环境持久性自由基及其介导的生物学损伤

张绪超,赵 力,陈 懿,李冬雪,胡 虹,储 刚,吴 敏,3*



环境持久性自由基及其介导的生物学损伤

张绪超1,赵 力1,陈 懿1,李冬雪2,胡 虹2,储 刚1,吴 敏1,3*

(1.昆明理工大学环境科学与工程学院,云南 昆明 650500；2.昆明理工大学医学院,云南 昆明 650500；3.云南省土壤固碳与污染控制重点实验室,云南 昆明 650500)

近年来,新型环境风险物质环境持久性自由基(EPFRs)被发现广泛分布于不同来源的环境介质中,如燃烧颗粒物、土壤/沉积物、天然有机质等.因其稳定性、持久性,且可以随着环境介质迁移和转化,EPFRs的生态环境风险可能被忽视.基于此,本文系统总结了存在于环境介质中的EPFRs,并归纳其分布特征;阐述了其介导的组织损伤,包括肺损伤、心血管损伤、神经毒性损伤、DNA以及细胞色素等生物大分子损伤;详述了主要由氧化应激、炎症、免疫反应以及代谢异常引起的损伤机理;最后,总结并展望了有关研究所存在的问题和未来研究方向,以期为EPFRs的生态健康风险评价和政策标准制定提供参考.

环境持久性自由基；地球表层系统；活性氧；环境风险；影响机理

环境持久性自由基(EPFRs)因其能在环境中稳定存在,且稳定时间长达数月甚至更久,被视为一种新型环境风险物质[1-5].目前,EPFRs能够在燃料燃烧、生物质热解、垃圾焚烧以及金属冶炼等人为活动过程中被释放,存在于大气颗粒物(PM)和土壤等环境介质中,对人体具有不可知的潜在危害以及潜在的环境毒理效应.EPFRs能随着环境介质迁移并进入生物体内,可能诱导机体产生氧化应激反应,导致机体出现炎症和免疫反应,破坏机体正常代谢.近年来,关于EPFRs的相关研究主要集中在对其产生的机理分析[6-10]和对污染物环境行为的影响研究[11-13].然而,针对EPFRs本身环境风险的系统研究,以及其存在的环境介质风险的全面评价仍然缺乏.主要原因:有关EPFRs的研究还没有得到足够的重视,现阶段存在EPFRs的环境介质污染物(如焦化地土壤)风险的检测、评价以及产生风险机理的解释,通常只考虑了金属元素和多环芳烃类化合物(PAHs)等传统污染物[14-16];研究者忽视了实验过程中传统有机溶剂萃取以及其他化学分析方法,可能会把持久性半醌类自由基转换为苯酚、对苯醌类分子污染物[17].此外,研究发现含有EPFRs的颗粒物引起的细胞毒性比颗粒物本身更强,导致细胞功能缺陷更严重[18-20].现有的国家标准还未将EPFRs纳入污染物管控范畴, 这可能致使当环境介质污染物(如大气颗粒物)的水平远远低于标准时,仍然会对公共健康产生威胁[21-23].本文从EPFRs存在的环境介质、介导产生的生物学损伤和引起损伤的机理三部分(图1),论述了EPFRs的研究现状,总结了EPFRs 在环境风险评估中的不足,为今后EPFRs的研究、风险控制和政策制定提供基础数据和技术指导.

图1 EPFRs的环境介质、损伤机理及其影响

1 EPFRs存在的环境介质

1.1 大气颗粒物中的EPFRs

1.1.1 室外大气颗粒物 大气颗粒物是EPFRs存在的环境介质之一[24-25].有研究报道,可通过使用电子顺磁共振仪(EPR)检测PM中的持久性半醌类自由基的信号,并且随颗粒物粒径变小,EPFRs浓度变高[28].通常,粒径越小的PM因其倾向于沉积在下呼吸道和肺泡,更容易引起呼吸道毒性和功能障碍[29]; EPFRs也会随其迁移到相应的组织部位,引起更广泛的组织损伤[30].在从美国各城市收集的PM样品中已经发现了类似半醌类自由基的存在,体外细胞实验表明EPFRs可以造成细胞的DNA损伤[18].近期研究表明,含有EPFRs的PM会引起并加重人体免疫、呼吸和心血管系统方面的疾病[30-32].

以往研究PM对呼吸系统的损伤时,一般考虑常规燃烧污染物(如PM、有机污染物和重金属)的贡献[33-34],却忽视了EPFRs的存在.Franklin等[35]和Wang等[36]先后注意到急性心血管疾病和癌症的发生,无法使用传统环境污染物的毒性风险进行解释, EPFRs却有可能诱发这些疾病.Dellinger等[1,3,37]鉴定了几乎所有燃烧源的产物都会存在EPFRs,同时开发了一套使用颗粒物-自由基的模型化合物进行实验的方法.利用模型化合物,证明EPFRs在环境暴露引起的疾病中的主导作用,以及EPFRs能引起比环境介质本身更强的生物活性和毒性[20,30,32,38].此外,在塑料燃烧后产生的颗粒烟雾排放物和残留固体灰分中都检测到以碳和氧为中心的EPFRs,进入空气后,能不断进行迁移从而产生更大范围的风险[39].

综上所述,各种燃料(如油、煤、木材、木炭、烟草)和塑料垃圾燃烧时,不仅会产生大量传统的燃烧副产物,也会产生稳定的EPFRs.这些EPFRs随着环境介质进行迁移转化,使风险提高.目前,对于垃圾焚烧等过程中纳米级颗粒物的归趋及其形成的EPFRs的风险研究相对较少.因此,PM中的EPFRs潜在的环境风险应得到足够的重视和关注.

1.1.2 室内空气颗粒物 室内PM主要来源于烹饪炉具产生的油烟烟雾、生物质燃烧过程中的混合物及香烟烟雾等介质,在这些介质中检测到与室外PM相似的EPFRs信号[40-41].研究表明,香烟烟雾的烟焦油中的 EPFRs主要是醌/氢醌类复合体[42-43];此类EPFRs在体外容易与氧气反应生成羟基自由基等活性氧自由基(ROS),ROS可能引起机体的氧化损伤.研究结果显示电子烟同样存在健康风险,其烟雾中的EPFRs信号强度高达7×1011radicals/puff; 将小鼠暴露在电子烟烟雾2周后,小鼠肺部出现了明显的氧化应激反应和巨噬细胞引起的炎症反应[44].含有EPFRs的香烟烟雾会削弱病人针对细菌和病毒的先天及适应性免疫应答反应,增加慢性阻塞性肺疾病发病率和死亡率[45-46].Wang等[36]从居民住宅区收集到人们日常使用的低阶煤中检测到EPR信号高达2.49× 1019spins/g,而且煤燃烧炉烟囱出口的烟尘EPR信号强度可达3.10×1019spins/g,这些EPFRs在18个月后依然保持在一个数量级上;研究者注意到当地肺癌的高发生率无法完全用传统的化学物质分析,据此推测这可能与长期暴露在EPFRs的环境中有关.因此,婴幼儿、老人及病人等在室内时间长的人群需要格外注意家庭烟囱烟气和烟雾的影响,这些室内空气颗粒物是EPFRs存在的重要环境介质.

1.2 土壤/沉积物中的EPFRs

土壤/沉积物是环境中有机污染物主要的汇,其组成主要有有机质、金属氧化物、粘土矿物等,构成了EPFRs形成的必要条件[3,36].Nwos等[47]证明不需要经过生物途径,土壤即可形成持续时间足够长的自由基.这说明土壤有机质和金属氧化物可能产生EPFRs.

研究发现,五氯苯酚污染的土壤和沉积物中有很强的EPFRs信号,其强度最强可高出空白对照土壤30倍,并且在超过10a时间里EPFRs仍不断产生[48-49].另一研究发现,通过低温热处理修复被污染的土壤反而可以增强EPFRs的强度[4].最近,在燃煤区域的土样中检测到类似的EPFRs信号.在云南宣威地区,发现土壤中含有大量EPFRs,并推测该发现可能是这一地区癌症高发的原因之一[36].Jia等[26]在焦化地周边的土壤中检测到EPFRs的强度达到3×1017radicals/g,同时说明了PAHs对EPFRs的形成起着主要作用.在自然条件下,采煤和焦化厂附近的土地会形成EPFRs,改变湿度和光照会形成其他类型的EPFRs,这些新的EPFRs可能具有不同的性质和毒性[50].研究者从土壤里提取了腐殖质(土壤有机质主要成分),从中检测到半醌类自由基和以碳为中心的芳香类的EPR信号,其强度也会因为湿度和光照的改变而变化[50-52],在土壤中, EPFRs参与氧化还原过程,而在水体环境中,它可以诱导产生ROS[25,53-54],使土壤生物处在氧化胁迫的环境下.Liao等[55]和赵力等[56]检测到生物炭中有以氧和碳为中心的EPR信号,使用羟基捕获剂5,5-二甲基-1-吡咯啉-N-氧化物(DMPO),成功捕获到生物炭诱导水体产生的羟基自由基.因此,土壤/沉积物中的EPFRs是确实存在的,但其对周边地区的人群和动植物的健康风险还需要进一步研究.

1.3 水体中的EPFRs

从德国和冯诺斯坎底亚采集的23个地表水样中提取到的天然有机质检测到有机自由基浓度最高可达到1.84´1017spins/g[48].研究发现球形纳米颗粒和纤维会自发形成一种新的稳定的三苯甲基自由基,这个自发反应可以发生在室温水溶液中,甚至低温冷冻的极端环境中[57],这也使得这类EPFRs的风险难以控制.鉴于纳米材料的广泛生产和使用,包括水体在内的各种环境介质中,纳米材料所形成的EPFRs引起的生态风险和人体健康问题值得关注.另外,含有EPFRs的生物炭也会以各种途径进入水体,从而对水中的生物产生威胁.

综上所述,EPFRs普遍存在于环境介质中(大气圈、岩石圈和水圈等).环境介质的组成、性质以及环境行为会影响EPFRs的类型以及其环境行为,EPFRs也可以随着环境介质在环境中迁移转化,导致EPFRs风险增加.此外,目前评估环境介质中污染物风险时,没有考虑到EPFRs的存在,导致风险评估的误差.

2 EPFRs对生物体的环境健康风险

本文主要以人和动物为例,介绍EPFRs介导的组织损伤.EPFRs可以通过呼吸直接进入呼吸系统或直接暴露的方式,引发肺部、心血管、免疫和神经系统等在内多种组织的损伤(表1).

表1 EPFRs存在的环境介质及其影响

续表1

注: 表中列出了EPFRs对动物、植物和人的影响. ①飞灰:由工业废料焚化产生[61];② MCP230:由5%的氧化铜和95%的二氧化硅(直径小于0.2μm)颗粒组成,并在大于230°C的温度下负载邻氯苯酚或邻二氯苯,分别称之为MCP230或DCB230[20];③Slican/MCP:合成方法同MCP230[62];④DCB230:合成方法同MCP230[3,63];⑤生物炭:氮气环境中,将水稻、玉米和小麦秸秆分别在不同温度下热解(200~500°C)冷却到室温得到[55];⑥puff与g(克)相对应,此单位暂无对应中文翻译,每puff在原文中对应35mL体积气体.*:值和强度分别是电子顺磁共振仪器(EPR)中用来分析自由基类型和电子自旋数的值,标*表示原文中未出现,这里从其参考文献中摘录;EPFRs强度的绝对定量还没有统一的标准,而其强度与EPR信号吸收峰的面积成正比,因此一般使用吸收峰的积分面积与标准样品1,1-二苯基-2-苦基肼基(DPPH)做对比,并用质量或体积标准化后计算出相对强度,文献中的单位常使用spins/g或radicals/g或radicals/puff.通常,g-Factor<2.0030时,EPFRs是以碳为中心的自由基;2.00302.0040时,EPFRs是以氧为中心的自由基[10,55];“-”表示文章中没有相应的数据.

2.1 肺损伤

外源化学物可经呼吸道和其他途径到达肺组织,引起肺的损伤.流行病学研究表明,环境空气中PM数量增加与死亡率升高、哮喘恶化、呼吸道感染等疾病有一定的关系[76-77].如前文所说,EPFRs会随着颗粒物迁移并进入呼吸系统,从而增加疾病患病率或加重病情.

起初,研究人员在香烟烟雾中发现醌类/氢醌类复合物可产生超氧化物损伤细胞,最终导致肺气肿和癌症的发生[43].使用EPR检测了长时间吸烟者、癌症患者和煤炭矿工工人的肺部组织存在EPFRs,并观察到相对严重的病情[58-59,78-79].机动车辆和垃圾燃烧产生的颗粒物会对肺上皮细胞[80]和肺部[76,81]造成损害,这些PM中含有与香烟烟雾相似的半醌类自由基信号,在肺部沉积位置参与氧化还原过程不断产生ROS[76],甚至与过渡金属等协同作用产生氧化应激反应[81],引发肺功能异常[80,82].

Dellinger等[3,37,83]合成了一种与PM有相似EPR信号的模型化合物.利用模型化合物,发现沉积在呼吸道中的EPFRs通过生成ROS使肺部产生氧化应激和炎症反应对肺部造成危害,与没有EPFRs的对照相比,实验组产生的ROS引发连锁脂质过氧化反应破坏了支气管上皮细胞(BEAS-2B)的细胞膜完整性[18],降低了细胞内的谷胱甘肽和抗氧化酶的水平,表现出更强的细胞毒性[20,62].最近的试验说明EPFRs有改变免疫反应的可能,暴露在EPFRs的环境后,肺部便处于氧化应激状态,这种状态抑制了免疫应答反应[69].用收集的车辆尾气中的颗粒物进行试验,肺部的免疫应答反应被延迟,病毒感染的可能性增加,通过捕获液相中的超氧阴离子和羟基自由基以及毒性实验,证实了含有EPFRs的PM引起的氧化应激是造成细胞毒性和肺组织损伤的主要可能机制[84-85].

同时,EPFRs会引起气道中的淋巴细胞、嗜中性粒细胞、细胞因子的改变,导致气道高反应性,增加肺部炎症[65,67],这种症状甚至会破坏子代的肺部免疫发育[30,68].哮喘的发展和恶化可能与EPFRs引发的氧化应激有关,EPFRs诱导抗原呈递细胞成熟,使肺部发生炎症而加重哮喘[67].此外,EPFRs可诱导上皮间质转化,不可逆的改变气道结构和功能,显著影响肺部的发育[38].感染流感后,肺部巨噬细胞减少,抗细菌/病毒和宿主防御体系受损,疾病严重程度增加,进而引起发病率和死亡率升高[44,69,75].

综上,氧化应激和炎症反应以及免疫抑制是造成呼吸系统功能降低的重要机制.而认识到EPFRs的存在可以帮助人们重新理解致病机制,如哮喘加重的原因.

2.2 心血管损伤

有毒污染物会增加心率和心律失常的发生率,加剧动脉粥样硬化、冠心病和外周动脉疾病,增加心绞痛、心肌缺血、中风等疾病的发病率,研究表明, EPFRs与这些疾病的发生存在一定相关关系[86-87].

尽管超细颗粒物可以进入细胞并引起主动脉粥样硬化[88-89],但细颗粒物中的EPFRs风险往往被忽视了.利用DCB230,发现EPFRs使心脏处于促炎状态,增加肺动脉压,降低心脏左心室基线功能,并在短暂的缺血再灌注后加重左心室功能障碍,表现出明显的心脏毒性[19,66,71].此外,EPFRs刺激产生的氧化应激能引起左心室肌细胞中的线粒体去极化,启动细胞凋亡程序,造成心肌细胞的细胞毒性[74].

EPFRs介导的心血管损伤的潜在机制可能是氧化应激和炎症反应改变了免疫应答反应,导致局部乃至全身的炎症,从而触发疾病的发生.然而,目前的研究只是通过氧化应激的标志物和已经发生的炎症反应来解释疾病的发生过程,没有给出具体的致病机理以及EPFRs直接引起损伤的观测.

2.3 神经毒性作用

EPFRs能够引起机体氧化应激反应,而氧化应激在神经退行性病变中起到重要作用.以中枢神经系统为例,通常该部位存在较低浓度的抗氧化酶,因此生物大分子最容易受到氧化.在阿尔兹海默症、帕金森氏病、运动神经元病等疾病的临床研究中,氧化应激可以引起神经元的缺失和神经变性[90].研究者利用模式生物秀丽隐杆线虫()首次探讨了土壤改良剂生物炭中的EPFRs的神经毒性,结果表明生物炭中的EPFRs在高浓度的时候会显著抑制的身体弯曲频率和相对运动长度,并有抑制化学感知功能的可能性,这对于生物炭在应用过程中被忽视的风险进行了补充和校正[91].

2.4 DNA和细胞色素等生物大分子损伤

研究发现香烟烟焦油水提取物中的半醌类自由基会使DNA产生切口[60],存在于PM、TiO2、石棉、陶瓷/玻璃纤维等介质中的EPFRs也能引起这样的损伤[92],通过检测DNA羟基化产物说明EPFRs能促进ROS的产生从而引起氧化损伤[61,93-94].为研究氧化应激的调控机制,研究者使用电子显微镜观察到较小尺寸(<2.5μm)的PM出现在线粒体上,表明EPFRs可随之迁移进入细胞内并引起线粒体严重的结构损伤[88,94].此外,EPFRs还会抑制肝微粒体中的细胞色素P450的正常功能,使P450参与的代谢不能正常进行,从而影响生物体代谢和消除异物的能力[70,72-73].

综上,EPFRs通过损伤细胞结构和正常细胞内蛋白质的表达,致使代谢异常,最终导致机体的发育异常和疾病发生.EPFRs引起的氧化应激和代谢异常具有潜在的危害作用.

3 EPFRs介导的损伤机制

EPFRs与机体接触之后,其损伤的风险来源主要有2部分:EPFRs在体外产生ROS,让机体处于氧化胁迫状态;EPFRs进入体内产生ROS,损伤生物体内的生物大分子,从而造成损伤.EPFRs对机体是否有直接作用和损伤,现有的研究还很少提及到.本文总结了EPFRs所能引起的损伤机理和途径(图2),并将其主要归为氧化应激、炎症和免疫反应,以及代谢异常.

图2 EPFRs损伤机理

1.EPFRs诱导细胞体内ROS产生并与细胞膜作用;2.ROS与线粒体膜作用;3.ROS与溶酶体膜作用;4.ROS与蛋白质作用;5.ROS与多聚核苷酸作用;6.EPFRs与内质网上的细胞色素P450作用;7.EPFRs与线粒体直接作用;8.EPFRs诱导细胞因子(如IL-6)释放;9.EPFRs在细胞体外诱导ROS产生

3.1 氧化应激

ROS引起的氧化应激是EPFRs介导生物损伤的主要原因.ROS的氧化能力一般比较强,化学性质非常活泼,如羟基自由基(×OH)、超氧阴离子(O- 2×)、单线态氧(1O2)等[90],其存在时间往往较短,因此称之为瞬时自由基.EPFRs通过氧化还原循环不仅可以在体外刺激产生ROS[58],也可以诱导体内产生ROS[30,38,90],ROS大量聚集后可损害细胞中几乎所有的生物大分子(如脂质、糖、蛋白质和多聚核苷酸),这种损害引起的次生产物还可继续产生与ROS同样的损害作用,并有可能破坏抗氧化防御体系引起细胞和组织的生理及病理的损伤,造成机体的广泛损伤,即氧化损伤[90].

在体外实验中,香烟烟雾、PM和DCB230中的醌类/氢醌类自由基参与氧化还原循环,减少了分子氧,产生超氧化物,形成H2O2和×OH,通过共价结合的方式损伤DNA[58],且添加抗氧化物质如超氧化物歧化酶(SOD)等能够清除瞬时自由基,减轻其损伤程度[15,38,58,94].ROS还可以通过氧化膜磷脂(即脂质过氧化)在细胞膜上引发连锁反应,并在膜内产生H2O2,脂质过氧化导致丙二醛和8-异构前列腺素等氧化产物的产生,现阶段主要是通过检测这些产物确定氧化应激的程度[95],同时丙二醛能与蛋白质和酶发生交联反应而扩大损伤,同样地这些损伤可以用白藜芦醇来减缓[20,30,62].使用来自骨髓的抗原呈递树突状细胞(DCs)也发现谷胱甘肽(GSH)的明显变化,说明EPFRs有可能诱导DCs的成熟,从而引起Th17细胞炎症[67].使用HL-1心肌细胞检测EPFRs对细胞的毒性作用,发现线粒体膜电位在早期开始下降(线粒体去极化),伴随着胱天蛋白酶增加,细胞凋亡通路被激活,后期释放出乳氨酸脱氢酶(细胞死亡标志物)证明细胞已经死亡[32,74].

类似的,当EPFRs通过各种方式进入体内也会对机体产生损伤.EPFRs使细胞产生氧化应激反应时,过量的ROS会通过自由基链式反应,迅速扩散并改变酶、脂质、蛋白质、多聚核甘酸的结构和功能,最终诱发机体各种肺部、心血管等疾病[30,90].EPFRs增强DCs抗原摄取和共刺激受体表达,导致白细胞介素IL-13增加和干扰素IFN-γ减少,辅助性T细胞数量增加[96],这将可能导致哮喘的发生[67,82]. MCP230/DCP230能够在细胞中产生ROS,伴随着氧化应激反应和炎症反应,体内基线心脏功能改变,在短暂的缺血再灌注后加重左心室功能障碍[62,66].此外,EPFRs会引起溶酶体和线粒体膜改变,氧化应激驱使BEAS-2B经历上皮-间质转化(EMT),导致气道结构和功能的不可逆损伤[38].心肌细胞暴露在DCB230后会死亡,死亡的内在凋亡途径关键是线粒体膜去极化,其次是细胞色素从线粒体转移到细胞质,最终导致胱天蛋白酶激活聚合酶,结果就是细胞凋亡导致疾病发生和加重[70,73-74].

总之, EPFRs可以诱导产生ROS,且ROS与各个生物大分子相互作用,引起细胞膜、溶酶体膜和线粒体膜结构和功能改变,激活细胞凋亡通路,引起细胞和组织凋亡,最终导致机体正常功能障碍.但是,这些EPFRs影响细胞的分子机理以及信号通路还需要深入研究.

3.2 炎症和免疫反应

解释EPFRs不利的健康影响时,炎症的产生也是关键的损伤机制,这是EPFRS诱导ROS和氧化应激能力的直接后果[43].未被清除的ROS导致细胞因子和趋化因子的基因表达,引起细胞内信号传导级联反应的激活,炎症便开始在目标组织中局部以及全身产生,并导致远离损伤部位的广泛促炎作用[97-98].因此,EPFRs可能是加重人类疾病恶化的重要风险因素.

半醌类自由基经氧化还原过程产生ROS,而ROS能引起炎症反应[80].EPFRs导致肺的炎症反应,伴随着粘膜状态和嗜酸性粒细胞的形态改变,上皮修复机制丧失,并造成呼吸功能障碍和疾病恶化.研究表明,城市中重要的空气污染物是PM,PM中的EPFRs可能会通过调节促炎细胞因子的释放来调节上皮细胞的功能[82].MCP230能够在肺部支气管上皮细胞中诱导细胞毒性,而且MCP230在较长的暴露时间和等效剂量下诱发的毒性更大[14,20,65].除了损伤肺部外,吸入DCB230能产生全身性炎症,诱导炎性细胞因子IL-6的增加[19,38].此外,暴露于EPFRs后的心脏会产生促炎反应,使心脏更容易受到缺血性损伤[71].所以,EPFRs介导的损伤机理可能是炎症和免疫反应所导致的结果.

3.3 代谢异常

代谢异常时也会诱发疾病的产生.一方面,正常细胞代谢本身会产生传统的瞬时的自由基;另一方面,来自外部各种介质中(如PM、香烟烟雾、生物炭等)的EPFRs也可以诱导产生不稳定的自由基[90],而后者往往是影响正常代谢过程的主要原因.

在代谢的过程中细胞色素P450(酶)起到了关键性作用,最近发现其与许多疾病的发生有着密切的关系.P450可能参与ROS的生成,进而引发上述包括氧化应激等反应过程的发生.PM中的EPFRs可能会被P450代谢酶活化成反应性亲电代谢物,这些物质会对靶细胞产生各种毒性作用[15].此外,EPFRs还可以导致不同形式的P450酶活性的不可逆抑制[70,72],使接触EPFRs的个体更加容易受到环境中存在的毒素和致癌物质的有害影响[73].因此,EPFRs可以通过影响细胞色素,引发细胞凋亡,导致机体功能受损.EPFRs导致机体损伤不是单一机理的作用,往往是综合作用过程.深入研究EPFRs损伤机理,可以有效控制环境介质中的EPFRs风险.

综上所述,EPFRs对生物的影响,一般需要经历氧化还原的过程,引发ROS的产生,通过产生氧化应激反应,造成炎症和免疫反应,破坏正常的代谢等方式,使机体的正常功能受损,从而引发风险.

4 结语

新型环境污染物EPFRs的环境介质几乎分布于大气圈(如颗粒物)、岩石圈(如土壤)和水圈(如天然有机质)各个圈层,通过环境介质在圈层间迁移转化,不断对生物圈内的生物产生影响并有可能造成威胁.影响现有风险研究无法继续深入的主要原因如下:一,EPFRs存在的环境介质的成分非常复杂,造成风险量化困难;二,EPFRs与传统污染物的相互作用会导致风险的不确定性,如传统污染物与EPFRs是否存在协同作用加重疾病程度;三,大多数研究中使用的环境介质都存在颗粒团聚和沉降等问题[4].进行毒性实验时,人为地使环境介质分散在溶液中可能会导致EPFRs性质发生变化,从而不能很好的模拟EPFRs的实际情况,造成风险评估偏差.为了更好的研究和控制其风险,未来还需要解决以下存在的问题.

4.1 加强存在EPFRs环境介质风险的全面评估.以往研究PM、土壤和纳米材料等环境介质风险时未关注介质中的EPFRs,因此针对这些环境介质的风险评估应考虑EPFRs的潜在作用,从而更有效地指导和控制环境介质的不利影响.

4.2 EPFRs影响细胞的分子机理和信号通路.未来可以借鉴分子生物学的手段来探讨EPFRs对细胞膜、脂质和蛋白质等的作用,这将有助于了解控制相应疾病的发生和治疗.此外,EPFRs对生物的直接影响仍需深入研究,如EPFRs是否可以直接损伤肺部.

4.3 EPFRs风险量化和模型化合物优化问题.建立标准化的模型和分析方法量化风险,使得毒性结果具有可比性.

4.4 EPFRs风险控制相关政策问题.利用可比较的模型和方法,增加有关EPFRs对生物影响的基础研究,为政策制定提供依据.

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Overlooked risks and influences of environmentally persistent free radicals in the ambient media.

ZHANG Xu-chao1, ZHAO Li1, CHEN Yi1, LI Dong-xue2, HU Hong2, CHU Gang1, WU Min1,3*

(1.Faculty of Environmental Science and Engineering, Kunming University of Science and Technology, Kunming 650500, China；2.Medical School, Kunming University of Science and Technology, Kunming 650032, China；3.Yunnan Provincial Key Lab of Carbon Sequestration and Pollution Control in Soils, Kunming 650500, China)., 2019,39(5)：2180~2189

Environmentally persistent free radicals (EPFRs) are a class of pollutants with emerging concern. They are detected in various environmental media, such as combustion products, soil/sediment, and natural organic matter, and have been attracted a great deal of research interest because of their potential toxic impacts to organisms. In this paper, the detection of EPFRs in ambient media was firstly been summarized. The negative effect or toxicity mediated of EPFRs was been described, including pulmonary injuries, cardiovascular disorders, neurotoxicities and biomacromolecule damages (such as protein, enzyme, and DNA). The mechanisms of these adverse effects (inducing oxidative stress, inflammatory and immune response and metabolic disorder) of EPFRs were discussed. We also discussed the urgently needed future research direction on EPFRs. This paper aims to provide reference for the potential risk assessment, health assessment and policy formulation of EPFRs in the environment.

environmental persistent free radicals；earth surface system；reactive oxygen species；environmental risks；mechanism

X826,R994.6

A

1000-6923(2019)05-2180-10

张绪超(1994-),男,安徽六安人,昆明理工大学硕士研究生.主要研究方向为持久性自由基的环境风险,现阶段主要利用秀丽隐杆线虫来探讨生物炭的毒性风险来源.发表论文2篇.

2018-09-10

云南省重点研发计划资助(2018BC004);国家自然科学基金地区项目(41663013);国家自然科学基金重点项目(U1602231)

*责任作者, 教授, minwup@hotmail.com