Thiolated arsenicals in arsenic metabolism: Occurrence, formation, and biological implications

Arsenic (As) is a notoriously toxic pollutant of health concern worldwide with potential risk of cancer induction, but meanwhile it is used as medicines for the treatment of different conditions including hematological cancers. Arsenic can undergo extensive metabolism in biological systems, and both toxicological and therapeutic effects of arsenic compounds are closely related to their metabolism. Recent studies have identified methylated thioarsenicals as a new class of arsenic metabolites in biological systems after exposure of inorganic and organic arsenicals, including arsenite, dimethylarsinic acid (DMAV), dimethylarsinous glutathione (DMAIIIGS), and arsenosugars. The increasing detection of thiolated arsenicals, including monomethylmonothioarsonic acid (MMMTAV), dimethylmonothioarsinic acid (DMMTAV) and its glutathione conjugate (DMMTAVGS), and dimethyldithioarsinic acid (DMDTAV) suggests that thioarsenicals may be important metabolites and play important roles in arsenic toxicity and therapeutic effects. Here we summarized the reported occurrence of thioarsenicals in biological systems, the possible formation pathways of thioarsenicals, and their toxicity, and discussed the biological implications of thioarsenicals on arsenic metabolism, toxicity, and therapeutic effects.     

Preliminary studies on the stability of arsenolipids: Implications for sample handling and analysis

Human health risk assessments concerning arsenic are now estimating exposure through food in addition to exposure through drinking water. Intrinsic to this assessment is sample handling and preparation that maintains the arsenic species in the form that they occur in foods. We investigated the stability of three arsenolipids(two arsenic fatty acids, As FA-362 and As FA-388, and one arsenic hydrocarbon As HC-332), common constituents of fish and algae, relevant to sample storage and transport, and to their preparation for quantitative measurements. The fate of the arsenolipids was followed by high performance liquid chromatography/electrospray triple quadruple mass spectrometry(HPLC/ESIMS) analyses.Storage of the compounds dry as pure compounds or mixed in fish oil at up to 60?C did not result in significant changes to the compounds, although losses were observed by apparent adsorption onto the plastic walls of the polypropylene tubes. No losses occurred when the experiment was repeated with glass tubes. When the compounds were stored in ethanol for up to 15 days under acidic, neutral, or alkaline conditions(each at room temperature), no significant decomposition was observed, although esterification of the fatty acids occurred at low p H. The compounds were also stable during a sample preparation step involving passage through a small silica column. The results indicate that these typical arsenolipids are stable when stored in glass at temperatures up to 60?C for at least 2 days, and that,consequently, samples of food or extracts thereof can be transported dry at ambient temperatures, i.e. without the need for cool conditions.     

Cellular arsenic transport pathways in mammals

Natural contamination of drinking water with arsenic results in the exposure of millions of people world-wide to unacceptable levels of this metalloid. This is a serious global health problem because arsenic is a Group 1 (proven) human carcinogen and chronic exposure is known to cause skin, lung, and bladder tumors. Furthermore, arsenic exposure can result in a myriad of other adverse health effects including diseases of the cardiovascular, respiratory, neurological, reproductive, and endocrine systems. In addition to chronic environmental exposure to arsenic, arsenic trioxide is approved for the clinical treatment of acute promyelocytic leukemia, and is in clinical trials for other hematological malignancies as well as solid tumors. Considerable inter-individual variability in susceptibility to arsenic-induced disease and toxicity exists, and the reasons for such differences are incompletely understood. Transport pathways that influence the cellular uptake and export of arsenic contribute to regulating its cellular, tissue, and ultimately body levels. In the current review, membrane proteins (including phosphate transporters, aquaglyceroporin channels, solute carrier proteins, and ATP-binding cassette transporters) shown experimentally to contribute to the passage of inorganic, methylated, and/or glutathionylated arsenic species across cellular membranes are discussed. Furthermore, what is known about arsenic transporters in organs involved in absorption, istribution, and metabolism and how transport pathways contribute to arsenic elimination are described.     

饮水型砷暴露对小鼠多系统脏器的毒性作用

为揭示饮水型砷暴露对机体的毒性,系统研究了砷摄入对实验动物基础生理和多系统脏器的毒性损伤作用.选雄性ICR小鼠为受试动物,以自由饮用含砷10 mg·L^-1的水溶液进行染毒,连续染毒60 d后检测发现,饮水砷暴露对小鼠一般体征和体重无显著影响,肝脏脏器系数显著降低,心脏、肺脏、肾脏和睾丸脏器系数降低,但无统计学意义.砷染毒组血清谷丙转氨酶（ALT）和谷草转氨酶（AST）活性显著升高,总胆固醇（TC）和甘油三酯（TG）含量显著升高,高密度脂蛋白胆固醇（HDL-C）含量显著降低,低密度脂蛋白胆固醇（LDL-C）含量显著升高;肝脏、小肠、心脏、肺脏、肾脏和睾丸组织中还原型谷胱甘肽（GSH）含量和超氧化物歧化酶（T-SOD）活性显著降低,过氧化氢（H₂O₂）和丙二醛（MDA）含量显著升高,并出现程度不同的组织形态结构损伤.研究结果表明,饮水砷暴露可诱发实验小鼠肝脏功能异常、生理代谢紊乱,导致消化系统、循环系统、呼吸系统、泌尿系统与生殖系统等多系统脏器组织的氧化损伤和结构病变,砷暴露对机体的毒性作用存在组织器官差异性,对肝脏的损伤较严重.     

Determination of total arsenic by photo-decomposition of organoarsenic compounds and hydride generation electrothermal atomic absorption spectrometry

A method was developed for the determination of total arsenic concentration in less than ng/ml level by decomposition of organoarsenicals using photo -oxidation combined with in situ trapping of arsenic hydride on a palladium coated graphite tube with subsequent atomization and detection by AAS. The organoarsenicals include monomethylarsenic, dimethylarsenic, arsenobetaine, arsenocholine, o -aminobenzenarsenate and p -aminobenzenarsenate. The method is simple and sensitive. Detection limit was obtained from different arsenic compounds over the range from 0. 058 to 0.063 ng/ml as As (based on three times of the standard deviation of 10 blank measurements) and the relative standard deviations for ten replicate measurements were from 2.0 to 3.8%. The calibration curves of arsenic compounds including inorganic and organic arsenicals were linear over the range from 0.1 to 3.0 ng/ml as As. The recommended method has been applied to the determination of total arsenic in tap and lake water samples at ng/ml leve     

Inorganic arsenic: A non-genotoxic carcinogen

Inorganic arsenic induces a variety of toxicities including cancer. The mode of action for cancer and non-cancer effects involves the metabolic generation of trivalent arsenicals and their reaction with sulfhydryl groups within critical proteins in various cell types which leads to the biological response. In epithelial cells, the response is cell death with consequent regenerative proliferation. If this continues for a long period of time, it can result in an increased risk of cancer. Arsenicals do not react with DNA. There is evidence for indirect genotoxicity in various in vitro and in vivo systems, but these involve exposures at cytotoxic concentrations and are not the basis for cancer development. The resulting markers of genotoxicity could readily be due to the cytotoxicity rather than an effect on the DNA itself. Evidence for genotoxicity in humans has involved detection of chromosomal aberrations, sister chromatid exchanges in lymphocytes and micronucleus formation in lymphocytes, buccal mucosal cells, and exfoliated urothelial cells in the urine. Numerous difficulties have been identified in the interpretation of such results, including inadequate assessment of exposure to arsenic, measurement of micronuclei, and potential confounding factors such as tobacco exposure, folate deficiency, and others. Overall, the data strongly supports a non-linear dose response for the effects of inorganic arsenic. In various in vitro and in vivo models and in human epidemiology studies there appears to be a threshold for biological responses, including cancer.     

金属有机框架材料吸附去除水中有机砷的研究进展

有机砷作为饲料添加剂在家禽养殖中被广泛使用,并伴随着家禽粪便大量进入环境中. 进入环境后有机砷容易被生物降解或(光)化学氧化转化为剧毒的无机砷,危害环境和人体健康. 因此,高效处理有机砷污染受到广泛关注. 金属有机框架(metal organic frameworks, MOFs)材料因其具有孔隙率和比表面积大、孔道尺寸可调、易功能化改性和材料性能可定制等特点,在水体污染物的去除中展现了良好的应用前景. 本文综述了目前MOFs材料作为吸附剂去除水环境中有机砷的最新研究进展,介绍了吸附有机砷MOFs材料的种类、制备方法和吸附性能,总结了MOFs材料吸附有机砷的关键影响因素,并归纳了不同类型MOFs材料吸附的再生方法和稳定性. 最后,指出了当前MOFs存在的技术缺陷及限制工程应用的关键因素,并提出相对应的建议及解决措施.      

Assessment of global industrial-age anthropogenic arsenic contamination

Arsenic, a carcinogenic trace element, threatens not only the health of millions of humans and other living organisms, but also global sustainability. We present here, for the first time, the global industrial-age cumulative anthropogenic arsenic production and its potential accumulation and risks in the environment. In 2000, the world cumulative industrial-age anthropogenic arsenic production was 4.53 million tonnes. The world-wide coal and petroleum industries accounted for 46% of global annual gross arsenic production, and their overall contribution to industrial-age gross arsenic production was 27% in 2000. Global industrial-age anthropogenic As sources (as As cumulative production) follow the order: As mining production >As generated from coal >As generated from petroleum. The potential industrial-age anthropogenic arsenic input in world arable surface in 2000 was 2.18 mg arsenic kg^–1, which is 1.2 times that in the lithosphere. The development of substitute materials for arsenic applications in the agricultural and forestry industries and controls of arsenic emissions from the coal industry may be possible strategies to significantly decrease arsenic pollution sources and dissipation rates into the environment.     

两个品种水稻对砷的吸收富集与转化特征及其健康风险

以2个水稻品种威优402号和Ⅱ优416号为实验材料,采用温室栽培方法研究对比两个品种水稻在人工添加砷处理(0、10、20和40mg·kg-1)和模拟自然砷污染(贵州高砷土和北京褐土的混合土,质量比为1∶1)胁迫条件下的生长发育状况,分析砷在水稻不同部位的累积、形态转化及其健康风险.砷处理显著地抑制了两个品种水稻的生长,水稻地上与地下部生物量、株高和穗数随砷处理水平的提高均出现明显的下降,但Ⅱ优416号的下降幅度明显低于威优402号.两个品种水稻籽粒中砷含量随砷处理水平提高也显著升高,人工添加砷各处理条件下,两个品种水稻稻谷中砷含量没有显著性差异;而在模拟自然砷污染土中,Ⅱ优416号稻谷中砷含量平均值为0.062mg·kg-1,明显低于威优402号稻谷平均值的0.278mg·kg-1.两个品种水稻各部位砷的转运系数在低砷处理时(10mg·kg-1)出现显著的升高,而在其他处理条件下保持不变.无论何种水稻品种,水稻各部位砷形态的组成和比例无显著性差异,水稻根、茎、叶中主要为无机砷,稻谷中无机和有机砷各占60%和40%.依据WHO相关建议标准,种植水稻品种Ⅱ优416号的健康风险要明显低于种植威优402号.     

卟啉作为人体早期砷暴露生物标志的研究

采用氢化物发生原子吸收分析了贵州省燃煤污染型砷中毒区和非砷中毒区（对照）居民尿样中砷浓度,采用高效液相色谱法分析了卟啉浓度,考察了燃煤污染造成的人体砷暴露与尿液中卟啉排泄改变的关系,寻求慢性砷中毒早期健康效应的生物标志物.结果显示,与对照组相比,砷暴露组尿卟啉Ⅲ（uroporphyrin-Ⅲ）和粪卟啉Ⅲ（coproporphyrin-Ⅲ）显著增高（P＜0.01,P＜0.01）,粪卟啉Ⅰ（coproporphyrin-Ⅰ）比对照组增高,但不显著;不同性别组间比较,对照组和暴露组的中龄（20～40岁）群体尿液中,尿卟啉Ⅲ的浓度在男性和女性群体之间呈显著性的差异（P<0.01）,其它年龄组中,这一指标在不同性别群体之间未见显著性差异;不同年龄分层比较,低龄组（＜20岁）尿卟啉Ⅲ和粪卟啉Ⅲ比对照显著增高（P＜0.01,P＜0.01）,中龄组（20～40岁）和高龄组（＞40岁）粪卟啉Ⅲ比对照显著增高（P＜0.05,P＜0.05）;此外,砷暴露组尿液中砷与总粪卟啉和总卟啉呈正相关（r=0.623,r=0.549）.结果表明,人体砷暴露会导致尿液中卟啉排泄的改变,提示卟啉有可能作为慢性砷中毒早期健康效应的生物标志.     

The dynamic changes of arsenic biotransformation and bioaccumulation in muscle of freshwater food fish crucian carp during chronic dietborne exposure

Dietary uptake is the major way that inorganic arsenic (iAs) enters into benthic fish; however, the metabolic process of dietborne iAs in fish muscle following chronic exposure remains unclear. This was a 40-day study on chronic dietborne iAs [arsenite (AsIII) and arsenate (AsV)] exposure in the benthic freshwater food fish, the crucian carp (Carassius auratus), which determined the temporal profiles of iAs metabolism and toxicokinetics during exposure. We found that an adaptive response occurred in the fish body after iAs dietary exposure, which was associated with decreased As accumulation and increased As transformation into a non-toxic As form (arsenobetaine). The bioavailability of dietary AsIII was lower than that of AsV, probably because AsIII has a lower ability to pass through fish tissues. Dietary AsV exhibited a high potential for transformation into AsIII species, which then accumulated in fish muscle. The largely produced AsIII considered more toxic at the earlier stage of AsV exposure should attract sufficient attention to human exposure assessment. Therefore, the pristine As species and exposure duration had significant effects on As bioaccumulation and biotransformation in fish. The behavior determined for dietborne arsenic in food fish is crucial for not only arsenic ecotoxicology but also food safety.     

上海夏季PM2.5中有机物的组分特征、空间分布和来源

有机物是大气细颗粒物(PM_(2.5))的重要组成部分,其来源和组分非常复杂,是大气科学研究的难点和热点.本研究定量表征了上海地区夏季3个不同功能站点PM_(2.5)中78种有机组分,分析了其组成特征及空间差异,并采用后向轨迹、指示物、特征比值等方法对其来源进行了探讨.结果表明,上海西部郊区青浦和徐汇的有机组分检出浓度相近,约为(317±129)ng·m~(-3),高于东部沿海.78种有机组分中,脂肪酸类物质的占比最高,之后依次为左旋葡聚糖、正构烷烃和多环芳烃,藿烷的占比最低.基于示踪物比值法初步分析结果表明,上海地区的颗粒有机物主要来源于汽油车尾气排放,此外中心城区和西部郊区在观测期间受到了一定程度的生物质燃烧污染,可能与西北方向的污染输送有关.就具体组分而言,在西部郊区青浦,脂肪酸主要来自于陆生植物排放,而在东部沿海地区临港,其还会受到海洋浮游植物和微生物的影响;PAH特征比值的分析表明煤燃烧和机动车尾气对多环芳烃具有重要贡献.相关研究结果有助于对上海有机气溶胶的污染特征及来源的深入认识,为开展颗粒有机物的防治提供一定的基础支撑.     

Ozone and secondary organic aerosol formation potential from anthropogenic volatile organic compounds emissions in China

Volatile organic compounds (VOCs) are major precursors for ozone and secondary organic aerosol (SOA), both of which greatly harm human health and significantly affect the Earth''s climate. We simultaneously estimated ozone and SOA formation from anthropogenic VOCs emissions in China by employing photochemical ozone creation potential (POCP) values and SOA yields. We gave special attention to large molecular species and adopted the SOA yield curves from latest smog chamber experiments. The estimation shows that alkylbenzenes are greatest contributors to both ozone and SOA formation (36.0% and 51.6%, respectively), while toluene and xylenes are largest contributing individual VOCs. Industry solvent use, industry process and domestic combustion are three sectors with the largest contributions to both ozone (24.7%, 23.0% and 17.8%, respectively) and SOA (22.9%, 34.6% and 19.6%, respectively) formation. In terms of the formation potential per unit VOCs emission, ozone is sensitive to open biomass burning, transportation, and domestic solvent use, and SOA is sensitive to industry process, domestic solvent use, and domestic combustion. Biomass stoves, paint application in industrial protection and buildings, adhesives application are key individual sources to ozone and SOA formation, whether measured by total contribution or contribution per unit VOCs emission. The results imply that current VOCs control policies should be extended to cover most important industrial sources, and the control measures for biomass stoves should be tightened. Finally, discrepant VOCs control policies should be implemented in different regions based on their ozone/aerosol concentration levels and dominant emission sources for ozone and SOA formation potential.     

固定源排放污染物健康风险评价方法的建立

将AERMOD模型应用于健康风险评价中,建立固定源排放污染物的健康风险评价方法,直接预测污染源排放毒性污染物通过某种暴露途径引起的健康风险.以兰州市三大电厂在采暖期和非采暖期排放可吸入颗粒物(PM_(10))中多环芳烃(PAHs)和其中的苯并[a]芘(Ba P)对不同年龄、不同性别的人群在呼吸暴露下的健康风险(包括致癌风险值和非致癌危险指数)为例,结合兰州市采样点处PM_(10)中PAHs的实测数据,分析三大电厂排放PM_(10)中PAHs和Ba P对人群呼吸暴露下的健康风险在采样点处的贡献率.结果表明贡献率与性别和年龄无关,与时间段和风险类别有关,非采暖期的贡献比采暖期的大,非致癌危险指数的贡献比致癌风险值的大.通过与传统方法的对比验证该方法的可靠性.该方法适用于所有固定源排放毒性污染物的健康风险评价以及环境影响评价中环境风险的评价.     

Toxic metals in amniotic fluid and altered gene expression in cell-free fetal RNA

Both exposures to toxic metals, as well as deficiencies in essential metals, during pregnancy has been linked to a variety of negative reproductive outcomes. The exact etiologies of such outcomes and the effects of fetal exposure to these metals are largely unknown. Therefore, the ability to assess levels of these elements is critical to determining the underlying causes of such conditions and the effects that both essential and nonessential metals have on fetal development. Thus, using cell-free fetal RNA from amniotic fluid, we set out to measure the association between amniotic fluid levels of toxic and essential metals and fetal gene expression. We find that arsenic was associated with increased expression of 3 genes known to play roles in both birth-related and reproductive effects. The results highlight the potential for detrimental health effects of prenatal metals exposure and the potential to identify biomarkers of environmental exposure during this critical developmental period.     

基于正定矩阵分解的傍河水源地土壤重金属污染源分析

以宁夏吴忠市金积傍河水源地为研究对象,在综合分析水源地区内土壤介质特征基础上,在水源地区域范围内采集了15个土壤样品,分析了区域范围内土壤重金属砷、镉、铬、铜、铅、镍、锰等7个因子空间分布状况,采用正定矩阵分析方法定性识别土壤重金属来源及各项来源空间污染贡献率。结果显示,金积水源地土壤重金属含量均未超过国家土壤环境二级标准,低于区域土壤背景值,其中土壤重金属污染受自然来源总贡献率为34.1%,受工业污染影响来源贡献率26.2%,受农业污染影响来源贡献率21.1%,受畜禽养殖粪便堆放及施肥作用影响的贡献率为18.6%。污染来源及其污染贡献程度分析结果为水源地供水安全和环境保护提供了重要的科学依据。     

生物炭复合青霉菌修复砷污染土壤对其微生物群落功能多样性的影响

真菌修复砷污染土壤是一种能够有效吸附固化环境中砷的重要措施.生物炭作为目前修复重金属的热点,其多空疏松的结构、较高的离子交换量、丰富的有机碳含量等都说明了其在土壤修复中的地位.为了探究生物炭与青霉菌在修复砷污染土壤的同时对土壤中微生物活性及其多样性的影响,在室内孵育条件下,运用Biolog法研究了3×3随机区组试验（3个生物炭梯度分别为0%、2%、4%,3个青霉菌梯度分别为0%、10%、20%）下土壤微生物对不同类型碳源的利用能力以及多种功能性指数的影响.结果表明:①添加青霉菌与生物炭后,土壤中有效砷含量较对照组显著下降,从而影响其微生物群落功能多样性.②砷污染土壤中微生物群落功能多样性、碳源利用丰富度随生物炭浓度梯度的升高呈先升后降的趋势.③高接菌量（20%）与低接菌量（10%）对砷污染土壤中微生物群落功能多样性的影响没有显著性差异.④2%生物炭与10%青霉菌处理土壤中微生物群落功能多样性、碳源利用丰度最高.⑤青霉菌对胺类及少部分酸类碳源的利用能力较弱（AWCD < 0.5,AWCD为Biolog微平板孔中溶液吸光值平均颜色变化率）,对氨基酸类中大部分碳源以及脂类碳源的代谢能力较强（AWCD>1.0）,对糖类、酚酸类的代谢能力稍弱（AWCD为0.3~1.0）,青霉菌对D-半乳糖醛酸、L-天冬酰胺酸、L-丝氨酸、L-精氨酸、r-羟基丁酸这5种碳源的利用率最高（AWCD>1.2）.研究显示,低浓度生物炭可增加砷污染土壤中微生物群落多样性,生物炭含量的继续增加会对微生物产生抑制作用;青霉菌添加到砷污染土壤后,会显著提升砷污染土壤中微生物的群落功能多样性,改善砷污染土壤中微生的物群落结构;青霉菌的优势碳源大多为植物根系分泌物,可为后续青霉菌与超积累植物复合修复砷污染土壤提供参考.      

城市土壤和地表灰尘重金属污染研究进展与展望

随着城市化和工业化的不断推进,城市土壤和地表灰尘重金属污染日趋严重,对城市环境和人类健康构成威胁,已成为国内外城市环境研究的热点问题.从重金属污染水平及其时空特征、污染源解析方法、生态和健康风险这3个主要方面,对国内外城市土壤和地表灰尘重金属研究成果进行了梳理和归纳.分析了当前研究存在的不足,并对未来研究进行了展望,即研究土壤和地表灰尘重金属在不同条件下的相互影响机制,通过丰富验证方法加强重金属来源解析模型结果的可靠性研究,加强来源驱动下重金属化学形态差异和地表灰尘短期累积污染过程的研究,完善暴露参数并深入探究重金属的化学形态对其生态和健康风险的影响,以提高风险预测水平.     

四平市南湖重金属污染及健康风险评价研究

在分析南湖水质的基础上,对重金属进行Pearson相关性分析,并进行了健康风险评价。结果表明Cr、Cu、Zn未超过生活饮用水卫生标准,Cd 和Pb严重超标。 Cu、Zn、Cd、Cr污染存在一定的同源性,而Mn、Fe、Ni、Pb污染具有多源性。污染物通过皮肤接触途径造成的危害要远小于饮水途径,致癌物风险比非致癌物高1～8个数量级,其中Cd对总风险贡献率为62.16％,成为主要的风险污染物。8个监测点都检测到致癌物,且风险度高于可接受水平,应引起环境治理部门的关注。     

焚烧厂周边居民重金属污染物多途径暴露的健康风险

焚烧厂排放的重金属污染物会通过不同途径富集于周围环境介质中,如土壤、地表水、地下水、大气、蔬菜和家禽等.焚烧厂周边人群通过上述各种环境介质暴露于重金属,并产生累计的健康危害.然而目前研究很少关注人群通过多途径暴露的累计健康风险.本研究调查了一座典型医疗废物焚烧厂周边不同环境介质中的重金属含量,分析其与人体暴露关系,并计算了其不同途径暴露的健康风险及累计风险.结果表明重金属产生的非致癌风险大小As(298.1)Cr(35.4)Mn(14.0)Pb(7.0)Cu(2.3)Hg(1.9)Zn(1),致癌风险大小依次为As(1.32×10-2)Cr(1.31×10-2)10-5,均超过风险可接受水平;食用自产蔬菜是主要的暴露途径(贡献率为68%~92%)其次为自养家禽贡献率为10%左右.这说明区别于通常关注的通过土壤、水体、空气等介质暴露的风险相比,食用研究区周边的动植物产品导致的风险更大,需要引起重点关注;不确定分析结果表明考虑污染物浓度不确定条件下,场地健康风险大约有0.54~2.28倍的增加;风险管理研究表明通过截断食用本地蔬菜和家禽,除Cr的致癌风险外,其他重金属对厂区居民的健康风险水平会迅速降低至可接受水平.