水环境中有机磷酸酯的污染现状及其生物毒性

曾佳敏,钟仕花,钱 伟,袁圣武,朱小山,3*

水环境中有机磷酸酯的污染现状及其生物毒性

曾佳敏1,钟仕花2,钱 伟1,袁圣武1,朱小山1,3*

(1.清华大学深圳国际研究生院海洋工程研究院,广东 深圳 518055；2. 深圳市农产品质量安全检验检测中心,广东 深圳 518055；3.南方海洋科学与工程广东省实验室(珠海),广东 珠海 519000)

为有效评估有机磷酸酯(OPEs)潜在的生态健康风险,综述了OPEs在全球水和沉积物中的污染现状,并重点关注OPEs对水生生物的毒性效应,根据浮游生物、游泳生物和底栖生物等不同生物类群的特点分析其潜在的毒性作用机制,进而展望本领域未来的研究方向和科学问题,以期有效评估OPEs的生态效应和健康风险,推动我国OPEs食品安全监控和生态毒理学研究,为规范其绿色应用提供参考.

水环境；有机磷酸酯(POEs)；污染；生物富集；毒性效应

有机磷酸酯(OPEs)是一类磷酸酯合成衍生物,因其良好的阻燃性能广泛应用于建材、纺织、化工以及电子等行业[1-2].近年来,随着多溴联苯醚(PBDEs)等溴化阻燃剂在全世界范围内被禁止使用, OPEs作为阻燃剂的使用量快速增长,从2011年的500kt增加到2018年的2800kt[1-4].OPEs根据取代基结构不同可以分为烷烃类OPEs、含氯类OPEs和芳烃类OPEs三大类,表1列举了常见OPEs及其理化性质.不同结构的OPEs其使用范围有所不同,其中含氯类OPEs和芳烃类OPEs主要作为塑料制品、纺织物、电子设备以及建筑、家装材料的阻燃剂;烷烃类OPEs则主要用作增塑剂、去泡剂、液压剂等[5].大部分OPEs主要以物理混合方式而非化学键合成方式添加到聚合物材料中,在产品生命周期中极易通过挥发、浸出、磨损和溶解等过程从材料中释放到周围环境.目前,在水和沉积物中均已检测到大量OPEs的存在[5].通过生物体的呼吸、摄食等生命活动,也有越来越多的OPEs在生物体内累积,并沿食物链进行传递,可能对整个生态系统造成危害.因此,OPEs已被认定为一类新型有机污染物,并受到全球的高度关注[1].早在2000年,含氯类OPEs被列入欧盟优先控制污染物名单[6].2014年欧盟开始限制儿童玩具中磷酸三(2-氯乙基)酯(TCEP)和磷酸三(1,3-二氯异丙基)酯(TDCPP)的使用[7].美国也针对消费品中的有机磷阻燃剂纷纷出台禁/限用要求,包括所有卤系有机磷酸酯阻燃剂,尤其是TCEP、TDCPP等[8].但迄今为止,关于OPEs在水环境中的赋存状态、污染程度和毒性效应的相关研究仍较少.为更全面有效地评估OPEs潜在的生态和健康风险,本文在分析全球水环境中OPEs污染现状基础上,重点总结OPEs对水生生物的毒性效应及其毒性机制,概括了目前研究中存在的问题,并提出未来的研究方向.

表1 常见OPEs的名称及理化性质

①数据来自US EPA(2020),其中logKOW为正辛醇-水分配系数(Octanol-Water Partition Coefficient),WS为水中溶解度,Vr为蒸汽压;②TCP为磷酸三邻甲苯基酯(Tri‑o‑cresyl phosphate,78-30-8)、磷酸三间甲苯基酯(Tri‑m‑cresylphosphate,563-04-2)、磷酸三对甲苯基酯(Tri‑p‑cresyl phosphate,78-32-0)混合物,图中分子结构用磷酸三对甲苯基酯结构式表示.

1 水环境中OPEs的污染现状

水环境是OPEs的重要归宿之一.如图1所示,大量生产的OPEs主要经以下几种途径进入水环境:①生产、生活中OPEs经污水处理厂出水排放[9-10];②固体废物处理厂等集中处理、填埋区渗滤液中OPEs的点源排放[11-12];③生产和生活场景中室内灰尘、粉尘中OPEs无管理排放,并随大气环流、降雨等过程再输入陆地及海洋中[13-15].OPEs一旦进入水环境,便受到不同水动力作用的影响,发生复杂的迁移、转化,其存在形式、分布状况及毒性效应不断改变.OPEs因其理化性质的差异,在水中的稳定性各不相同.例如,TMP极性强、水溶解度大且易挥发,而TEHP则难溶于水且不易挥发.在中性条件下,大多数磷酸三酯不易水解,但是在碱性条件下或有磷酸酯酶存在时,水解过程会显著加剧[16].含氯类OPEs如TCEP、TCPP和TDCPP在水环境中很难发生转化或者降解[17].水溶性较差的OPEs,可能更容易吸附在沉积物中;即便部分水溶性好的OPEs,也可通过和水体中有机质、胶体和浮游生物等颗粒相结合,再经重力作用沉降到沉积物中.OPEs在水和沉积物中的大量存在,使得水环境被认为是OPEs最终的“汇”.目前,全球各类水体和沉积物中,均已检测到大量OPEs的存在(表2和3).

图1 水环境中OPEs的来源及迁移途径示意

1.1 水相中OPEs的污染现状

表2和图2总结了全球范围内部分水体包括海洋、河流、湖泊和城镇污水中OPEs的浓度水平.从水中总浓度来看,OPEs在水相中的全球浓度分布极不均匀,地表水浓度最高已超过1000ng/L,例如澳洲城市地表水[18-19];但也有不少地区浓度低至1ng/L,甚至未检出,如美国密歇根湖水或北极海水[20-21].人类的生产和生活活动或是造成OPEs分布不均的关键因素.高度城市化地区附近的水体中OPEs含量较高,水环境中可检测到数百ng/L或更高浓度的OPEs,例如韩国洛东江[22](483.45ng/L)、日本东京湾水体[23](284ng/L)、法国罗纳河[24](128.90ng/L)、悉尼地表水[19](1060ng/L)等.而人类活动较低的地区,例如美国密歇根湖及其支流中检测到OPEs的水平相对较低,范围从10～50ng/L[20,25].另外,海水中OPEs的浓度比淡水中要低.即便在OPEs浓度较高的香港海域[23],其浓度值(181.93ng/L)仍远小于陆地水域中的OPEs浓度.是否由于OPEs在海洋中被大量海水稀释,还是其他原因,仍有待查证.

表2 全球水体环境中OPEs的浓度数据(ng/L)

续表2

图2 水环境中OPEs的浓度分布

此外,不同地区和不同类型水环境中优势OPEs种类明显不同.在韩国河流、美国五大湖及其支流、日本东京湾水体中,TCEP和TCPP等含氯类OPEs的含量最为丰富[22-23,25-26].这与含氯类OPEs具有更强的持久性,在水中难以降解有关[6].而与国外相比,国内检测到的OPEs并非都以含氯类为主.TEP等烷烃类OPEs在中国黄河口、渤海湾近海水样中分布也十分广泛[23,27];中国南方珠江三角洲地区烷烃类OPEs占48%,含氯类OPEs占21%[23].这反映了不同地区使用的OPEs数量、类型和工业开发活动的差异[1].

1.2 沉积相中OPEs的污染现状

OPEs通过自身沉降或与水中其他物质结合后共沉降进入沉积物中.但目前,相对水体而言,有关沉积物中OPEs的调查还较少.表2和图3总结了全球范围内,OPEs在部分河流、湖泊及海洋沉积物中的浓度分布.OPEs在所有调查区域均有检出,甚至在海底[28]和南极[29]等人迹罕至之处的沉积物中也检测到OPEs的存在,进一步证实OPEs的全球污染.沉积物中OPEs总浓度范围从几十到数百ng/g dw(干重),较其在水中的变化小,可能与OPEs在沉积物中的迁移性能较弱有关,这也说明沉积物可能是OPEs的重要赋存库,可在长时间尺度上不断积累.有趣的是, OPEs在沉积物中的总浓度与其在水相中总浓度规律类似,在不同国家之间以及同一国家不同地域之间的污染程度存在明显差异(图3).这一现象很大程度上归因于人类活动的地域差异,以及不同地区间OPEs使用量、应用类型和经济发展水平等方面的差异.例如,在海底岩芯(41.6ng/g dw)和南极沉积物(3.66ng/g dw)中检测到较低的OPEs浓度[28-29];而在发达的欧洲Evrotas、Adige和Sava三大流域[30]、西班牙流域[31]、荷兰西谢尔特河口[32]、美国旧金山湾区[33]的沉积物样品中均检测到较高浓度的OPEs.

中国沉积物中OPEs的污染现状也不可小觑.截至目前,已调查区域尽管仅有渤海沿海海域[28,34]、太湖[35]、珠江三角洲地区[36-37]和广西沿海湾区[38]等地.但所有调查区域均有检出,其中渤海莱州湾沉积物中OPEs浓度高达300ng/g dw[34];珠江三角洲地区沉积物中也检测到高OPEs含量,浓度范围为8.30～ 470ng/g dw[37];太湖沉积物中OPEs总浓度相对较低,范围是3.38～14.26ng/g dw[35].从已有数据来看,我国和世界其他地区沉积物OPEs的污染程度类似,但是在主要OPEs污染物种类方面稍有不同:欧美沉积物中含氯类OPEs如TCPP、TCEP等占总OPEs浓度的比例较中国的高;中国沉积物中主要以TnBP、TBOEP等烷烃类OPEs为主,也有一定比例的TCEP、TCPP等含氯类OPEs存在(图3).

图3 沉积环境中OPEs的浓度分布

表3 全球沉积物中OPEs的浓度数据(ng/g dw)

续表3

2 OPEs对水生生物的毒性效应及机制

OPEs已在水环境中大量存在并随时间推移不断富集,其对水生生物和人类健康的风险受到全球环境和毒理学家的高度重视.目前,已有大量报道证实OPEs在水生生物体内累积,但是有关OPEs毒性效应及其作用机制的研究仍较少[34,39].最新研究证实OPEs暴露能对浮游生物、鱼类和底栖生物等造成伤害(表4),但总体所用受试生物及被研究OPEs种类仍较少,且缺乏环境浓度下长期慢性暴露等毒性数据,相关毒理学机制也有待进一步明确.

表4 不同OPEs对水生生物毒性效应

注:① L(E)C50值、NOEC值来源于文献[17].

2.1 OPEs对浮游生物的毒性效应

目前,OPEs对浮游生物的毒性效应研究仍较少,已知仅有TnBP、TDCPP和TPHP 3种OPEs的浮游植物毒性以及TnBP、TBOEP、TCEP、TCPP、TDCPP、TPHP和TCP 7种OPEs的浮游动物毒性研究结果(表4).

如图4所示,OPEs对浮游植物的毒性表现为:生长抑制、渗透压调节干扰、细胞膜损伤和细胞形态的改变,其机制与OPEs引起的氧化应激和脂质过氧化以及细胞的代谢功能受损有关.对不同的OPEs种类而言,TDCPP(2～10mg/L)显著抑制斜生栅藻和三角褐指藻的生长,随暴露剂量增加生物量减少,表现出明显的剂量-效应关系[42-43].在植物细胞中,叶绿体被认为是活性氧物质(ROS)产生的主要场所[44].进入藻类细胞后,TDCPP通过抑制光合作用、叶绿素合成和光系统中的光捕获,导致藻体内ROS增加,脂质过氧化水平升高,产生膜破坏使个体凋亡,最终抑制种群增长.代谢组学和转录组学鉴定出52种差异代谢物,其中与脂质代谢相关的代谢物水平下调[42];与光合作用天线蛋白、碳代谢、细胞周期和过氧化物酶体有关的基因表达也下调,为上述现象提供了关键证据[43].TPHP的暴露也会抑制斜生栅藻和小球藻的生长,但小球藻随着暴露时间增加,细胞生长呈现恢复趋势.代谢组学分析表明,TPHP诱导小球藻脂质代谢物(MGDG和DGDG)累积,通过呼吸增强补偿应激反应中的能量损失,并改善膜结构以抵消渗透压增强压力,提升耐受性;而暴露于TPHP后斜生栅藻出现渗透压增强(缬氨酸,脯氨酸和棉子糖增加)和膜脂解代谢反应增强[45]现象,使耐受性下降.Liu等同样发现,TnBP暴露下三角褐指藻细胞的变形和细胞膜受损的现象,并证实TnBP暴露诱导ROS增加,然后通过脂质过氧化引发膜损伤,改变膜的完整性和通透性,最终触发细胞凋亡[46].实际上,脂质成分是细胞膜的重要结构成分,也是细胞渗透调节的关键因子,此类OPEs通过氧化伤害对细胞脂质代谢产生影响可能是其重要的致毒机制.

图4 OPEs对浮游植物的毒性途径示意(修改自文献[43])

OPEs对浮游动物的毒性效应已经开始受到关注.浮游动物中大型溞和卤虫是两类公认的标准实验生物.表4总结了7种OPEs(TnBP、TBOEP、TCEP、TCPP、TDCPP、TPHP和TCP)对大型溞的急性毒性效应.可见,不同的OPEs其毒性效应相差甚远,芳烃类TPHP的急性48h-EC50(50% Effiective Concentration,半数有效浓度(下同))为1～1.35mg/L,其次是含氯类TDCPP为3.8～4.6mg/L,而同为含氯类的TCPP则毒性较小,其48h-EC50为131mg/L. OPEs对浮游动物的毒性大小还与其浓度高低和暴露时间长短呈正相关,随着暴露浓度增高和暴露时间增加而增强.例如,TnBP的6h-EC50(52～93mg/L)高于24h-EC50(5.8～35mg/L);同样,TBOEP的24h- LC50(50% Lethal Concentration,半数致死浓度(下同)) (84mg/L)高于48h-LC50(75mg/L).卤虫作为受试生物的OPEs急性毒性数据较少,TnBP的急性24h-EC50为54.6mg/L,TDCPP的急性48h-EC50为15～17mg/L.对比急性暴露,低浓度慢性暴露条件下浮游动物的响应更能反映OPEs的生态毒理效应.Giraudo等人率先报道了环境相关浓度OPEs对大型蚤的长期毒性效应[47].发现10µg/L TBOEP可以在大型溞中产生氧化应激和内分泌干扰作用,其效应可在世代间迁移:例如亲代(F0)中编码过氧化氢酶()和谷胱甘肽S～转移酶()的基因均被下调,随后在F1代中过氧化氢酶(CAT)等活性显著降低;F0代中的卵黄蛋白原两种亚型(和)、蜕皮激素受体()、激素核受体()和血红蛋白()基因转录水平显著升高,随后影响了大型溞多世代生长发育.对比急性暴露(48h)和慢性暴露条件(20d)下卤虫()的生长发育,发现急性暴露至8mg/L TDCPP并不会影响卤虫体长,但长期暴露于环境相关浓度(200 µg/L TDCPP),会显着降低体长,提高死亡率,影响卤虫生长发育;此外,两种条件均会引起代谢变化,急性暴露触发甘油和海藻糖等与渗透作用相关的代谢物水平升高,以调节渗透压变化;慢性暴露则下调甘油磷脂代谢,这可能导致能量存储机制和脂质结构的改变[48].可见,低浓度长期暴露,会影响浮游动物生长、发育与生殖,而氧化应激、内分泌干扰以及参与遗传信息处理、生物系统、细胞过程等生理生化代谢途径的差异可能是其主要的毒性机制[49].总体而言,在OPEs浮游动物毒性效应研究中,受试的物种和OPEs种类仍偏少,环境相关浓度的暴露和慢性长期暴露研究不多,亟需进一步开展毒性机制的探讨和深入分析.

此外,基于不同OPEs物化性质的差异,在复杂的实际环境中其毒性效应也会产生不同影响.例如,TPHP的LogOW(4.59)比TCEP和TBOEP的LogOW值(1.44、3.75)高,TPHP更容易吸附在溶解性有机物(DOM)上,从而改变OPE的生物利用度和亚致死毒性.Kovacevic等[50]也发现DOM不会改变单独TCEP和TBOEP暴露的代谢变化,但会产生与单独暴露TPHP不同的代谢反应,例如,在5mg 有机碳/L DOM,存在下,暴露于TPHP后大型溞体内代谢产物百分比发生变化,其中葡萄糖含量显著降低,亮氨酸显著升高,而仅TPHP暴露则未观察到.而且,不同种类OPEs间可能存在联合毒性作用,有必要对几种OPEs进行联合毒性实验,并关注浮游生物体内OPEs的生物转化机制和生物转化产物的毒性.例如Choi等[51]基于非目标筛选表征大型溞中TPHP的生物转化产物和途径,发现TPHP主要的生物转化机制是半胱氨酸结合和硫酸化,某些生物转化产物(如磷酸二苯酯、羟基化磷酸三苯酯和巯基磷酸三苯酯)可能会引起生物毒性.

2.2 OPEs对鱼类的毒性效应

表4总结了目前OPEs的鱼类毒性效应研究结果.可见,不同的OPEs对同种鱼类的L(E)C50值差别很大,反映了不同OPEs的毒性存在显著的差异.例如TCP和TCEP对虹鳟()以及TCP和TCPP对蓝鳃鱼()的96h-LC50值,差距均高达1000倍以上.而且同种OPEs在不同物种中也存在差异.TPHP暴露下,美洲原银汉鱼()的96h-LC50(95mg/L)是杂色鱂()(0.31～0.56mg/L)的300倍.总体而言,TnBP、TDCPP、TPHP、TCP的毒性较强,对水生生物具有轻微至高毒性.而暴露于TDCPP中的斑马鱼胚胎、暴露于TCP中的蓝鳃鱼以及暴露于TPHP中的鲫鱼则十分敏感,其96h-L (E)C50均小于1,表明最容易受到侵害.

鱼是人类食品的重要来源,也是OPEs水生生态毒理学研究的重点.尽管OPEs对鱼类的毒性效应,已有一定数量的研究报道,但有关OPEs的潜在致毒机制目前尚未有定论.相关的研究主要集中在OPEs对模式生物稀有鮈鲫()和斑马鱼()的神经毒性、发育和生殖毒性等方面. Hong等[52]近期报道了芳烃类OPEs(TPHP)对成年雄性鮈鲫的毒性:TPHP显著提高了鱼脑中血脑屏障的通透性,激活了神经炎症反应,不利于阻止有害物质进出脑组织;TPHP还明显抑制细胞增殖,并显著降低鱼小脑垂体神经元(Ce)的树突状乔化,导致鱼的学习和记忆功能受损.其他OPEs,如TDCPP,在200 µg/L处理下,神经营养因子(例如,,和)的转录受到明显抑制,这表明OPEs可能通过靶向神经营养因子和神经胶质蛋白引起神经毒性作用[53].除了神经毒性,OPEs对水生生物的遗传毒性也日益受到关注.以TDCPP为例(图5),它显著激活了DNA损伤反应(DDR)信号,进而改变与DNA损伤相关的途径,包括DNA修复抑制以及促进细胞凋亡和细胞周期停滞等[54].Hong等[55]则通过高通量测序(HTS)评估microRNA和isomiR (microRNA的变体)转录效果,并以此来评估三类OPEs(TBOEP、TDCPP、TPHP)对稀有鮈鲫的肝脏毒性,发现TBOEP,TDCPP和TPHP暴露条件下均分别检测到不同种microRNA的差异表达.

图5 TDCPP诱导的稀有鮈鲫DNA损伤的系统观点[54]

OPEs对水生生物生长和发育的毒性研究主要以斑马鱼为受试生物.Zeng等[56]还报道了环境相关浓度烷烃类TBOEP对斑马鱼生长的影响,发现雌性体内的TBOEP平均含量均高于雄性,体长和体重显著减少,且相关基因在生长激素/胰岛素样生长因子(GH/IGF)轴和下丘脑～垂体～甲状腺(HPT)轴上的转录受到影响,雌性血浆中甲状腺素(T4)含量降低,同时促甲状腺激素β亚基()mRNA水平降低.为了更加明确TBOEP暴露后的性别差异和亲本转移, Huang等[57]进一步研究后认为TBOEP暴露所呈现出的明显性别差异,可能与产卵期间TBOEP的排出有关.斑马鱼子代幼鱼中检测到TBOEP残留也证明上述观点.此外,暴露于TBOEP,斑马鱼性腺发育出现明显延迟,下丘脑～垂体～性腺(HPG)轴基因转录发生改变[57].HPG轴在生殖系统的发育和调节中起着至关重要的作用.下丘脑分泌促性腺激素释放激素刺激垂体分泌卵泡刺激素和黄体生成激素,进而刺激性腺释放17-雌二醇(E2)和睾丸激素(T).TBOEP暴露导致血浆中E2和T浓度上升,且较低浓度的TBOEP仅能改变雌性的T/E2比值,表明TBEOP对女性的生殖影响更大[57].除此之外,斑马鱼暴露于含氯类和芳烃类OPEs也可以显著增加血浆中T和E2的浓度[58-59].因此,OPEs可能是通过影响生物体内激素的平衡,进而影响生长,产生发育毒性;长期OPEs暴露还将导致该污染物向其后代转移,产生代际毒性.

在OPEs的发育毒性方面.近来已探明含氯类OPE(TDCPP)导致斑马鱼尾鳍畸形的分子机制与尾鳍发育相关的转录因子的错误表达有关[60].TDCPP还是斑马鱼胚胎中血管和肌肉发育的有效破坏者.Dishaw等[61]发现10µmol/L TDCPP具有致畸性和明显的毒性,100µmol/L可显著改变斑马鱼的游泳活动,显示TDCPP的毒性可能与神经发育和肌肉发育的破坏有关.Li等[62]也发现短链含氯类OPEs (TCPP和TCEP)对斑马鱼胚胎神经发育的不利影响.与前人对鮈鲫的神经毒性研究[53]相似,TCEP和TCPP对乙酰胆碱的含量和乙酰胆碱酯酶的活性没有影响,但污染物暴露显著下调了与神经发育相关的选定基因和蛋白质的表达,造成显著的发育毒性.

近年来,借助组学技术,OPEs的毒理学机制研究取得了新的进展.以TPHP为例,高通量蛋白质组学研究表明其急性暴露对斑马鱼幼鱼的发育毒性与视蛋白基因的表达改变有关[63]:TPHP暴露引起五种视蛋白基因(视紫红质zfrho,紫外线视蛋白,蓝色视蛋白,绿色视蛋白,,,,红色视蛋白)的转录显著下调.而代谢组学分析发现,TPHP还显著抑制斑马鱼氨基酸代谢,降低缬氨酸、亮氨酸和异亮氨酸水平,抑制氨酰tRNA生物合成过程,同时引起葡萄糖糖酵解过程和三羧酸循环发生障碍[64].以上原因可能是TPHP引起斑马鱼发育畸形的主要原因.尽管目前仅针对TPHP开展研究,但上述研究结果为深入理解OPEs的水生生物毒性机制奠定了坚实的基础.

2.3 OPEs对底栖生物的毒性效应

与水相相比,沉积物中含有更多的OPEs,底栖动物可能更易于受到OPEs的污染威胁.但目前大多数OPEs的毒性研究都以水层生物为受试生物,有关OPEs对底栖生物的毒性仍缺乏系统性认知.目前仅有少量研究以亚洲淡水蛤()和海洋贻贝()为受试生物考察OPEs对底栖生物的潜在负面影响.

烷烃类OPEs(TBOEP和TnBP)长期暴露对亚洲淡水蛤的抗氧化酶活性(CAT、SOD)和丙二醇(MDA)含量产生影响,具体表现为CAT和SOD活性随暴露剂量(20～2000 µg/L)的增加呈现先降低,后增加的趋势[3].可能是SOD和CAT在低浓度时无法及时清除过量的ROS,导致机体抗氧化活性下降,但在高浓度暴露下,由于淡水蛤闭壳效应的影响产生虹吸行为导致抗氧化酶活性呈增加趋势,并使MDA含量降低.对于含氯类OPEs(TCPP和TDCPP),蛤消化腺通过大量摄取TDCPP产生ROS,诱导SOD活性上升,使MDA含量显著增加,随后干扰细胞正常的氧化还原平衡并降解蛋白质、DNA和脂质,导致细胞凋亡[65];而贻贝血细胞内SOD活性和MDA含量的升高,同样证实TCPP的氧化伤害是导致细胞凋亡的原因之一[66].芳烃类OPE(TPHP)与含氯类OPEs类似,可导致贻贝消化腺中抗氧化酶(GPX、SOD和CAT)活性与基因转录水平的上调,表现出明显的氧化应激现象[67-68].上述研究揭示,OPEs对底栖生物的毒性效应可能在于引发机体氧化应激,使抗氧化功能紊乱,最终产生损害;该过程受OPEs种类、暴露时间、剂量以及生物生理生化行为(如闭壳效应和虹吸行为)等因素的多重影响.值得一提的是,双壳类生物虹吸行为对其具有一定的保护功能,反之,该行为的抑制则可作为机体功能紊乱的标志[3].

底栖生物对OPEs暴露的响应,除了氧化应激之外,体内OPEs的生物转化或解毒过程是决定其毒性效应的另一个关键.一般而言,生物体通过激活I期和II期生物转化和多异生物抗性(MXR)系统来保护生物免受外源污染物侵害.例如,研究证实TDCPP可在亚洲淡水蛤消化腺内容易发生生物转化,BDCPP是其主要的I期转化产物;与母体TDCPP相比,BDCPP减低消化腺细胞凋亡、显著缓解虹吸抑制,降低对底栖生物的毒性[65].此外,GST(谷胱甘肽S转移酶)和细胞色素P450作为重要的生物转化酶,也参与了底栖生物消化腺OPEs的生物转化和解毒过程[3].例如,TDCPP暴露下,亚洲淡水蛤细胞色素P450家族蛋白基因()、谷胱甘肽系统基因()的表达水平随暴露剂量(50～5000µg/L)显着降低[65];暴露于TBOEP后,谷胱甘肽系统基因(、)表达水平也显著降低[3].除上述生物转化酶外,其他生物标记物(如神经肽[69]、乙酰胆碱酯酶(AChE)[70]等)也受到重视.已证实,在长期低水平TDCPP(10μg/L)暴露下,贻贝体内AChE活性的抑制和蛋白质分子水平上受体型酪氨酸蛋白磷酸酶N2型(PTPRN2)的下调均标志着该化合物可引起神经毒性[70].

上述研究表明,OPEs的底栖生物毒性不容忽视,尽管已有少量前瞻性研究,但明确OPEs底栖生物毒性机制、开发更有效的生物标志物等仍有待更多的研究.

3 结语

OPEs已经在许多国家和地区、甚至是极地水域中被检出,检出浓度逐渐升高,其潜在的负面效应不容忽视;检出的OPEs以烷烃类和含氯类为主,但具体种类及浓度水平在不同的国家和地区间有较大差异,这与人类活动的地域差异、不同地区间OPEs使用量、应用类型和经济发展水平等相关.

进一步对OPEs的水生生物毒性及其作用机制进行分析,发现OPEs暴露会对包括浮游生物、鱼类和底栖生物在内的整个水生生态系统造成伤害,主要表现为生长抑制、组织病变、发育和生殖毒性、神经毒性和细胞凋亡等;其毒性作用机制十分复杂,既与基因的转录和表达、蛋白质的表达有关,也有激素代谢调节和神经递质因子的变化有关,酶活性的抑制以及氧化应激也被证明是可能的致毒机制.

当前,OPEs的环境与生物毒性数据不够完善, 缺乏OPEs水生生物富集及沿食物链传递和生物放大的研究,且浓度的大小、暴露时间、环境条件以及毒性实验的设计和条件等多种因素均会影响OPEs的毒性表现,难以得出OPEs致毒机制的一致规律,更难以对其环境效应和健康风险实施有效的评估.

为深入了解OPEs的生态毒性及其健康效应,未来需建立一套相对完整, 科学的OPEs毒性测试标准方法,包括OPEs物理化学性质表征, 模型生物选取, 暴露方式和毒性效应指标等,保证不同的调查和实验结果间的可比性. 考虑到OPEs存在较高的生物富集及其食物链传递潜能,在关注OPEs高剂量急性效应(当前毒性研究的主要内容)的同时,更需要关注OPEs长期低剂量或环境水平的暴露及其生态毒性效应,包括在生物体内的归趋、富集和遗传毒性等, 也包括OPEs沿食物链传递的影响,及对种群,群落及生态系统产生的生态风险,以使研究结果更加贴近真实环境的情况.

另外,在自然环境中,污染物并非孤立存在,而是与其他污染物混合存在且受各种环境因子影响,不仅会改变其迁移、转化和生物毒性,往往还对生物体产生联合毒性效应.因此需要重视OPEs在环境条件下的生物转化和水解或光降解过程.经过转化或降解,OPEs是否可能生成毒性更强/更弱的代谢产物或副产物(如OP二酯和羟基化代谢物等)亟需深入研究.也需要加强研究OPEs在水环境中与其他共存污染物可能产生的协同、拮抗等复合污染生态效应.

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Pollution status and ecotoxicity of organophosphate esters (OPEs) in aquatic environment.

ZENG Jia-min1, ZHONG Shi-hua2, QIAN Wei1, YUAN Sheng-wu1, ZHU Xiao-shan1,3*

(1.Institute of Marine Engineering, Shenzhen International Graduate School, Tsinghua University, Shenzhen 518055, China；2.Shenzhen Agricultural Products Quality and Safety Inspection and Testing Center, Shenzhen 518055, China；3.Guangdong Laboratory of Southern Ocean Science and Engineering (Zhuhai), Zhuhai 519000, China)., 2021,41(9)：4388～4401

To effectively assess the potential ecological health risks of organophosphate esters (OPEs), this study gave an overview of the global OPE pollution in water and sediment with a focus on their toxic effects on aquatic organisms. The potential toxicity mechanisms were also analyzed in different kinds of biota including plankton, nekton and benthos, and the future research directions and scientific issues in aquatic environmental studies were finally prospected. This study would be helpful for effective assessment of ecological effects and health risks of OPEs. It would also positively promote the food safety monitoring and ecotoxicology research of OPEs, and provide reference for regulating their green applications.

aquatic environment；organophosphate esters (OPEs)；pollution；bioaccumulation；toxicity

X52

A

1000-6923(2021)09-4388-14

曾佳敏(1997-),女,湖南常德人,清华大学环境工程专业硕士研究生,主要从事有机磷酸酯生态环境毒理研究.发表论文1篇.

2021-02-07

国家自然科学基金(41877352,42077227);广东省基础与应用基础研究基金项目(2021A1515010158);深圳市基础研究重点项目(JCYJ20180507182227257)

* 责任作者, 副研究员, zhu.xiaoshan@sz.tsinghua.edu.cn