宋鵬程,陸書(shū)玉,2*,魏永杰,羅麗娟,陳嘵倩

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上海市大氣顆粒物生物毒性及二噁英呼吸暴露風(fēng)險(xiǎn)評(píng)價(jià)

宋鵬程1,陸書(shū)玉1,2*,魏永杰3,羅麗娟4,陳嘵倩5

(1.東華大學(xué)環(huán)境科學(xué)與工程學(xué)院,上海 201620；2.上海市環(huán)境科學(xué)學(xué)會(huì),上海 200003；3.中國(guó)環(huán)境科學(xué)研究院,北京 100012；4.上海市輻射環(huán)境監(jiān)督站,上海 200065；5.上海市檢測(cè)中心,上海 201203)

使用Vibrio fischeri發(fā)光細(xì)菌法,評(píng)價(jià)了工業(yè)區(qū)和居民區(qū)大氣顆粒物懸浮液的細(xì)菌毒性,并對(duì)顆粒物暴露后的老鼠毒性效應(yīng)進(jìn)行了分析和討論;應(yīng)用HRGC-HRMS研究了工業(yè)區(qū)大氣中二噁英濃度水平及組分特征,并在此基礎(chǔ)上開(kāi)展了二噁英呼吸暴露風(fēng)險(xiǎn)評(píng)價(jià).結(jié)果顯示:工業(yè)區(qū)大氣顆粒物的細(xì)菌毒性要明顯高于居民區(qū),表明急性毒性結(jié)果與局地污染排放密切相關(guān);不同粒徑分布的大氣顆粒物細(xì)菌毒性結(jié)果產(chǎn)生顯著差異,證明毒性成分主要吸附在較細(xì)粒徑的顆粒物上.強(qiáng)有力的證據(jù)表明,顆粒物暴露后的肺組織病理?yè)p傷與氧化性自由基過(guò)量產(chǎn)生有關(guān),因此與自由基相關(guān)的毒理機(jī)制可作為下一步深入研究的路徑.4個(gè)采樣點(diǎn)主動(dòng)采樣、被動(dòng)采樣和大氣沉降樣品二噁英濃度范圍分別為0.034~1.29pg/m3、0.031~0.103pg/m3和0.226~4.67pg/(m2·d),平均值分別為0.366pg/m3、0.063pg/m3和1.82pg/(m2·d);優(yōu)勢(shì)組分分別為2,3,4,7,8-PeCDF、2,3,4,6,7,8-HxCDF、1,2,3,6,7,8-HxCDF和1,2,3,4,7,8-HxCDF,2,3,4,7,8-PeCDF、1,2,3,7,8-PeCDD、2,3,7,8-TCDD和2,3,7,8-TCDF,2,3,4,7,8-PeCDF、1,2,3,7,8-PeCDD、2,3,4,6,7,8-HxCDF和1,2,3,6,7,8-HxCDF.成人和兒童呼吸暴露量最大值分別為9.74×10-2pg/(kg·d)和1.28×10-1pg/(kg·d),均低于0.4pg/(kg·d)(呼吸進(jìn)入人體的每日允許攝入量),表明暴露風(fēng)險(xiǎn)處于可接受水平.

大氣顆粒物；生物毒性；費(fèi)氏弧菌；二噁英；呼吸暴露

眾所周知,細(xì)顆粒物已被認(rèn)定為一類具有遺傳毒性的致癌物[1].人體通過(guò)肺泡進(jìn)行氣體交換,肺是與大氣顆粒物相互作用首要部位[2].目前,關(guān)于大氣顆粒物的健康效應(yīng)的研究方法主要集中在動(dòng)物暴露實(shí)驗(yàn)和動(dòng)物流行病學(xué)統(tǒng)計(jì)分析.大量流行病學(xué)研究表明顆粒物污染大幅度增加肺癌、呼吸道疾病、心血管、腦血管疾病的發(fā)病風(fēng)險(xiǎn)[3-5],毒理學(xué)機(jī)制主要有基因毒性、活性氧(ROS)自由基誘導(dǎo)、氧化應(yīng)激性等[6-7].近年來(lái),一些微生物測(cè)試手段被用于大氣顆粒物環(huán)境毒性研究中,如Aammi等[8]采用發(fā)光細(xì)菌Vibrio fischeri、SOS顯色反應(yīng)法評(píng)估了伊斯坦布爾不同工業(yè)特征區(qū)域的大氣顆粒物的急性毒性、基因毒性, Lemos等[9]用沙門氏菌/微粒體實(shí)驗(yàn),研究了受石油化工影響區(qū)域的PM2.5對(duì)不同基因毒性標(biāo)記物的敏感性.

顆粒物吸附的毒性物質(zhì)種類繁多,以持久性有機(jī)污染物(POPs)最受關(guān)注,如多環(huán)芳烴(PAHs)、多氯聯(lián)苯(PCBs)、二噁英等[10],但尚無(wú)法有效建立污染物與其毒性效應(yīng)間的定量關(guān)系.通常將多氯代二苯并對(duì)二噁英(PCDDs)和多氯代二苯并呋喃(PCDFs)統(tǒng)稱為二噁英[11],在其210種單體中,具有生理毒性為2,3,7,8-位均被氯取代的17種化合物,簡(jiǎn)稱有毒異構(gòu)體;其中,以2,3,7,8-TCDD的毒性最強(qiáng),被稱為“世紀(jì)之毒”,是目前發(fā)現(xiàn)最毒的化合物之一[12].二噁英屬于無(wú)意產(chǎn)生的一類化合物,于1977年在城市生活垃圾焚燒爐煙氣和飛灰中被首次發(fā)現(xiàn)[13],由于來(lái)源過(guò)于廣泛,不能通過(guò)禁止生產(chǎn)或者禁止使用的行政手段來(lái)進(jìn)行污染控制量[14].鑒于其高毒性、持久性、生物累積、遠(yuǎn)距離遷移等特性,二噁英的監(jiān)測(cè)分析和風(fēng)險(xiǎn)評(píng)估工作一直是科研工作者研究重點(diǎn)及決策管理部門工作難點(diǎn)[11].Li等[15]、應(yīng)媛媛[16]、Chen等[17]、何曉蕾[18]曾經(jīng)對(duì)上海大氣環(huán)境中二噁英濃度水平進(jìn)行了監(jiān)測(cè)研究,但整體上上海市大氣顆粒物中二噁英的相關(guān)研究數(shù)據(jù)相對(duì)較少.本研究通過(guò)大規(guī)模、長(zhǎng)周期、被動(dòng)和主動(dòng)相結(jié)合的手段,開(kāi)展了上海市某工業(yè)區(qū)大氣環(huán)境中PCDD/Fs監(jiān)測(cè)分析,在迄今為止的文獻(xiàn)記載中尚不多見(jiàn).

上海是國(guó)家中心城市和長(zhǎng)江三角洲經(jīng)濟(jì)圈的龍頭城市,顆粒物是上海市環(huán)境空氣的主要污染物,顆粒物暴露下的毒性效應(yīng)和環(huán)境風(fēng)險(xiǎn)引起社會(huì)各界廣泛關(guān)注.目前,許多顆粒物暴露毒性研究主要針對(duì)單一動(dòng)物開(kāi)展,且系統(tǒng)性、連貫性的研究較少.本研究分別以細(xì)菌、動(dòng)物、人為主線,先后從細(xì)菌毒性(工業(yè)區(qū)、居民區(qū))、老鼠暴露肺部損害(暴露箱暴露、氣管灌注)、人群二噁英呼吸暴露風(fēng)險(xiǎn)(基于監(jiān)測(cè)分析數(shù)據(jù))3個(gè)方面對(duì)顆粒物的毒性效應(yīng)進(jìn)行了較為系統(tǒng)的研究.使用主動(dòng)采樣和被動(dòng)采樣相結(jié)合的手段,通過(guò)大規(guī)模、長(zhǎng)周期采樣對(duì)上海某工業(yè)區(qū)TSP樣品、氣相物質(zhì)、大氣沉降物樣品的17種2,3,7,8-PCDD/Fs含量進(jìn)行了監(jiān)測(cè)分析,不僅補(bǔ)充了上海市二噁英基礎(chǔ)數(shù)據(jù)信息,而且為開(kāi)展區(qū)域二噁英污染防控工作提供了科學(xué)依據(jù).

1 材料與方法

1.1 樣品采集

PM2.5樣品采樣點(diǎn)位于浦東中心城區(qū)某樓頂,距地面約20m,是典型的居民區(qū)采樣點(diǎn),受局地污染源排放影響較小;氣態(tài)污染物與TSP(主動(dòng)采樣)、氣相物質(zhì)(被動(dòng)采樣)和大氣沉降物的采樣點(diǎn)位于上海市某典型工業(yè)區(qū);樣品采集信息見(jiàn)表1.

1.2 實(shí)驗(yàn)方法和研究?jī)?nèi)容

1.2.1 發(fā)光細(xì)菌急性毒性 將表1“A05”采樣點(diǎn)6個(gè)PM2.5樣品膜剪碎,置于15mL滅菌超純水中超聲15min(80Hz),重復(fù)上述過(guò)程1次.在第3次超聲時(shí),加入20mL超純水超聲20min(80Hz),得到各個(gè)PM2.5待測(cè)樣品懸浮液. TSP和大氣沉降物懸浮液抽提步驟如下:(1)將TSP濾膜剪成1cm×3cm大小碎塊,稱重后置于藍(lán)蓋瓶中,加入100mL滅菌超純水,超聲振蕩30min,轉(zhuǎn)移至新藍(lán)蓋瓶中,再按上述步驟進(jìn)行兩次超聲,逐次轉(zhuǎn)移懸浮液至新藍(lán)蓋瓶中,直至新藍(lán)蓋瓶中懸液體積達(dá)300mL,懸浮液置于4℃冰箱備用,使用前用0.22μm的針頭過(guò)濾器對(duì)上述懸浮液進(jìn)行抽濾;(2)采用whatman濾膜(孔徑0.45μm)過(guò)濾大氣沉降溶液,干燥后稱重大氣沉降的重量,然后重復(fù)(1)中步驟進(jìn)行懸浮液抽濾.各待測(cè)樣品懸浮液信息見(jiàn)表2.

表1 樣品采集信息

表2 樣品懸浮液信息及毒性測(cè)試結(jié)果

1.2.2 老鼠暴露實(shí)驗(yàn) 本課題組先后通過(guò)暴露箱培養(yǎng)和氣管灌注2種方式開(kāi)展了顆粒物暴露下的動(dòng)物肺部毒性研究.如之前開(kāi)展實(shí)驗(yàn)[21],孕鼠及其8周齡大仔鼠被分別放置于暴露箱(呼吸環(huán)境空氣)和對(duì)照箱(呼吸經(jīng)HEPA膜過(guò)濾后的環(huán)境空氣)中進(jìn)行暴露實(shí)驗(yàn).同一實(shí)驗(yàn)室內(nèi)2個(gè)大小相同,第一批次實(shí)驗(yàn)動(dòng)物為30只12周大的懷孕SD大鼠,具體實(shí)驗(yàn)設(shè)計(jì)如下:(1)在妊娠4d后,大鼠被隨機(jī)分為兩組:18只進(jìn)入未經(jīng)過(guò)濾的暴露組,其余12只進(jìn)入設(shè)有HEPA網(wǎng)的對(duì)照組;(2)在妊娠第19d安樂(lè)死對(duì)照組及暴露組部分孕鼠;(3)未安樂(lè)死的部分孕鼠生下仔鼠后,分別在各自暴露箱里培育至8周成年后,實(shí)行安樂(lè)死.(4)提取老鼠血液和肺組織,進(jìn)行生物標(biāo)記物和肺臟病理分析.

在氣管灌注實(shí)驗(yàn)中,40只7周大C57雄鼠,隨機(jī)分為4組,飼養(yǎng)至8周大時(shí),開(kāi)始?xì)夤芄嘧?shí)驗(yàn).按照日均暴露濃度35,70,140,0μg/m3,對(duì)應(yīng)設(shè)置日灌注量為1.7,3.5,7.0μg的濃度梯度暴露組和生理鹽水對(duì)照組.完成灌注實(shí)驗(yàn)后,安樂(lè)死各實(shí)驗(yàn)組小鼠進(jìn)行肺臟病理分析.

1.2.3 二噁英監(jiān)測(cè)與分析 用毒性當(dāng)量(TEQ)和毒性當(dāng)量因子(TEF)來(lái)評(píng)價(jià)二噁英對(duì)環(huán)境或人體健康的潛在效應(yīng);TEF指有毒異構(gòu)體與毒性最強(qiáng)的2,3,7,8-TCDD毒性當(dāng)量的比值,其中2,3,7,8-TCDD的TEF為1[22].17種有毒異構(gòu)體TEF及濃度均值(TEQ)分別見(jiàn)表3[23-25]和表4.

表3 17種二噁英有毒異構(gòu)體毒性當(dāng)量因子

注: WHO-TEF、I-TEF分別是世界衛(wèi)生組織(WHO)、北大西洋公約組織(NATO)制定的毒性當(dāng)量.

表4 4個(gè)采樣點(diǎn)17種二噁英有毒異構(gòu)體毒性當(dāng)量濃度平均值

1.2.4 二噁英人體呼吸暴露健康風(fēng)險(xiǎn)評(píng)價(jià) 根據(jù)VLIER-HUMAAN暴露模型公式和參數(shù)[26],按照式(1)評(píng)估人群二噁英呼吸暴露量.

Inh =r×air×r×f/ BW (1)

式中:Inh為呼吸暴露劑量,pg/(kg·d);r為呼吸量,m3/d,大人該值設(shè)為20,兒童為7.6;air為空氣中二噁英的平均濃度,pg/m3;f為空氣在肺泡中氣體交換的保留分?jǐn)?shù),0.75;t為暴露時(shí)間分?jǐn)?shù),即暴露時(shí)間與24h的比值;BW為體重,kg.

2 結(jié)果與討論

2.1 細(xì)菌毒性

5個(gè)采樣點(diǎn)的發(fā)光細(xì)菌急性毒性結(jié)果(表2)顯示:工業(yè)區(qū)4個(gè)采樣點(diǎn)中,某些采樣點(diǎn)上TSP和大氣沉降物表現(xiàn)出不同程度的急性毒性效應(yīng);除A04采樣點(diǎn)外,其他采樣點(diǎn)呈現(xiàn)出中急性毒性(A01、A03)或高急性毒性(A02);而居民區(qū)A05采樣點(diǎn)6個(gè)PM2.5中有2個(gè)樣品為低急性毒性,其余4個(gè)為無(wú)急性毒性.從整體上看,工業(yè)區(qū)大氣顆粒物的細(xì)菌毒性要明顯高于居民區(qū),由此可以推斷,相比居民區(qū),工業(yè)區(qū)采樣點(diǎn)受周圍污染源影響較為明顯,造成某些采樣點(diǎn)Vibrio fischeri細(xì)菌急性毒性呈現(xiàn)中、高毒性的結(jié)果;而民區(qū)采樣點(diǎn)受局地污染影響較小,PM2.5吸附毒性物質(zhì)成分較少或濃度較低,可能是其Vibrio fischeri細(xì)菌急性毒性“低毒或無(wú)毒”的原因.

此外,A01、A03采樣點(diǎn)同一季節(jié)的不同粒徑范圍的大氣顆粒物樣品細(xì)菌毒性結(jié)果產(chǎn)生顯著差異,A01、A03采樣點(diǎn)TSP(粒徑￡100μm)的毒性明顯高于大氣沉降顆粒(粒徑310μm)的細(xì)菌急性毒性.這一研究結(jié)果表明毒性成分主要集中吸附在較細(xì)粒徑的顆粒物上,同時(shí)也佐證了當(dāng)下普遍認(rèn)可的研究結(jié)論-“細(xì)顆粒物比粗顆粒物危害更大”.

2.2 顆粒物暴露動(dòng)物毒性

暴露箱培養(yǎng)和氣管灌注實(shí)驗(yàn)均顯示,顆粒物暴露對(duì)肺組織造成損傷,主要病例特征為肺部炎癥和纖維化,這與其他一些類似研究結(jié)論相吻合[27-29].在生物液樣品測(cè)試中,MDA(丙二醛)、8-isoprostane(8-異前列腺素)和GSH(谷胱甘肽轉(zhuǎn)移酶) 常作為氧化應(yīng)激性標(biāo)記物出現(xiàn).相比對(duì)照組,暴露組孕鼠及其仔鼠血液中MDA濃度分別增加了85.6%和86.7%,仔鼠肺中MDA和8-isoprostane濃度分別增加了286%和50.8%. MDA和8-isoprostane來(lái)源于自由基與脂質(zhì)的過(guò)氧化反應(yīng),其含量的高低間接反映了機(jī)體細(xì)胞受自由基攻擊的嚴(yán)重程度[30-32],這與“ROS誘導(dǎo)損傷”機(jī)制吻合,說(shuō)明顆粒物暴露造成活性自由基大量生成(如ROS),進(jìn)而影響機(jī)體健康.此外,暴露組孕鼠及其仔鼠血液中GSH濃度降低了65.6%和54.0%,由于GSH可以清除機(jī)體內(nèi)的自由基和活性氧,是體內(nèi)重要的抗氧化劑,是細(xì)胞抗氧化能力的標(biāo)志[33],說(shuō)明顆粒物暴露致使體內(nèi)氧化與抗氧化系統(tǒng)失衡,偏向于氧化環(huán)境,從而影響機(jī)體功能正常表達(dá).與自由基相關(guān)的毒性機(jī)制仍需進(jìn)一步研究然而這些研究成果都是基于顆粒物暴露后的病理指標(biāo)分析,并不能說(shuō)明暴露危害路徑和機(jī)制,自由基相關(guān)的毒性機(jī)制可作為深入研究的路徑.

本課題組曾對(duì)顆粒物暴露后的肺部差異基因進(jìn)行研究分析,發(fā)現(xiàn)DNA和核糖體合成、免疫和消化系統(tǒng)的基因功能聚類產(chǎn)生異常.目前已證實(shí)的“基因毒性、ROS誘導(dǎo)損傷、氧化應(yīng)激”等毒理學(xué)過(guò)程,均與基因異常表達(dá)密切相關(guān),如ROS誘導(dǎo)氧化應(yīng)激性被認(rèn)為在PM2.5暴露下細(xì)胞毒性機(jī)制中起重要作用[31,34].有研究表明PM2.5暴露通過(guò)ROS誘導(dǎo)氧化應(yīng)激性損傷,主要包括DNA損傷和修復(fù)、細(xì)胞死亡,炎癥和遺傳調(diào)控[6,35].因此基因表達(dá)和基因損傷研究可能是揭示顆粒物暴露危害機(jī)制的關(guān)鍵手段.

2.3 二噁英分布特征

主動(dòng)采樣能夠在短時(shí)間內(nèi)采集氣體樣品,但會(huì)造成PCDD/Fs檢測(cè)結(jié)果產(chǎn)生較大波動(dòng)[36].而被動(dòng)采樣采樣周期長(zhǎng),可以彌補(bǔ)主動(dòng)采樣的不足,與主動(dòng)采樣數(shù)據(jù)互為補(bǔ)充,較全面地了解區(qū)域污染情況.4個(gè)采樣點(diǎn)主動(dòng)、被動(dòng)采樣和大氣沉降樣品,二噁英濃范圍分別為0.034~1.29pg/m3、0.031~ 0.103pg/m3和0.226~4.67pg/(m2·d),平均值分別為0.366pg/m3、0.063pg/m3和1.82pg/(m2·d).4個(gè)采樣點(diǎn)二噁英濃度(TEQ)分布見(jiàn)表5.

表5 4個(gè)采樣點(diǎn)二噁英濃(TEQ)度分布

4個(gè)采樣點(diǎn)二噁英濃度均值見(jiàn)圖1.可以看出,冬季大氣環(huán)境中二噁英濃度明顯高于夏季,其原因主要是冬季大氣穩(wěn)定度較高,混合層高度較低,平均風(fēng)速較低,導(dǎo)致較高的大氣污染物落地濃度.

圖1 4個(gè)采樣點(diǎn)二噁英濃度均值

2.4 二噁英組分特征

考慮到毒性當(dāng)量因子的計(jì)算影響,17種2,3,7,8-PCDD/Fs的毒性當(dāng)量?jī)?yōu)勢(shì)組分與濃度含量?jī)?yōu)勢(shì)組分分布有所差異.主動(dòng)采樣條件下,部分樣品中的2,3,7,8-TCDD、1,2,3,7,8-PeCDD、1,2,3, 4,7,8-HxCDD 和1,2,3,7,8,9-HxCDD低于檢測(cè)限,優(yōu)勢(shì)組分為2,3,4,7,8-PeCDF、2,3,4,6,7, 8-HxCDF、1,2,3,6,7,8-HxCDF和1,2,3,4,7,8- HxCDF,見(jiàn)圖2a.

被動(dòng)采樣條件下,部分樣品中123789- HxCDF、2378-TCDD和123478-HxCDD低于檢測(cè)限,優(yōu)勢(shì)組分為23478-PeCDF、12378-PeCDD、2378-TCDD和2378-TCDF,具體信息見(jiàn)圖2b.

大氣沉降物中部分樣品2,3,7,8-TCDD、1,2,3,7,8-PeCDD低于檢測(cè)限,優(yōu)勢(shì)組分為2,3, 4,7,8-PeCDF、1,2,3,7,8-PeCDD、2,3,4,6,7,8- HxCDF和123678-HxCDF,具體信息見(jiàn)圖3.

圖3 大氣沉降物優(yōu)勢(shì)組分

2.5 二噁英呼吸暴露風(fēng)險(xiǎn)評(píng)價(jià)

二噁英具有難生物降解、長(zhǎng)代謝半衰期和強(qiáng)親脂性的特點(diǎn),不僅可以通過(guò)鼻、口呼吸進(jìn)入肺部組織,還可以通過(guò)食物鏈攝取方式在體內(nèi)累積和富集[37].由圖4可知,二噁英人體暴露的介質(zhì)主要有大氣、土壤、植物、水和魚(yú),空氣吸入、食物攝取、皮膚接觸是進(jìn)入人體的主要途徑[38-39].本課題基于環(huán)境大氣中的二噁英監(jiān)測(cè)數(shù)據(jù),對(duì)成人和兒童的呼吸暴露量風(fēng)險(xiǎn)進(jìn)行了研究.

按照式(1):Inh =r×air×r×f/,計(jì)算呼吸暴露劑量Inh.假設(shè)個(gè)體室外和室內(nèi)暴露濃度相同,t成人取0.616,兒童取0.457;BW成人為70kg,兒童為15kg.則Inh成人= 0.132Cair,Inh兒童= 0.174Cair.

圖4 二噁英人體暴露途徑

表6 成人和兒童二噁英呼吸暴露量

將大氣主動(dòng)采樣、被動(dòng)采樣二噁英檢測(cè)數(shù)據(jù)代入后,分別得到成人和兒童的呼吸暴露量;按照WHO提出的人體每日可耐受攝入量TDI [4pg/ (kg·d)]為參考標(biāo)準(zhǔn)計(jì)算呼吸暴露占標(biāo)率.大氣主動(dòng)、被動(dòng)采樣條件下,成人呼吸暴露量分別為1.85~9.74′10-2pg/(kg·d)、0.40~1.36′10-2pg/ (kg·d);兒童呼吸暴露量分別為0.24~1.28′10-2pg/ (kg·d)、0.53~1.79′10-2pg/(kg·d).具體內(nèi)容見(jiàn)表6.可以看出,4個(gè)采樣點(diǎn)二噁英呼吸暴露量均呈現(xiàn)冬季大于夏季現(xiàn)象,這種現(xiàn)象在主動(dòng)采樣條件下較為明顯.

根據(jù)《關(guān)于進(jìn)一步加強(qiáng)生物質(zhì)發(fā)電項(xiàng)目環(huán)境影響評(píng)價(jià)管理工作的通知》(環(huán)發(fā)[2008]82號(hào))附件-生物質(zhì)發(fā)電項(xiàng)目環(huán)境影響評(píng)價(jià)文件審查的技術(shù)要點(diǎn)中“環(huán)境風(fēng)險(xiǎn)”評(píng)估要求:風(fēng)險(xiǎn)評(píng)價(jià)標(biāo)準(zhǔn)參照人體每日可耐受攝入量4pgTEQ/kg執(zhí)行,經(jīng)呼吸進(jìn)入人體的允許攝入量按每日可耐受攝入量10%執(zhí)行(即占標(biāo)率為10%).本研究中,大氣主動(dòng)、被動(dòng)采樣條件下,成人呼吸暴露量占標(biāo)率分別為0.46~2.44%、0.10~0.34%;兒童呼吸暴露量占標(biāo)率分別為0.75~3.2%、0.13~0.45%;均低于10%,處于可接受的水平.

3 結(jié)論

3.1 工業(yè)區(qū)、居民區(qū)大氣顆粒物細(xì)菌毒性分別為“中、高”和“低”毒性.相比居民區(qū),工業(yè)區(qū)顆粒物吸附毒性物質(zhì)成分較多或濃度較高,可能是其“細(xì)菌毒性明顯高于居民區(qū)”的原因,同時(shí)也表明毒性結(jié)果與局地污染排放密切相關(guān).

3.2 同一采樣點(diǎn)(A01、A03)在同一季節(jié)所采集的不同粒徑范圍的大氣顆粒物細(xì)菌毒性結(jié)果產(chǎn)生顯著差異,即TSP(粒徑￡100μm)毒性明顯高于大氣沉降顆粒(粒徑310μm)的細(xì)菌急性毒性,說(shuō)明毒性成分主要集中吸附在較細(xì)粒徑的顆粒物上.

3.3 老鼠暴露實(shí)驗(yàn)表明,顆粒物暴露后的肺部病理?yè)p傷與氧化性自由基過(guò)量產(chǎn)生有關(guān),自由基相關(guān)的毒理機(jī)制可作為下一步深入研究的路徑.

3.4 主動(dòng)采樣,二噁英濃度(TEQ)范圍為0.034~ 1.29pg/m3,平均濃度為0.366pg/m3,優(yōu)勢(shì)組分為2,3,4,7,8-PeCDF、2,3,4,6,7,8-HxCDF、1,2,3,6,7, 8-HxCDF和1,2,3,4,7,8-HxCDF;被動(dòng)采樣,二噁英濃度(TEQ)范圍為0.031~0.103pg/m3,平均濃度為0.063pg/m3,優(yōu)勢(shì)組分為2,3,4,7,8-PeCDF、1,2, 3,7,8-PeCDD、2,3,7,8-TCDD和2,3,7,8-TCDF;大氣沉降樣品二噁英濃度(TEQ)范圍為0.226~ 4.67pg/(m2·d),平均濃度為1.82pg/(m2·d),優(yōu)勢(shì)組分為2,3,4,7,8-PeCDF、1,2,3,7,8-PeCDD、2,3,4,6,7, 8-HxCDF和1,2,3,6,7,8-HxCDF.冬季環(huán)境大氣中二噁英濃度明顯高于夏季,主要原因是冬季大氣穩(wěn)定度較高,不利于污染物轉(zhuǎn)移擴(kuò)散.

3.5 成人和兒童呼吸暴露量最大值分別為9.74×10-2pg/(kg·d)和1.28×10-1pg/(kg·d),均低于WHO推薦的呼吸進(jìn)入人體的每日允許攝入量[0.4pg/(kg·d)],表明暴露風(fēng)險(xiǎn)處于可接受水平.

[1] 王 嬡,黃 薇,汪 彤,等.患心血管病老年人夏季PM2.5和CO的暴露特征及評(píng)價(jià)[J]. 中國(guó)環(huán)境科學(xué), 2009,(9):1005-1008.

[2] Guan W, Zheng X, Chung K F, et al. Impact of air pollution on the burden of chronic respiratory diseases in China: Time for urgent action [J]. The Lancet, 2016,388(10054):1939-1951.

[3] Ostro B, Malig B, Broadwin R, et al. Chronic PM2.5exposure and inflammation: Determining sensitive subgroups in mid-life women [J]. Environmental Research, 2014,132:168.

[4] Shaughnessy W J, Venigalla M M, Trump D. Health effects of ambient levels of respirable particulate matter (PM) on healthy, young-adult population [J]. Atmos. Environ., 2015,123:102-111.

[5] Leiva G M A, Santiba?ez D A, Ibarra E S, et al. A five-year study of particulate matter (PM2.5) and cerebrovascular diseases [J]. Environmental Pollution, 2013,181:1-6.

[6] Vattanasit U, Navasumrit P, Khadka M B, et al. Oxidative DNA damage and inflammatory responses in cultured human cells and in humans exposed to traffic-related particles [J]. International J. Hygiene and Environmental Health, 2014,217(1): 23-33.

[7] Líbalová H, Kr?ková S, Uhlí?ová K, et al. Analysis of gene expression changes in A549cells induced by organic compounds from respirable air particles [J]. Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis, 2014,770:94-105.

[8] Aammi S, Karaca F, Petek M. A toxicological and genotoxicological indexing study of ambient aerosols (PM2.5~10) using in vitro bioassays [J]. Chemosphere, 2017,174:490-498.

[9] Lemos A T, Lemos C T D, Flores A N, et al. Genotoxicity biomarkers for airborne particulate matter (PM2.5) in an area under petrochemical influence [J]. Chemosphere, 2016,159:610- 618.

[10] 董繼元,劉興榮,張本忠,等.上海市居民暴露于多環(huán)芳烴的健康風(fēng)險(xiǎn)評(píng)價(jià)[J]. 生態(tài)環(huán)境學(xué)報(bào), 2015,(1):126-132.

[11] 裴新輝,謝群慧,胡 芹,等.二噁英對(duì)免疫系統(tǒng)影響的研究進(jìn)展[J]. 環(huán)境化學(xué), 2011,(1):200-210.

[12] 楊永濱,鄭明輝,劉征濤.二惡英類毒理學(xué)研究新進(jìn)展[J]. 生態(tài)毒理學(xué)報(bào), 2006,(2):105-115.

[13] Ding, Yingming, Wang, et al. Seasonal trend of ambient PCDD/Fs in Tianjin City, northern China using active sampling strategy [J]. 環(huán)境科學(xué)學(xué)報(bào)(英文版), 2012,24(11):1966-1971.

[14] 陳小亮.中美二噁英相關(guān)標(biāo)準(zhǔn)的比較[J]. 中國(guó)環(huán)境管理, 2014, (3):26-30.

[15] Li H, Feng J, Sheng G, et al. The PCDD/F and PBDD/F pollution in the ambient atmosphere of Shanghai, China [J]. Chemosphere, 2008,70(4):576-583.

[16] 應(yīng)媛媛.上海市典型區(qū)域大氣和土壤樣品中二噁英初探[D]. 上海:華東理工大學(xué), 2010.

[17] Chen T, Li X, Yan J, et al. Distribution of polychlorinated dibenzo-dioxins and dibenzofurans in ambient air of different regions in China [J]. Atmospheric Environment, 2011,45(36): 6567-6575.

[18] 何曉蕾.上海地區(qū)大氣中二噁類分布特征的初步研究[J]. 城市環(huán)境與城市生態(tài), 2014,(6):8-13.

[19] Wang X H, Fan L Y, Wang S, et al. Relationship between acute and chronic toxicity for prevalent organic pollutants in Vibrio fischeri based upon chemical mode of action [J]. Journal of Hazardous Materials, 2017,338:458-465.

[20] ISO. ISO 11348-3:2007. Water quality - Determination of the inhibitory effect of water samples on the light emission of Vibrio fischeri (Luminescent bacteria test) - Part 3: Method using freeze-dried bacteria [S]. 2007.

[21] Song P C, Li Z G, Li X, et al. Transcriptome Profiling of the Lungs Reveals Molecular Clock Genes Expression Changes after Chronic Exposure to Ambient Air Particles: [J]. International J. Environ. Res. Public Health, 2017,14(1):90.

[22] 徐夢(mèng)俠.城市生活垃圾焚燒廠二惡英排放的環(huán)境影響研究[D]. 杭州:浙江大學(xué), 2009.

[23] Govers H A J, Krop H B. Partition constants of chlorinated dibenzofurans and dibenzo-p-dioxins [J]. Chemosphere, 1998, 37(9):2139-2152.

[24] CCMS N. Scientific bases for the development of international toxicity equivalency factor (I-TEF) method of risk assessment for the complex mixtures of dioxins and related compounds [M]. Washington D. C. North Atlantic Treaty Organization/Committee on Challenges of Modern Society, 1988.

[25] Van den Berg M, Birnbaum L, Bosveld A T, et al. Toxic equivalency factors (TEFs) for PCBs, PCDDs, PCDFs for humans and wildlife. [J]. Environmental Health Perspectives, 1998,106(12):775-792.

[26] Nouwen J, Cornelis C, De F R, et al. Health risk assessment of dioxin emissions from municipal waste incinerators: The Neerlandquarter (Wilrijk, Belgium). [J]. Chemosphere, 2001, 43(4):909-923.

[27] Liu X, Jin X, Su R, et al. The reproductive toxicology of male SD rats after PM2.5exposure mediated by the stimulation of endoplasmic reticulum stress [J]. Chemosphere, 2017,189:547- 555.

[28] Gao R, Ku T, Ji X, et al. Abnormal energy metabolism and tau phosphorylation in the brains of middle-aged mice in response to atmospheric PM2.5exposure. [J]. J. Environ. Sci., 2017,62(12): 145-153.

[29] Hu Y, Wang L S, Li Y, et al. Effects of particulate matter from straw burning on lung fibrosis in mice [J]. Environmental Toxicology & Pharmacology, 2017,56:249.

[30] Tsikas D, Rothmann S, Schneider J Y, et al. Development, validation and biomedical applications of stable-isotope dilution GC–MS and GC–MS/MS techniques for circulating malondialdehyde (MDA) after pentafluorobenzyl bromide derivatization: MDA as a biomarker of oxidative stress and its relation to 15(S)-8-iso-prostaglandin F2α and nitric oxide (NO) [J]. Journal of Chromatography B, 2016,1019:95-111.

[31] Ma M, Li S, Jin H, et al. Characteristics and oxidative stress on rats and traffic policemen of ambient fine particulate matter from Shenyang [J]. Sci. Total Environ., 2015,526:110-115.

[32] Elfsmark L, ?gren L, Akfur C, et al. 8-Isoprostane is an early biomarker for oxidative stress in chlorine-induced acute lung injury [J]. Toxicology Letters, 2018,282:1-7.

[33] Schmitt B, Vicenzi M, Garrel C, et al. Effects of N-acetylcysteine, oral glutathione (GSH) and a novel sublingual form of GSH on oxidative stress markers: A comparative crossover study. [J]. Redox Biology, 2015,6:198-205.

[34] Coronas M V, Vaz Rocha J A, Favero Salvadori D M, et al. Evaluation of area contaminated by wood treatment activities: Genetic markers in the environment and in the child population [J]. Chemosphere, 2016, 144:1207-1215.

[35] Topinka J, Rossner P, Milcova A, et al. DNA adducts and oxidative DNA damage induced by organic extracts from PM2.5in an acellular assay [J]. Toxicology Letters, 2011,202(3):186-192.

[36] W?giel M, Chrz?szcz R, Ma?lanka A, et al. Study on the determination of PCDDs/Fs and HCB in exhaust gas. [J]. Chemosphere, 2011, 85(3):481-486.

[37] 黃 超,陳 凝,楊明嘉,等.二噁英類的毒性作用機(jī)制及其生物檢測(cè)方法[J]. 生態(tài)毒理學(xué)報(bào), 2015,10(3):50-62.

[38] Lohmann R, Jones K C. Dioxins and furans in air and deposition: a review of levels, behaviour and processes [J]. Science of the Total Environment, 1998,219(1):53-81.

[39] Oh J E, Choi J S, Chang Y S. Gas/particle partitioning of polychlorinated dibenzo-p-dioxins and dibenzofurans in atmosphere; evaluation of predicting models [J]. Atmospheric Environment, 2001,35(24):4125- 4134.

Biotoxicity effects and respiratory risk assessment of PCDD/Fs exposured to atmospheric particulates in Shanghai.

SONG Peng-cheng1, LU Shu-yu1,2*, WEI Yong-jie3, LUO Li-juan4, CHEN Xiao-qian5

(1.College of Environmental Science and Engineering, Donghua University, Shanghai 201620, China；2.Shanghai Society of Environmental Sciences, Shanghai 200003, China；3.Chinese Research Academy of Environmental Sciences, Beijing 100012, China；4.Shanghai Radio-Environment Supervision Agency, Shanghai 200065, China；5.Shanghai Academy of Public Measurement, Shanghai 201203, China)., 2018,38(5)：1961~1969

Bacterial toxicity of atmospheric particulate suspensions in residential and industrial areas was evaluated with Microtox test (), and the toxicity effects of rats after particulate exposure were also analyzed and discussed. HRGC-HRMS was applied to study concentration level and composition characteristic of PCDD/Fs, in addition, dioxin respiratory exposure risk assessment was conducted based on the data analysis. Results showed that the acute toxicity of atmospheric particulate in industrial site was higher than those in residential site, which indicated that acute toxicity was closely related to local pollution. The bacterial toxicity results of airborne particles with different particle sizes were significantly different, which suggested that toxicant was mainly adsorbed on finer particles. Exposure experiment studies provided overwhelming evidence that pathological damage of lungs after particulate exposure was correlative with overproduction of oxidative free radical, so toxicological mechanism associated with free radicals could be used as a pathway for further in-depth study. Concentration of PCDD/Fs ranged from 0.034~1.29pg/m3in active sampling, from 0.031~0.103pg/m3in passive sampling, and from 0.226~4.67pg/(m2·d) in atmospheric deposition sampling respectively, with a mean concentration of 0.366pg/m3, 0.063pg/m3and 1.82pg/(m2·d) respectively. Dominant composition characteristics of PCDD/Fs were 2,3,4,7,8-PeCDF, 2,3,4,6,7,8-HxCDF, 1,2,3,6,7,8-HxCDF, 1,2,3,4,7,8-HxCDF for active sampling,2,3,4,7,8-PeCDF, 1,2,3,7,8-PeCDD, 2,3,7,8-TCDD, 2,3,7,8-TCDF for passive sampling, and 2,3,4,7,8-PeCDF, 1,2,3,7,8-PeCDD, 2,3,7,8-TCDD, 2,3,7,8-TCDF for atmospheric deposition sampling respectively. Maximum respiratory exposures of adult [9.74×10-2pg/(kg·d)]and children [1.28×10-1pg/(kg·d)] were lower than 0.4pg/(kg·d)-1(maximum allowed daily intake), which indicated an acceptable level of inhalation exposure risk.

atmospheric particulates；biotoxicity；；PCDD/Fs；respiratory exposure

X171.5,X823

A

1000-6923(2018)05-1961-09

2017-11-17

上海市環(huán)境保護(hù)局環(huán)?？蒲许?xiàng)目專項(xiàng)(滬環(huán)科2013第79號(hào),滬環(huán)科2014第38號(hào))

* 責(zé)任作者, 教授級(jí)高級(jí)工程師, sisrlu@126.com

宋鵬程(1987-),男,河南信陽(yáng)人,東華大學(xué)博士研究生,主要從事大氣顆粒物污染控制及毒性效應(yīng)方面的研究.發(fā)表論文3篇.