ʒ5000)孵育1h,TBST液漂洗3次,每次10min,ECL发光法成像,Image J1.52软件计算其灰度值并进行统计学分析㊂1.3.4㊀制备石蜡切片及染色H&E染色:将切片取出平衡至室温,之后依次放入二甲苯Ⅰ㊁二甲苯Ⅱ各反应10min;连续下行酒精梯度各3min;自来水冲洗2min;苏木素染液浸染6min;自来水冲洗6min;盐酸酒精分化液分化1s,流水冲洗5min;伊红染液染色7min,流水冲洗3 min;连续上行酒精梯度各2min;二甲苯Ⅰ㊁二甲苯Ⅱ各10min;中性树脂封片㊂采用Olympus系统观察染色结果㊂Nissl染色:将切片取出平衡至室温,之后依次放入二甲苯Ⅰ㊁二甲苯Ⅱ各反应10min;连续下行酒精梯度各3min;自来水冲洗2min;将载玻片放入Nissl试剂盒中的试剂A液中,56ħ浸染1h;之后取出载玻片用纯水清洗3遍,每次1min;将载玻片放入Nissl试剂盒中的试剂B液中分化40s;连续上行酒精梯度各1min;二甲苯Ⅰ㊁二甲苯Ⅱ各反应5min;中性树脂封片㊂采用Olympus系统观察染色结果㊂1.4㊀统计学方法数据采用Graphpad8.0软件进行统计学分析,实验数据均用x ʃSEM表示㊂所有数据先进行方差校验,符合正态分布后进行统计分析㊂多组间比较用单因素方差分析(One-way ANOV A),两两比较用330㊀生态毒理学报第18卷Dunnet t 法,P 0.05具有统计学差异㊂2㊀结果(Results )2.1㊀一般状态及体质量变化情况大鼠ACE 暴露9周的体质量变化趋势如图1所示,ACE 干预后每周称量一次空腹体质量,前6周各组体质量稳定上涨无明显差异;第7周㊁第8周和第9周,与对照组相比,ACE 暴露组大鼠体质量上涨均明显下降,具统计学意义(P <0.05㊁P <0.01㊁P <0.001)㊂对照组大鼠摄食㊁饮水和精神状态一般状况良好,毛发顺滑,而ACE 暴露组大鼠毛发粗糙,顺滑度下降㊂2.2㊀行为学实验2.2.1㊀开放旷场实验(OFT)图2(a)展示的是3组大鼠在OFT 实验中的典型轨迹图;图2(b)展示的是3组大鼠旷场内的总运动距离统计结果㊂与对照组比较,ACE -40组大鼠的运动距离显著减少(P <0.05);图2(c)展示的是3组大鼠在中央区运动距离统计结果㊂与对照组比较,ACE -40组大鼠在中央区运动距离明显减少(P <0.01);图2(d)展示了大鼠在中央区运动时间统计结果㊂与对照组比较,ACE -15组(P <0.05)和ACE -40组(P <0.05)大鼠在中央区运动时间明显减少㊂图1㊀啶虫脒(ACE )暴露9周大鼠体质量变化(x ʃSEM ,n =6)注:与对照组比较,*表示P <0.05,**表示P <0.01,***表示P <0.001㊂Fig.1㊀The effect of acetamiprid (ACE)on themean body weight of SD rat (x ʃSEM,n =6)Note:Compared with control group,*represents P <0.05,**represents P <0.01,and ***represents P <0.001.图2㊀ACE 暴露下各组大鼠的OFT 实验结果(x ʃSEM ,n =6)注:(a)大鼠在OFT 实验中的典型轨迹图;(b)运动总距离;(c)中央区移动距离;(d)中央区运动时间;*表示P <0.05,**表示P <0.01㊂Fig.2㊀OFT results of SD rat after exposed to ACE (x ʃSEM,n =6)Note:(a)Trajectories of SD rat after treated with ACE in OFT;(b)Total distance;(c)Movement distance in central area;(d)Duration of movement in the central area;*represents P <0.05,and **represents P <0.01.第2期李姝霖等:新生大鼠啶虫脒亚慢性暴露致成年后神经系统毒性的研究331㊀2.2.2㊀Morris 水迷宫(MWM)3组大鼠逃逸潜伏期统计结果如图3(a)所示㊂与对照组比较,ACE 暴露组逃逸潜伏期变长(P<0.01),与ACE -15组比较,ACE -40组逃逸潜伏期明显延长(P <0.05);3组大鼠在目标象限停留时间统计结果如图3(b)所示㊂与对照组比较,ACE 暴露组在目标象限停留时间减少(P <0.05㊁P <0.01)㊂3组大鼠在MWM 空间探索期典型轨迹图如图4(a)所示;跨平台次数统计结果如图4(b)所示㊂与对照组比较,ACE -40组跨平台次数减少(P <0.01),与ACE -15组比较,ACE -40组明显减少(P <0.01);3组大鼠在平台所在象限的游泳速度统计结果如图4(c)所示㊂与对照组比较,ACE 暴露组游泳速度明显减慢,其中ACE -15组(P <0.05)和ACE -40组(P <0.01)均与对照差异显著㊂2.3㊀氧化应激相关指标及抗氧化酶活性测定如图5所示,与对照组比较,ACE 暴露组大鼠大脑皮质组织MDA 浓度升高,ACE -40组(P <0.05)㊂与ACE -15组比较,ACE -40组MDA 浓度显著升高(P <0.01)㊂ACE 暴露组海马组织中MDA 浓度也升高,ACE -15组和ACE -40组均与之差异显著(P <0.01)㊂图3㊀ACE 暴露下各组大鼠的MWM 定位巡航期实验结果(x ʃSEM ,n =6)注:(a)逃逸潜伏期;(b)目标现象停留时间;*表示P <0.05,**表示P <0.01㊂Fig.3㊀Results of SD rat after exposed to ACE in MWM of positioning cruise period (x ʃSEM,n =6)Note:(a)Escape latency;(b)Target quadrant residence time;*represents P <0.05,and **represents P <0.01.图4㊀ACE 暴露下各组大鼠的MWM 空间探索期实验结果(x ʃSEM ,n =6)注:(a)大鼠在MWM 实验中的轨迹图;(b)跨平台次数;(c)目标现象游泳速度;*表示P <0.05,**表示P <0.01㊂Fig.4㊀Results of SD rat after exposed to ACE in MWM of space exploration period (x ʃSEM,n =6)Note:(a)Trajectories of SD rat after treated with ACE in MWM;(b)Target crossing;(c)Swimming speed in the target quadrant;*represents P <0.05,and **represents P <0.01.332㊀生态毒理学报第18卷㊀㊀ACE暴露后大鼠大脑皮质(a)和海马(b)中的SOD活性如图6所示,与对照组比较,ACE-40组大鼠大脑皮质组织SOD活性显著减少㊂而海马组织SOD活性升高,ACE-15组㊁ACE-40组与对照差异具有统计学意义(P<0.01)㊂2.4㊀Western Blot检测大鼠大脑皮质和海马组织中IL-1β㊁IL-10蛋白表达量结果㊀㊀如图7所示,与对照组比较,皮质中IL-1β蛋白表达量在ACE-15组和ACE-40组均增高(P<0.01);而IL-10蛋白表达含量均降低(P<0.01㊁P<0.001),与ACE-15组比较,ACE-40组IL-10表达量明显减少(P<0.01)㊂海马中IL-1β蛋白表达量在ACE-15组和ACE-40组均增高(P<0.01㊁P<0.001);而IL-10蛋白表达含量均降低(P<0.01㊁P<0.001),与ACE-15组比较,ACE-40组IL-10表达量明显减少(P<0.01)㊂2.5㊀组织病理学ACE暴露下大鼠大脑海马形态结构上的变化如图8所示,H&E结果显示,与对照组比较,ACE-40组DG㊁CA3区出现神经元排列紊乱㊁稀疏和轮廓模糊等现象㊂ACE暴露下大鼠大脑海马神经元情况如图9所示,Nissl结果显示,与对照组比较,ACE 暴露组海马DG㊁CA3区神经元数量减少㊂3㊀讨论(Discussion)自新烟碱类杀虫剂问世以来,新烟碱已成为杀虫剂市场发展速度最快,使用率最高的杀虫剂之一,目前约占市场的1/3[18]㊂然而这类杀虫剂在发挥杀虫除草作用的同时,对环境[19]和非靶标动物[20]也具有危害㊂目前,已有新烟碱类杀虫剂暴露对哺乳动物造成多方面损伤的研究报道㊂Gasmi等[21]将成年大鼠ACE(3.14mg㊃kg-1)暴露90d后,发现线粒体结构损伤,呼吸链功能紊乱㊂Karaca等[22]将8 ~10周龄雄性SD大鼠进行ACE(25mg㊃kg-1㊁35 mg㊃kg-1)暴露90d后,肝肾功能出现一定的损伤㊂图5㊀ACE暴露下大鼠皮质和海马组织中MDA浓度检测结果(x ʃSEM,n=6)注:*表示P<0.05,**表示P<0.01㊂Fig.5㊀Results of MDA concentration in the brain cortex and hippocampus of SD rat after exposure to ACE(x ʃSEM,n=6)Note:*represents P<0.05,and**represents P<0.01.图6㊀ACE暴露下大鼠皮质和海马组织中SOD活性检测结果(x ʃSEM,n=6)注:**表示P<0.01㊂Fig.6㊀Results of SOD activity assay in the brain cortex and hippocampus of SD rat after exposure to ACE(x ʃSEM,n=6)Note:**represents P<0.01.第2期李姝霖等:新生大鼠啶虫脒亚慢性暴露致成年后神经系统毒性的研究333㊀图7㊀ACE 暴露下大鼠皮质和海马组织中IL-1β㊁IL-10蛋白表达量(x ʃSEM ,n =6)注:(a)大鼠皮质组织中IL -1β㊁IL -10蛋白表达量;(b)大鼠海马组织中IL -1β㊁IL -10蛋白表达量;**表示P <0.01㊂Fig.7㊀Expression of IL -1βand IL -10protein in cortical and hippocampal tissues of rats exposed to ACE (x ʃSEM,n =6)Note:(a)IL -1β,IL -10level in the cortex;(b)IL -1β,IL -10level in the hippocampus;**represents P <0.01.图8㊀H&E 染色:大鼠海马DG ㊁CA3区显微结构图注:(a),(d)对照组;(b),(e)15mg ㊃kg -1;(c),(f)40mg ㊃kg -1;标尺=40μm ,n =6;黑色箭头表示细胞结构松散㊂Fig.8㊀H&E staining:Microstructure of DG,CA3region of rat hippocampusNote:(a),(d)Control group;(b),(e)15mg ㊃kg -1;(c),(f)40mg ㊃kg -1;the bar =40μm,n =6;the black arrows indicate loose cell structure.Kagawa 和Nagao [23]将孕期小鼠经口ACE (5mg ㊃kg -1)暴露发现,在胚胎期第6天到第13天间小鼠皮质发育不全,神经发生减少,这提示孕期ACE 暴露会对发育中的神经系统产生毒性作用㊂Dhouib 等[24]对大鼠进行ACE (40mg ㊃kg -1)连续口服21d 实验,暴露后进行斜板测试和前爪握力测试,结果显示ACE(40mg ㊃kg -1)暴露能够产生对大鼠神经肌肉接头毒性作用㊂在海马体中,胆碱能系统对空间学习和记忆形成等认知功能起着至关重要的作用㊂Shamsi 等[25]认为ACE 对哺乳动物的n 型乙酰胆碱受体(nAChR)具有显著的亲和性,是导致哺乳动物学习记忆减退的原因㊂而出生后早期ACE 暴露,是否对其成年后学习记忆等认知功能产生影响,尚不清楚㊂因此,本研究采用OFT 和MWM 进行学习记忆与情绪变化的测试㊂334㊀生态毒理学报第18卷图9㊀Nissl染色:大鼠海马DG㊁CA3区显微结构图注:(a),(d)对照组;(b),(e)15mg㊃kg-1;(c),(f)40mg㊃kg-1;标尺=40μm,n=6;黑色箭头表示尼氏小体消失㊂Fig.9㊀Nissl staining:Microstructure of DG,CA3region of rat hippocampusNote:(a),(d)Control group;(b),(e)15mg㊃kg-1;(c),(f)40mg㊃kg-1;the bar=40μm,n=6;the black arrows indicate the disappearance of Nissl body.㊀㊀研究表明,行为变化是一种早期和敏感的毒理学指标[26]㊂OFT是探究动物在新环境中的焦虑行为和空间探索度的方法㊂已知ACE暴露会改变大鼠的社会性和焦虑行为,成年大鼠口服ACE平均剂量10mg㊃kg-1,连续7d,情境恐惧条件和修正降压行为模型下均表现出学习记忆障碍[27]㊂本研究OFT结果显示,大鼠在中央区运动距离和时间较对照组均减少了,表明ACE的干预对大鼠的精神状态造成了一定影响,大鼠探究行为受到ACE的抑制,回避和焦虑水平增高,适应环境能力下降㊂MWM 是评价动物空间学习记忆与认知功能的实验㊂MWM结果显示,在定位巡航期间,ACE暴露组逃逸潜伏期时间明显延长,表明新生大鼠在亚慢性ACE暴露后,成年期的学习记忆能力变差;在空间探索期,ACE-40组跨平台次数明显减少,表明口服ACE40mg㊃kg-1对大鼠新生期至成年阶段的空间记忆能力造成影响㊂行为学结果说明ACE亚慢性暴露能够对大鼠的认知行为造成影响㊂Ford和Ca-sida[28]的研究表明,与ACE同属新烟碱类杀虫剂的吡虫啉可以透过血脑屏障且蓄积在脑内,影响相应的蛋白表达,造成海马功能下降,表现为学习记忆等行为异常㊂Abd-Elhakim等[29]的研究表明,吡虫啉可造成大鼠在孔板实验和斜面实验中出现神经毒性表现㊂Bhardwaj等[30]的研究也发现长期暴露于吡虫啉的大鼠神经行为学实验表现异常,包括行进距离㊁运动时间等自发运动显著减少,这些研究结果都与本研究的结果一致㊂本研究中H&E与Nissl结果显示ACE-40组的海马神经元较对照组出现形态结构等变化,说明ACE40mg㊃kg-1对大鼠的海马神经元结构造成破坏,这与行为学的结果相对应㊂诸多研究表明,传统杀虫剂在体内代谢会产生活性氧(ROS)等产物,造成脂质过氧化,导致MDA的产生[31]㊂MDA是反映有害物质对生物体细胞氧化损伤的重要指标㊂大脑含有丰富的过氧化物脂肪酸,抗氧化能力相对较弱,因此特别容易受到氧化损伤[32]㊂在细胞水平上,ACE暴露可能以剂量依赖性的方式导致氧化应激介导的抗氧化状态改变[33]㊂本实验结果显示,ACE暴露后大脑皮质和海马均发生脂质过氧化,ACE暴露组MDA浓度较对照组明显升高㊂SOD是机体中一种重要的抗氧化酶,在本实验中脑皮质的SOD活性降低,而海马组织中SOD 活性却上升㊂Gasmi等[21]研究的结果也显示在海马组织中SOD活性上升㊂Panemangalore和Bebe[34]的研究显示,氧化产物的增加会导致SOD活性的抑制㊂Terayama等[35]研究显示,ACE在皮质和髓质㊁间脑㊁海马和纹状体中积累量不同㊂当积累量达到一定程度时机体抗氧化系统的代偿功能丧失,造成SOD的活性抑制,这可能是SOD在不同脑区活性不一致的原因,进一步支持了本研究结果㊂已有研究显示,氧化应激可以增加炎症反应,炎症也可以加重氧化应激[36]㊂炎症因子IL-1β可以反映机体炎症水平和组织的损伤程度[37]㊂Western第2期李姝霖等:新生大鼠啶虫脒亚慢性暴露致成年后神经系统毒性的研究335㊀Blot实验结果显示大脑皮质和海马组织中的IL-1β在ACE暴露组中均上升,抑炎因子IL-10在ACE 暴露组中减少,表明新生大鼠ACE亚慢性暴露能引起中枢神经系统炎症反应㊂之前有研究显示[38], ACE干预可以引起体内B细胞等免疫细胞增殖下调,免疫防御作用降低,产生氧化应激反应,使免疫细胞功能下降,激活巨噬细胞转变成M1型,促进炎症因子产生㊂有研究明确了炎症因子对神经元的损伤作用[39],因此,ACE40mg㊃kg-1的干预引起海马和皮质组织炎症的上调,造成神经元损害,从而出现行为与认知的改变㊂目前研究表明,ROS在炎症反应中起到第二信使的作用,能够促进炎症反应的发生㊂Santhanasabapathy等[40]研究发现在大鼠脑组织中氧化应激反应的发生伴有星形胶质细胞及小胶质细胞的激活,以及促炎因子IL-lβ㊁TNF-a和iNOS的表达升高,同时在大脑皮层㊁海马及纹状体中观察到神经退行性病变的发生,也与我们的研究结果一致㊂氧化应激与炎症的联系最终导致了神经元功能改变是ACE造成大鼠学习行为能力改变的重要原因㊂综上所述,本研究发现新生期大鼠ACE暴露9周可以导致大鼠成年后出现明显的学习记忆与认知功能减退以及海马神经元变化㊂氧化应激和炎症可能是ACE造成中枢神经发育毒性的机制㊂通信作者简介:田建英(1963 ),女,硕士,博士生导师,教授,主要研究方向为神经退行性变的环境机制㊂参考文献(References):[1]㊀Bass C,Denholm I,Williamson M S,et al.The globalstatus of insect 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2015新版啶虫脒乳油安全技术说明书

化学品安全技术说明书产品名称：%吡虫啉乳油按照GB/T 16483、GB/T 17519 编制编制日期：2015年3月10日版本：1.1第一部分化学品及企业标识化学品中文名称：%吡虫啉乳油化学品英文名称：acetamiprid企业名称：地址：邮编：传真号码：电子邮件地：联系电话：企业应急电话：产品推荐及限制用途：农用杀虫剂第二部分危险性概述紧急情况概述:本品低毒，遇明火，高热易燃。

受高热分解放出毒性气体。

GHS危险性类别：急性毒性-经口类别4急性毒性-经皮类别4标签要素：象形图：警示词：警告危险性说明：吞咽有害; 皮肤接触有害;防范说明：预防措施：使用本品应采取相应的安全防护措施，穿防护服戴防护手套、口罩等；避免皮肤接触及口鼻吸入。

使用中不可吸烟、饮水及吃东西，使用后及时清洗手、脸等暴露部位皮肤、并更换衣物。

应急响应：如皮肤接触，立即用水冲洗受污染皮肤；脱去污染的衣着，用肥皂水及清水彻底冲洗皮肤。

如眼睛接触，立即翻开上、下眼睑，用流动清水或生理盐水冲洗至少15min，就医。

如吸入：迅速脱离现场至空气新鲜处，保持呼吸通畅，输氧，进行人工呼吸和心脏按摩术，就医。

如食入：饮足量温水，催吐、就医。

安全储存：本品应贮存在阴凉干燥避光处，注意防潮，防晒，远离火源等热源。

配备相应品种和数量的消防设施。

存储区有合适的材料和措施收集泄漏物。

废弃处置：使用完本品，包装物不得随便丢弃，不得用于盛放农产品或其他食品，应选择安全地点妥善处置。

废弃的产品用控制焚烧法或土壤深埋法处理。

理化危害：因其溶剂为二甲苯，甲醇等有机溶剂遇明火可燃烧、爆炸。

健康危害：低毒，中毒表现有头痛、头晕、无力、恶心、呕吐、腹痛、腹泻、心律紊乱、心前区痛、呼吸困难、大汗、瞳孔缩小等。

环境危害：对环境安全第三部分成份/组成信息物质√混合物组分浓度或浓度范围CAS No.啶虫脒135410-20-7第四部分急救措施急救皮肤接触：立即用水冲洗受污染皮肤；脱去污染的衣着，用肥皂水及清水彻底冲洗皮肤。

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5.2 ACETAMIPRID (246)TOXICOLOGYAcetamiprid is the International Organization for Standardization (ISO)–approved name for (E)-N1-[(6-chloro-3-pyridyl)methyl]-N2-cyano-N1-methyl acetamidine (International Union of Pure and Applied Chemistry). Its Chemical Abstracts Service number is 135410-20-7. Acetamiprid is a neonicotinoid insecticide that is used for the control of sucking-type insects on leafy vegetables, fruiting vegetables, cole crops, citrus fruits, pome fruits, grapes, cotton and ornamental plants and flowers. Acetamiprid is being reviewed for the first time by the Joint FAO/WHO Meeting on Pesticide Residues at the request of the Codex Committee on Pesticide Residues.All critical studies contained statements of compliance with good laboratory practice.Biochemical aspectsAcetamiprid is rapidly absorbed, with a maximum concentration in blood being achieved in approximately 2–3 hours. The extent of absorption was more than 90% of the administered radioactivity. Acetamiprid is widely distributed in the tissues, with highest concentrations being found in the adrenal gland, liver and kidney following oral administration to the rat. The concentration of radioactivity in the brain was lower than the concentration in blood at all time points. No sex differences were observed. The major route of elimination was via urine (53–65%). The recovery of the radioactivity excreted in the bile was less than 20% of the administered dose, which suggests that the bile is not a major route of excretion. The disappearance of radioactivity from the body of the rat was rapid, and there was no indication of accumulation in any tissue. Less than 1% of the administered radioactivity remained in the tissues by day 4 following dosing. The major radioactive compounds in the excreta of rats were acetamiprid (~5–7%), the demethylated compound IM-2-1 (~15–20%), the nicotinic acid derivative IC-O (~8–11%) and the IC-O glycine conjugate IC-O-Gly (~10%). In addition, MeS-IC-O, IM-1-4, IM-2-4, IM-O, IM-1-3 and IM-2-3 were detected, each at less than 2% of the dose. There were several unknown compounds in the urine, with a maximum abundance of 1%. The main metabolic pathway of acetamiprid in rats is the transformation to IM-2-1 by demethylation. IM-2-1 is further metabolized to IC-O, with the release of IS-1-1 and IS-2-1 after cleavage from the side-chains of NI-25 (parent compound) and IM-2-1.Toxicological dataIn mice and rats, the oral median lethal dose (LD50) was in the range of 140–417 mg/kg body weight (bw). Dose-related reversible toxic signs (crouching, tremor, convulsion and mydriasis) were observed. The dermal LD50in rats was greater than 2000 mg/kg bw. When acetamiprid was administered by inhalation through nose-only exposure, the median lethal concentration (LC50) was greater than 1.15 mg/L of air. Mydriasis in many rats and tremor and convulsion in a few rats were observed when acetamiprid was administered by the oral route, and these effects disappeared after 1 day. Acetamiprid was not an irritant in studies of ocular or dermal irritation in rabbits or a dermal sensitizer in the Magnusson and Kligman maximization test in guinea-pigs.Short-term studies of oral toxicity in mice, rats and dogs were conducted using acetamiprid. These studies are characterized by similar toxic responses, such as decreased feed consumption and body weight.In a 13-week study in mice, the no-observed-adverse-effect level (NOAEL) was 400 ppm (equal to 53.2 mg/kg bw per day), on the basis of a significant decrease in total cholesterol level in females at 800 ppm (equal to 106.1 mg/kg bw per day). Tremor, decreased body weight gain, decreased feed consumption, decreased haemoglobin concentration, decreased serum total cholesteroland glucose levels, decreased urinary pH, increased liver to body weight ratio and centrilobular hypertrophy were observed at higher doses.In a 90-day study of oral toxicity in rats, the NOAEL was 200 ppm (equal to 12.4 mg/kg bw per day), on the basis of decreased body weight gain, decreased feed consumption and increased serum total cholesterol levels at 800 ppm (equal to 50.8 mg/kg bw per day).In three oral dog studies (4 weeks, 90 days and 1 year), initial body weight losses and decreased body weight gains were observed in males and females receiving the highest dietary concentrations of acetamiprid. In the 4-week study, the NOAEL was 22 mg/kg bw per day. However, an overall NOAEL for the other two oral dog studies was 800 ppm (equal to 32 mg/kg bw per day).In an 18-month study of toxicity and carcinogenicity in mice, decreased feed consumption was observed in males and females at 1200 ppm. At 400 ppm in males, body weights were decreased, and the body weight gain was statistically significantly decreased compared with controls through 13 weeks of study. At the end of 18 months, mean relative liver weights were increased in males and females receiving 1200 ppm and also in females receiving 400 ppm. On microscopic examination, treatment-related hepatocellular hypertrophy was seen in male and female mice receiving 1200 ppm after 12 and 18 months of treatment. These microscopic findings are considered to be an adaptive response of the liver to exposure to acetamiprid. The NOAEL was 130 ppm (equal to 20.3 mg/kg bw per day), based on transient decreased body weight observed at 400 ppm (equal to 65.6 mg/kg bw per day) in males. There was no evidence of any carcinogenic effect in mice.The 2-year study of toxicity and carcinogenicity in rats demonstrated an increased incidence of clinical signs, such as rales, hunched posture and laboured breathing, in the 400 and 1000 ppm dose groups. The body weights of the 1000 ppm males and females and the 400 ppm females (until week 100) were statistically significantly lower than those of controls during the study. Trace to mild centrilobular hepatocellular hypertrophy and vacuolation were seen at 400 ppm and above. Incidences of mammary gland adenocarcinomas and hyperplasias were increased in females at 1000 ppm (equal to 60 mg/kg bw per day); however, incidence levels were within normal limits for ageing Crl:CD rats, and therefore these lesions are considered to be unlikely to be due to an endocrine or carcinogen effect of acetamiprid. Because the observation of rales at 160 ppm was not correlated to the other clinical signs, such as laboured breathing, moribundity, hunched posture and decreased activity, the NOAEL in this study was 160 ppm (equal to 7.1 mg/kg bw per day), based on hepatocyte vacuolation at 400 ppm (equal to 17.5 mg/kg bw per day). Acetamiprid was not carcinogenic in rats.Acetamiprid was tested for genotoxicity in an adequate range of assays, both in vitro and in vivo. No significant result is obtained in these tests, except for chromosomal aberration induction in vitro. In vivo, there was no confirmation of chromosomal aberration in a number of tests, and there was no evidence of induction of deoxyribonucleic acid (DNA) damage.The Meeting concluded that acetamiprid is unlikely to be genotoxic in vivo.In view of the lack of genotoxicity in vivo and the absence of carcinogenicity in rats and mice, the Meeting concluded that acetamiprid is unlikely to pose a carcinogenic risk to humans.In a two-generation study in rats, the NOAEL for systemic parental toxicity was 100 ppm (equal to 6.67 mg/kg bw per day), on the basis of a decline in body weights and feed consumption and an increased incidence of hepatocellular hypertrophy and vacuolation at 280 ppm (equal to 18.9 mg/kg bw per day) and above. The NOAEL for offspring toxicity was 280 ppm (equal to 13.9 mg/kg bw per day), on the basis of decreases in body weight gain in both generations and reduced postnatal survival in the F2 offspring at 800 ppm (equal to 38.7 mg/kg bw per day). However, there are no effects on reproduction with treatment up to 800 ppm (equal to 38.7 mg/kg bw per day), the highest dose tested.In a study of developmental toxicity in rats, the NOAEL for maternal toxicity was 16 mg/kg bw per day, based on decreased feed consumption and body weight gain during the treatment period in maternal rats in the 50 mg/kg bw per day group at scheduled sacrifice. The developmental NOAELin rats was 16 mg/kg bw per day, based on the increased incidence of fetuses with shortening of the 13th rib at 50 mg/kg bw per day.In a study of developmental toxicity in rabbits, the NOAEL for maternal toxicity was 15 mg/kg bw per day, based on decreased feed consumption and body weight gain during the treatment period at 30 mg/kg bw per day. The developmental NOAEL was 30 mg/kg bw per day, the highest dose tested.The Meeting concluded that acetamiprid was not teratogenic in rats or rabbits.In an acute oral neurotoxicity study, increased urination frequency and reduced locomotor activity were observed at doses of 30 mg/kg bw and above. Other clinical signs of neurotoxicity (e.g., hunching, tremors) were observed at higher doses. No apparent effects on sensory systems or evidence of neuropathology was seen. The NOAEL was 10 mg/kg bw, based on evidence of increased urination frequency (males) and a statistically significant reduction of locomotor activity (males) at30 mg/kg bw.A 13-week dietary neurotoxicity study in rats did not result in any changes that were considered indicative of neurotoxicity. The NOAEL was 200 ppm (equal to 14.8 mg/kg bw per day), on the basis of lower body weights and feed consumption at 800 ppm (equal to 59.7 mg/kg bw per day).A developmental neurotoxicity study in rats revealed the NOAEL for maternal toxicity, developmental toxicity and developmental neurotoxicity to be 10 mg/kg bw per day, based on a reduction in body weight gain in dams during the first 3 days of dosing (gestation days 6–9), decreased feed consumption in F0animals, early postnatal mortality, reduced post-weaning body weights and deficits in auditory startle response without neuropathology or changes in brain morphometry in F1 animals at 45 mg/kg bw per day.Acetamiprid did not cause delayed neuropathy in hens.Studies for immunotoxicity in mice (highest dose tested was 157 mg/kg bw per day) and rats (highest dose tested was 67.7 mg/kg bw per day) indicated no specific effect on immune function as assessed by the measurement of antigen-specific T cell–dependent antibody formation.Toxicological data on impurities and metabolitesAcute toxicity studies and studies of genotoxicity have been undertaken for four compounds that are present as impurities in technical acetamiprid. None of them were genotoxic in a number of assays, and they had acute oral LD50values in rats between 603 and greater than 5000 mg/kg bw. Nine compounds identified as plant metabolites are IM-1-3, IM-1-4, IM-2-1, IM-2-3, IM-2-4, IM-0, IC-0, IS-1-1 and IS-2-1. None were genotoxic in a number of assays, and they had acute oral LD50 values in rats between 900 and greater than 5000 mg/kg bw. The NOAEL following repeated exposure of rats to diets containing IM-1-4 for 13 weeks was 600 ppm (equal to 36.5 mg/kg bw per day), based on effects on spleen (increased pigments in splenic sinusoids) at 1800 ppm (112.2 mg/kg bw per day) in treated males. The NOAEL for IM-0 in a 13-week study in rats was 800 ppm (equal to 48.9 mg/kg bw per day), on the basis of eosinophilic intranuclear inclusions seen in proximal tubular epithelium of kidneys at 4000 ppm (250.1 mg/kg bw per day) in males. All the impurities and metabolites were of lesser toxicity than the parent (acetamiprid).No adverse health effects or poisoning in manufacturing plant personnel or in operators and workers exposed to acetamiprid have been reported.Three cases of intentional poisoning with acetamiprid formulation have been reported. In one case, the concentration of acetamiprid in blood was measured at the time of reporting for treatment. In all cases, some signs similar to those associated with acute organophosphate intoxication were reported. Supportive treatments for a variety of signs were sufficient for recovery, and all recovered within 24–48 hours of the initiation of treatment.The Meeting concluded that the existing database on acetamiprid was adequate to characterize the potential hazards to fetuses, infants and children.Toxicological evaluationThe Meeting established an acceptable daily intake (ADI) of 0–0.07 mg/kg bw on the basis of the NOAEL of 7.1 mg/kg bw per day from the 2-year study of toxicity and carcinogenicity in rats, based on clinical signs and hepatocyte vacuolation seen at 17.5 mg/kg bw per day. A safety factor of 100 was applied. This ADI was supported by the NOAEL of 6.67 mg/kg bw per day observed in a two-generation study of reproductive toxicity in rats on the basis of decreased parental body weight gain and feed consumption and hepatocyte vacuolation at 18.9 mg/kg bw per day.The Meeting established an acute reference dose (ARfD) of 0.1 mg/kg bw on the basis of a NOAEL of 10 mg/kg bw in an acute neurotoxicity study in rats, based on evidence of neurotoxicity, decreased locomotor activity and increased urination frequency. This ARfD was supported by the NOAEL for maternal toxicity in the developmental neurotoxicity study of 10 mg/kg bw per day, based on reduced body weight gain in dams during the first 3 days of dosing (gestation days 6–9).A toxicological monograph was prepared.Levels relevant to risk assessmentSpecies Study Effect NOAEL LOAELMouse Eighteen-month study oftoxicity andcarcinogenicity a Toxicity 130 ppm, equal to20.3 mg/kg bw perday400 ppm, equal to65.6 mg/kg bw per dayCarcinogenicity 1200 ppm, equal to214.6 mg/kg bw perday b—Rat Two-year study oftoxicity andcarcinogenicity a Toxicity 160 ppm, equal to7.1 mg/kg bw per day400 ppm, equal to17.5 mg/kg bw per day Carcinogenicity 1000 ppm, equal to60 mg/kg bw per day b—Two-generation study of reproductive toxicity a Offspring toxicity 280 ppm, equal to13.9 mg/kg bw perday800 ppm, equal to38.7 mg/kg bw per dayReproductivetoxicity800 ppm, equal to38.7 mg/kg bw perday b—Parental toxicity 100ppm, equal to6.67 mg/kg bw perday280 ppm, equal to18.9 mg/kg bw per dayDevelopmental toxicity study c Maternal toxicity 16 mg/kg bw per day 50 mg/kg bw per day Embryo and fetaltoxicity16 mg/kg bw per day 50 mg/kg bw per dayAcute neurotoxicity study c Acuteneurotoxicity10 mg/kg bw 30 mg/kg bwDevelopmental neurotoxicity study c Developmentalneurotoxicity10 mg/kg bw per day 45 mg/kg bw per dayRabbit Developmental toxicity Maternal toxicity 15 mg/kg bw per day 30 mg/kg bw per daySpecies Study Effect NOAEL LOAEL study c Embryo and fetaltoxicity30 mg/kg bw per day b—Dog Ninety-day and 1-yearstudies of toxicity a,d Toxicity 800 ppm, equal to32 mg/kg bw per day1500 ppm, equal to55 mg/kg bw per daya Dietary administration.b Highest dose tested.c Gavage administration.d Two studies combined.Estimate of acceptable daily intake for humans0–0.07 mg/kg bwEstimate of acute reference dose0.1 mg/kg bwInformation that would be useful for the continued evaluation of the compoundResults from epidemiological, occupational health and other such observational studies of human exposureCritical end-points for setting guidance values for exposure to acetamipridAbsorption, distribution, excretion and metabolism in mammalsRate and extent of oral absorption Rapid and almost completely absorbed (> 90%) Distribution Widely distributed; highest concentrations in adrenal, liverand kidneyPotential for accumulation No evidence of accumulationRate and extent of excretion Rapid, more than 90% within 96 h, mainly via urine Metabolism in animals Moderately metabolized; the major radioactive compounds inthe excreta of rats were acetamiprid itself and IC-O glycineconjugateToxicologically significant compounds(animals, plants and the environment)Acetamiprid (parent compound)Acute toxicityRat, LD50, oral 140–417 mg/kg bwRat, LD50, dermal > 2000 mg/kg bwRat, LC50, inhalation > 0.30 mg/L (whole-body exposure)> 1.15 mg/L (nose-only exposure)Rabbit, dermal irritation Non-irritantRabbit, ocular irritation Non-irritantGuinea-pig, dermal sensitization (Magnussonand Kligman test)Non-sensitizerShort-term studies of toxicityTarget/critical effect Increased cholesterol, decreased body weight, decreased feedconsumptionLowest relevant oral NOAEL 53.2 mg/kg bw per day (13-week study in mice) GenotoxicityNot genotoxic in vivoLong-term studies of toxicity and carcinogenicityTarget/critical effect Increased clinical signs; hepatic vacuolationLowest relevant NOAEL 7.1 mg/kg bw per day (rats)Carcinogenicity Not carcinogenic in rats or miceReproductive toxicityReproduction target/critical effect NoneLowest relevant reproductive NOAEL 38.7 mg/kg bw per day, highest dose tested Developmental target/critical effect Skeletal anomaliesLowest relevant developmental NOAEL 16 mg/kg bw per day (rat)Neurotoxicity/delayed neurotoxicityAcute neurotoxicity target/critical effect Motor activity and increased frequency of urination Lowest relevant acute neurotoxic NOAEL 10 mg/kg bwSubchronic neurotoxicity target/critical effect Not neurotoxic (rats)Deficits in auditory startle responseDevelopmental neurotoxicity target/criticaleffectLowest relevant developmental neurotoxic10 mg/kg bw per day (rat)NOAELImmunotoxicity28-day immunotoxicity Not immunotoxic (mice and rats)Medical dataNo significant health effects were reported amongmanufacturing personnel; however, three cases of intentionalpoisoning have been reported with some signs similar to thoseof acute organophosphate poisoningSummaryValue Study Safety factor ADI 0–0.07 mg/kg bw Two-year rat study (supported by parental100toxicity in the multigeneration rat reproductionstudy)ARfD0.1 mg/kg bw Acute neurotoxicity, rat (supported by maternal100toxicity in the developmental neurotoxicity ratstudy)RESIDUE ND ANALYTICAL ASPECTSAcetamiprid is a neonicotinoid insecticide with contact and stomach action against a range of Hemiptera , Thysanoptera and Lepidoptera plant pests, acting as an agonist of the nicotinic acetylcholine receptor in the insect central nervous system. It exhibits translaminar activity in plants and is authorised for use in North America, Europe and in a number of countries in Asia and the Pacific.Residue and analytical aspects of acetamiprid were considered for the first time by the presentmeeting. The manufacturer submitted studies on metabolism, analytical methods, authorised uses, supervised field trials, the effects of processing, freezer storage stability, environmental fate in soil and rotational crop residues.Acetamiprid, ((E)-N 1-[(6-chloro-3-pyridyl)methyl]-N 2-cyano-N 1-methylacetamidine) ispartially soluble in water (3-4 g/litre), stable to hydrolysis and photolysis, has a log P OW of 0.8 and is soluble in acetone, methanol, ethanol, dichloromethane, and acetonitrile.The following abbreviations are used for the metabolites discussed below:Animal metabolismThe Meeting received acetamiprid metabolism studies on animals (rats, lactating goats and laying hens) using 14C-acetamiprid (labelled in the 2 and 6 positions of the pyrimidine ring).In rats, acetamiprid is rapidly and almost completely absorbed and is widely distributed intothe tissues, being found at highest concentrations in GI tract, adrenal gland, liver and kidney, following oral administration to the rat. The major route of elimination was via the urine and bile (relevant but not a major route in excreta). The disappearance of radioactivity from the body of the rat was rapid and there was no indication of accumulation in any tissue. Less than 1% of the administered radioactivity was left in the tissues by day four following dosing. The major radioactive compounds in the excreta of rats were acetamiprid (approx. 5–7%); the demethylated compound IM-2-NClCH 3CH 3C N CNCH 2N1(approximately 15–20%), the nicotinic acid derivative IC-O (approximately 8–11%) and the IC-O glycine conjugate IC-O-Gly (approximately 10%). In addition, MeS-IC-O, IM-1-4, IM-2-4, IM-O, IM-1-3 and IM-2-3 were detected, but they were less than 2% of dose. There were several unknown compounds in urine with a maximum abundance of 1%.The main metabolic pathway of acetamiprid in rats is the transformation to IM-2-1 by demethylation which is further metabolized to IC-O with the release of IS-1-1 and IS-2-1 after the cleavage from the side chains of IN-25 and IM-2-1.Lactating goats were orally dosed twice daily for 7 days with encapsulated [pyridine-2, 6-14dosing period, the goats were sacrificed 22 hours after the last administration.Most of the administered radioactivity (AR) was excreted via urine or faeces (about 95–99% AR) and less than 1% AR in milk (reaching a plateau after about 3 days). In tissues, radioactivity did not exceed 1.6% AR and in milk, about 94–96% TRR was found in the whey with about 3–5% TRR occuring in milk fat and precipitated milk proteins.The predominant residue in milk, liver and kidney was the IM-2-1 metabolite (70–89% TRR) and in muscle, the major residue was IM-2-2 (about 50% TRR), with the IM-2-3 and IM-2-4 metabolites also being found at 6% and 13% TRR respectively. Acetamiprid (parent) was only found in milk, at less than 10% TRR and < 0.005 mg/kg.Laying hens (five hens per dose group) were dosed each morning for 14 days with [pyridine-2, 6-14C]-acetamiprid at dietary equivalent levels of 1.1 ppm or 12.5 ppm. At the end of the 14-day dosing period, the hens were sacrificed about 24 hours after the last administration.Most of the applied radioactivity was excreted or found in the cage wash (93–97% AR). Small amounts of radioactivity were detected in edible organs/tissues (0.7–0.8% AR) with about 1.3% AR found in eggs (reaching a plateau after about 8–11 days). In liver and skin, residues were about 0.1% AR and 0.3% AR in muscle.The IM-2-1 metabolite was the predominant residue, at 83–86% TRR in egg white, about 60% TRR in egg yolk, 65–69% TRR in liver and 53–62% TRR in muscle and skin. The other metabolite found at more than 10% TRR was the IM-2-3 in muscle (17– 21% TRR). Metabolite IM-2-5 was the predominant residue in egg yolks (27% TRR) and IC-0 was found in skin at about 13% TRR. Acetamiprid (parent) was not found in any tissues or in eggs.In summary, acetamiprid metabolism in animals is similar, with more than 95% of the residues being eliminated in excreta and less than 2% remaining in tissues or present in eggs or milk. Residues of the parent acetamiprid were not found (except at low levels in milk), and the predominant residue in most animal products was the IM-2-1 (53–89% TRR) with IM-2-2 occurring in goat muscle at about 50% TRR). The IM-2-4 and IM-2-3 metabolites were also found in muscle at 13–21% TRR, with the IM-2-5 metabolite being found at about 27% TRR in egg yolks.The proposed metabolic breakdown of acetamiprid in both goats and hens involves degradation to IC-0 or demethylation to IM-2-1 with the IM-1-2 metabolite converting to the amide (IM-2-2) or IM-2-3 and the subsequent formation of the IM-2-4 and IM-2-5 metabolites.Plant metabolismThe meeting received plant metabolism studies in apples, eggplant, cabbage, cotton and carrot following foliar applications of [pyridine-2, 6-14C]-acetamiprid and an additional study with cabbages treated with [CN-14C]-acetamiprid (both as a foliar application and a soil treatment).In apple fruit, more than 98% of the radioactivity was recovered from the surface wash and14 days and to about 6% TRR for fruit sampled 28 and 62 days after treatment. Residues in flesh increased to 48% TRR after 14 days and to about 78% TRR at the end of the 62-day study period.Acetamiprid (parent) was the predominant residue, making up more than 79% TRR. Minor metabolites (IM-2-1 and IM-0-Glc) were found at maximum 3.7%TRR and 1.8%TRR, respectively.For apple leaves, more than 98% of the radioactivity was recovered from the surface wash and extracts from leaves. Initial residues in surface washes decreased from 99% to about 43% TRR at the end of the 90-day study period and the residues in the leaf extracts increased to about 51% TRR (11.8 mg/kg eq). Translocated radioactivity in untreated leaves was less 0.04 mg/kg.The majority of the radioactivity was the unchanged acetamiprid, making up 90% or more of the TRR in the first 14 days after treatment, declining to 49% TRR after 90 days. The main metabolite found above 5% TRR was the IM-2-1 metabolite, present at about 10% TRR after 62 days and about 16% TRR after 90 days. The only other metabolite present at more than 5% TRR was IM-0-Glc (max 8.3% TRR at day-90).leaves. Translocated radioactivity was negligible. Acetamiprid was the major residue, making up about 85–89% TRR in leaves and 94–95% TRR in fruit. Of the three identified metabolites, IM-2-1 was present in fruit at 0.4% TRR and 1.8% TRR in leaves and the IM-0 metabolite and its glycoside were identified in leaves at 0.6% TRR and 4.6% TRR respectively.For following foliar treatments with [pyridine-2, 6-14C]-acetamiprid, surfacestudy period (day-63). Residues in the extracts from washed plants increased accordingly, from 15% TRR (day-0) to 83.5% TRR (day-63). Acetamiprid was the major residue component in leaves, found at about 67–91% TRR with residues of the IM-2-1 metabolite increasing over the study period to a maximum of about 7% TRR (day-63). No parent residues were measured in mature cabbage heads with the wrapper leaves removed, with the major residue being the IC-0 metabolite (about 46% TRR or 0.03 mg/kg).In cabbages grown in soil treated with [pyridine-2, 6-14C]-acetamiprid, radioactivity wasday study period. Acetamiprid was also the only major residue in both leaves and roots, initially found at about 90% TRR (leaves) and 78% TRR (roots), decreasing to 60% TRR (leaves) and 50% TRR (roots) after 28 days. The IM-1-4 metabolite was the only other identified metabolite present at more than 5% TRR, being found in roots after 28 days.An additional study on cabbages treated with a foliar application of [CN-14C-acetamiprid]after 63 days, with residues in the extracts from washed leaves increasing to about 78% TRR at the end of the study period. The major residue was the unchanged acetamiprid, making up more than 98% TRR (to day-7) and about 65% TRR by day-68.For carrots treated twice with [pyridine-2, 6-14C]-acetamiprid as foliar sprays, total radioactivity in carrots (including tops) at harvest was less than 0.1 mg/kg acetamiprid equivalents, mostly in the tops (0.44 mg/kg), with about 0.08 mg/kg in the roots. The main components found at harvest (2 weeks after the second treatment), in the carrot tops were IM-0-Glc (33% TRR), the parent acetamiprid (27% TRR) and IM-1-4 (15% TRR) with no other components exceeding 6% TRR. In the carrot roots the main components were acetamiprid (30-34% TRR and 0.03 mg/kg) and IC-0 (17–31% TRR and 0.02 mg/kg).In cotton seed and gin trash from plants treated with four foliar applications of [pyridine-2, 6-14found at 50% TRR (1.4 mg/kg) in the 14-day PHI samples and at 45% TRR (0.71 mg/kg) in the 28-day PHI samples.. The IC-0 metabolite was the predominant residue in cotton seed, found in the 14-day PHI samples at 46% TRR (0.69 mg/kg), decreasing to 24% TRR (0.27 mg/kg) in the 28-day samples.。