Concentrations of polychlorinated dibenzo‐p‐dioxins and dibenzofurans in outdoor air of North‐Rhine‐Westphalia,Germany

Measurements of polychlorinated dibenzo‐p‐dioxins (PCDD) and dibenzofurans (PCDF) in outdoor air of North‐Rhine‐Westphalia were carried out. Fifty‐six samples were taken at different sites in areas of different land use and emission structures. A special filter system allowed analysis of the gas and particle phases separately. It was found that higher chlorinated PCDD/PCDF (7 or 8 chlorine atoms) are collected on glass fiber filter and lower chlorinated PCDD/PCDF (tetra‐ and penta‐CDD/CDF) are absorbed on polyurethane foam. The following isomers were determined: OCDD, OCDF and 11 isomers with chlorine substitution in 2,3,7,8‐position as well as the sum of TCDD, PeCDD, HxCDD, HpCDD, TCDF, PeCDF, HxCDF, HpCDF and the sum of PCDD (4–8) and PCDF (4–8). No 2,3,7,8‐TCDD could be detected but 2,3,7,8‐TCDF was found at 15 sites. Mean concentration in the Rhine‐Ruhr‐District for the sum of PCDD (4–8) and PCDF (4–8) was 3.2pg/m³ and 5.5pg/m³ respectively. Detection limit for TCDD and PCDD/PCDF (5–8) was 0.1–0.2 pg/m³ and 0.005–0.015 pg/m³ respectively. There is no significant indication that 2,3,7,8‐chlorinated isomers of PCDD/PCDF are predominantly decomposed by photochemical reactions in outdoor air.     

Protective effects of curcumin on antioxidant status,body weight gain,and reproductive parameters in male rats exposed to subchronic 2,3,7,8-tetrachlorodibenzo-p-dioxin

The aim of this study was to investigate the effects of curcumin (CUR) on antioxidant status, body weight (BW) gains, and some reproductive parameters in male rats exposed to subchronic doses of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Thirty-two rats were divided into four groups. The first group was kept as control. The second group (TCDD group) was given TCDD at a dose of 50 ng·kg^?1 BW per day; the third group (CUR group) was treated with CUR at a dose of 80 mg·kg^?1 BW per day. The fourth group (TCDD + CUR group) was given TCDD and CUR at the same doses simultaneously. Malondialdehyde (MDA) levels were significantly increased in the TCDD group. In addition, TCDD exposure decreased liver superoxide dismutase (SOD) activity, catalase (CAT) activities of kidney and brain, glutathione peroxidase (GSH-Px) activities of liver, kidney, and brain, and glutathione levels of liver, kidney, and heart. However, CUR treatment with TCDD exposure decreased MDA levels in all tissues and increased SOD activities of liver, kidney, and brain, CAT activity of heart, and GSH-Px activities of heart and brain. TCDD caused a decrease in BW gain, and CUR partially eliminated this effect of TCDD. In addition, while reproductive organ weights, sperm concentration, and sperm motility tended to decrease with TCDD exposure, these effects tended to be close to normal levels by CUR treatment. In conclusion, CUR was seen to be effective in the treatment and prevention of toxicity induced by subchronic TCDD exposure.     

Isomer‐specific determination and toxic evaluation of potentially hazardous coplanar PCBs,dibenzofurans and dioxins in the tissues of “Yusho” PCB poisoning victim and in the causal oil

In the light of new discoveries on the extremely toxic non‐ortho coplanar 3,3’,4,4'‐tetra‐ (T₄CB), 3,3’,4,4’,5‐penta‐(P₅CB) and 3,3'4,4’,5,5'‐hexachlorobiphenyl (H₆CB) and their mono‐ and di‐ortho analogs, tissue samples of a Yusho poisoning victim and Yusho causal oils were subjected to a thorough congener/isomer‐specific investigation for polychlorinated biphenyls (PCBs), polychlorinated dibenzofurans (PCDFs), polychlorinated dibenzo‐p‐dioxins (PCDDs). Among the many PCB congeners detected in Yusho oil, non‐ortho coplanar T₄CB constituted 3.1%, P₅CB‐0.17% and H₆CB‐0.0072% in total PCBs. Their concentrations in liver and adipose tissue were 130–700 (T₄CB), 54–720 (P₅CB) and 50–380 (H₆CB) pg/g on wet weight basis. The observed concentrations in adipose tissue were two to four fold higher than that detected in unexposed individuals. Among the PCDFs identified, toxic 2,3,7,8‐substituted isomers including 2,3,4,7,8‐P₅CDF were the dominant ones. Tetra‐ through hepta‐CDDs were detected in the oil, whereas octa‐CDD was the dominant isomer in the patient. A comparison with KC‐400 revealed enrichment of coplanar PCBs in Yusho oil along with toxic PCDFs. Enrichment was highest for 3,3'4,4'5,5'‐H₆CB followed by 3,3’,4,4'5‐P₅CB. A comparative toxic evaluation of these chemical groups in Yusho patient's adipose tissue based on “2,3,7,8‐T₄CDD Toxic Equivalent Analysis” revealed accountable toxic contribution from coplanar PCBs. This analysis also confirmed that 2,3,4,7,8‐P₅CDF was the principal causative agent in Yusho poisoning.     

Combined effects of 2,3,7,8-tetrachlorodibenzo- p -dioxin and polychlorinated biphenyl congeners in rats

The objective of this work was to evaluate potential interactions between 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and polychlorinated biphenyls congeners (PCBs) in rats. Groups of five adult female rats were given 0, 2.5, 25, 250, or 1000?ng TCDD/kg body weight/day or TCDD in combination with a mixture of PCB congeners at a concentration of 2 or 20?µg?kg^?1 body weight/day by gavage for 28 days. After the 28-day treatment period, the rats were killed for the analysis of biochemical, liver enzyme activities, and hematological and pathological end points. Growth suppression, increased absolute and relative liver weights, and decreased thymic weight were observed in the 1000?ng TCDD group alone, or the groups receiving a mixture of 1000?ng TCDD and 2 and 20?µg PCBs. TCDD-increased liver and thymic weights were not altered by PCBs; however, growth suppression was more pronounced in animals receiving 1000?ng TCDD and 2?µg PCBs. Increased hepatic microsomal methoxy resorufin-O-demethylase and ethoxy resorufin-O-deethylase activities occurred in 250 and 1000?ng?kg^?1 TCDD-treated animals, which were antagonized by PCBs. Effects of 250?ng TCDD on serum cholesterol and liver uridine diphosphate glucuronosyl transferase activity were reduced by 20?µg PCBs. Treatment with 1000?ng TCDD increased serum albumin, decreased liver vitamin A, increased kidney vitamin A, and liver microsomal glutathione-S-transferase activity, which were not affected by PCBs. Decreased hemoglobin, platelet, packet cell volume, and red cell indices were observed in TCDD-treated rats, but no interactive effects were seen. Histopathological evaluation revealed that liver, thyroid, and thymus were the target organs, but the effects of co-exposure to PCBs and TCDD were variable. These results indicate that the mixture effects of PCBs and TCDD may be additive, synergistic, or antagonistic depending on the dose level and end points measured.     

运动对2,3,7,8-四氯二苯并二噁英持续暴露大鼠肝脏氧化应激的影响

为探索运动对2,3,7,8-四氯二苯并二噁英(2,3,7,8-TCDD)持续暴露大鼠肝脏氧化应激的影响,本研究将7周龄雄性SD大鼠适应性喂养1周后,随机分为对照(NC)、运动对照(EC)、染毒1(NT1)、运动染毒1(ET1)、染毒2(NT2)、运动染毒2(ET2)、染毒3(NT3)、运动染毒3(ET3)、染毒4(NT4)及运动染毒4(ET4)共10组。染毒组(NTs、ETs)腹腔注射TCDD(溶于玉米油),对照组及各染毒组首次剂量依次为0、0.4、1.6、6.4、25.6μg·kg~(-1)(以单位体重计),之后每周给予上述剂量的21%作为维持剂量,持续染毒8周;运动组尾部负重5%游泳,每周5 d,每次30 min。实验结束取材,测定血清丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、肝组织超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)活性及丙二醛(MDA)、活性氧(ROS)含量。结果显示:1)染毒可升高各染毒组大鼠血清AST活性及NT4组大鼠血清ALT活性,增加NT2、NT3组肝脏MDA含量,而降低NT1、NT2组大鼠血清ALT活性;2)运动可升高大鼠血清AST及ALT活性,增加大鼠肝组织GSH-Px活性;3)运动可升高染毒大鼠血清AST活性(T1剂量),降低染毒大鼠血清ALT活性(T1剂量),降低染毒大鼠血清AST活性(T3剂量),升高染毒大鼠血清ALT活性(T3、T4剂量),增加染毒大鼠肝组织SOD活性(T2、T3剂量)、CAT活性(T1、T2、T3剂量)及GSH-Px活性(T2、T3、T4剂量),降低染毒大鼠肝组织MDA含量(T2、T3、T4剂量)及ROS含量(T1、T3剂量)。结果表明,2,3,7,8-TCDD持续暴露8周可引起大鼠肝细胞氧化应激损伤,并产生剂量依赖效应;而有氧运动可增加2,3,7,8-TCDD持续暴露(T2、T3剂量)大鼠肝组织抗氧化酶活性,有效降低氧化应激损伤而减轻肝毒性。     

Protein expression profile in the testis of rats chronically exposed to low-dose 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin

The chronic effects low-dose 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) were examined on protein expression profiles in rat testis, sperm, and serum gonadal hormones. A total of 32 male rats were randomly divided into three TCDD-exposed groups, administered either 140, 350, or 875 ng TCDD/kg/week for 29 weeks, respectively, and one control group receiving only corn oil. The proteins from rat testis were separated and analyzed by two-dimensional gel electrophoresis and mass spectrometry. TCDD induced significant decreases in sperm counts and serum gonadal hormone levels compared with controls. TCDD altered testicular protein expression levels. Several interesting volume-altered proteins that were related to the reproductive toxicities or other toxicities of TCDD were identified. Among these proteins, PERF15 was the only down-regulated protein; sperm protein SSP411, ubiquitin carboxyl-terminal hydrolase L-3, and eukaryotic translation elongation factor 1 gamma were up-regulated by TCDD. The differentially expressed proteins and other data provide further insight into the mechanisms of reproductive toxicity mediated by low-dose TCDD exposure.     

Polychlorinated -dibenzo-p-dioxins/furans and -dioxin-like biphenyls in eggs of common terns from lime island,St. Mary's river,Michigan, USA

Population collapse of common tern (Sterna hirundo) from Lime Island in the St. Mary's River, Michigan, USA were related to the 2,3,7,8-chlorine substituted dioxins, furans, dioxin-like PCBs, and other possible factors using unhatch egg target contaminant analysis. The most toxic congeners, 2,3,7,8-TCDD/DF was found in all samples at noticeable concentrations. Magnitude of sum 2,3,7,8-PCDD/DFs were within the range of 39–93?pg/g wet wt. Dioxin-like PCBs were within the range of 360–1230?ng/g wet wt. Great Toxic Equivalent Quantity (TEQ) contributions by 2,3,7,8-TCDF, 2,3,4,7,8-PeCDF, 2,3,7,8-TCDD, 1,2,3,7,8-PeCDD, and dioxin-like PCBs such as CB-77, CB-126 and CB-105 are considered greatly due to their influence of poor embryo development and consequent damage of embryos of common terns in egg injection studies. However, other organochlorines, heavy metals, and/or synergistic effects also taken in to account. On the whole, TEQs in the tern eggs were greater than the Lowest-Observable-Adverse Effect Level (LOAEL) for bald eagle (Haliaeetus leucocephalus) embryos observed in British Columbia, Canada. Concentrations of dioxin-like PCBs, dioxins, furans in the St. Mary's River food chain are at levels for concern for nesting colonial waterbirds. Eventually, the possible movements of analyzed chemicals downstream from a man-made flood event are discussed.     

Residues of PCDD,PCDF, and PCBs in some marine organisms in Lake Temsah,Ismailia, Egypt

Residues of PCDDs/F, non-ortho, mono-ortho PCBs, and other PCBs were monitored in the tissues of mullet fish, bolti fish, bivalves and crab taken from Lake Temsah, at Ismailia, Egypt.

Results showed that 2,3,7,8 Tetra CDD and 1,2,3,7,8 Penta CDD were the most frequently detected PCDD congeners. Similarly, 2,3,7,8 Tetra CDF, 1,2,3,7,8 Penta CDF and 2,3,4,7,8 Penta CDF were the most frequently detected PCDF congeners. No relationship was apparent between the concentrations of detected PCDDs congeners and the degree of chlorination, except with crab samples in which an increase in the chlorination coincided with a decrease in the concentrations of the congeners.

In PCDF congeners, detected residues have had a reversed relationship with chlorination increase. In PCDD congeners, Octa CDD had the highest detected concentrations in the two fish species, while in the bivalves and crab, 2,3,7,8 Tetra CDD had the highest concentrations. The mullet fish had the highest total PCDDs concentration, at 0.398?pg/g fresh weight, followed by crab at 0.395?pg/g fresh weight, then bivalves and bolti fish at 0.187 and 0.062?pg/g fresh weight, respectively. In all the examined organisms, the total concentrations of PCDFs were much higher than the total concentrations of the PCDD congeners. The WHO–TEQ values were 11.92, 39.12, 25, and 3.6?pg/g fresh weight, for mullet fish, bolti fish, bivlaves and crab, respectively. The concentration of the mono-ortho congeners CB 118 was the highest detected of all non-ortho and mono-ortho PCBs congeners, with values of 0.382, 0.022, 0.231 and 0.357?ng/g fresh weight, in mullet fish, bolti fish, bivalves and crab, respectively. The WHO–TEQ concentrations were 0.799, 0.003?pg/g fw, 0.05?pg/g fresh weight, 0.676?pg/g, and 0.799?pg/g fresh weight, for the same species, respectively. The total concentration of PCBs 28, 52, 95, 99, 101, 105, 110, 118, 138, 146, 149, 151, 153, 170, 177, 180, 187 were 6.86?ng/g fresh weight for mullet fish, 0.2?ng/g fresh weight, for bolti fish, 2.72?ng/g fresh weight for bivalves and 2.8?ng/g fresh weight for crab, respectively.     

Clam‐sediment accumulation factors for polychlorinated biphenyl congeners at a contaminated estuarine marsh

Clam‐sediment accumulation factors for hexa‐, hepta‐ and octa‐chlorobiphenyls were estimated at an intertidal marsh that has been contaminated with Aroclor 1268. Accumulation factors for PCB congeners with K _ow > 6.5 were in the range of 0.07–0.88, indicating that their uptake was hindered by steric factors, contamination levels, non‐equilibrium conditions and stronger affinity to sediment organic carbon. Biota‐sediment accumulation factors (BSAFs) were negatively correlated with log K _ow of superhydrophobic PCB congeners. BSAFs estimated based on 2,3,7,8‐TCDD equivalents of PCBs were 2‐fold greater than those derived from total PCB concentrations.     

2,3,7,8-四氯二苯并二噁英与Aroclor 1254单独与联合作用对大鼠外周血淋巴细胞DNA的损伤效应(Damage Effects of Individual and Combined Exposure to 2,3,7,8-Tetrachlorodibenzo-p-Dioxin and Aroclor 1254 on DNA in Peripheral Blood Lymphocyte of Rats)

为探讨2,3,7,8-四氯二苯并二噁英(TCDD)和多氯联苯(Aroclor 1254)联合染毒对大鼠外周血淋巴细胞DNA的损伤效应,将20只雄性Sprague-Dawley(SD)大鼠随机均分为4组,即对照组(橄榄油)、Aroclor 1254单独染毒组(10mg·kg-1)、TCDD单独染毒组(10μg·kg-1)和联合染毒组(TCDD 10μg·kg-1+Aroclor 1254 10 mg·kg-1).大鼠每天灌胃染毒1次,连续染毒6d.染毒过程中记录大鼠的体征和体重.末次染毒后24h取外周血,分离淋巴细胞,采用碱性单细胞凝胶电泳技术(彗星试验)检测外周血淋巴细胞DNA损伤,并采用CASP软件分析各组彗星的尾部DNA百分含量(Tail DNA%)、尾长(Tail Length)和尾矩(Tail Moment).结果表明,染毒结束时TCDD单独染毒和联合染毒组大鼠体重显著低于对照组,且联合染毒组表现更为明显.TCDD单独染毒组和联合染毒组大鼠外周血淋巴细胞DNA可见明显损伤,TailDNA%、Tail Length和Tail Moment均显著高于对照组(p<0.05),且联合染毒组大鼠细胞DNA损伤更为严重,但Arolor 1254单独染毒组大鼠未见明显DNA损伤.析因分析提示TCDD与Aroclor 1254对大鼠外周血淋巴细胞DNA损伤的联合毒性效应为协同作用.本研究结果表明TCDD与Aroclor 1254联合染毒可加重大鼠外周血淋巴细胞DNA损伤,在对PCBs与二噁英的混合暴露进行危险性评估时要注意这种联合毒性作用.     

2,3,7,8-四氯二苯并对二噁英对大鼠卵巢颗粒细胞雌二醇和孕酮分泌的影响

为研究2,3,7,8-四氯二苯并对二噁英(TCDD)对体外原代培养大鼠卵巢颗粒细胞活力和雌二醇(Estradiol,E2)、孕酮(Progestone,P)分泌的影响,探索TCDD对卵巢颗粒细胞的毒性作用阈值和程度,对未成熟SD大鼠卵巢颗粒细胞进行了原代培养,并设2组体外染毒实验:终浓度分别为0.1、1、10、100nmol·L-1TCDD染毒24h和10nmol·L-1TCDD染毒1、3、6、18、24h.染毒结束后采用MTT法检测细胞活力,RIA法检测收集培养液中的E2和P含量.结果表明,1、10、100nmol·L-1TCDD可显著抑制大鼠卵巢颗粒细胞活力和E2、P的分泌,与阴性对照、0.1%DMSO组、0.1nmol·L-1TCDD组比较差异均有显著性(p<0.05);10nmol·L-1TCDD染毒6、18、24h可明显抑制细胞活力和E2、P的分泌,与对照组和短期染毒组(1h、3h)差异均有显著性(p<0.05).痕量的TCDD可显著降低大鼠卵巢颗粒细胞活力并抑制细胞E2和P分泌,对大鼠卵巢颗粒细胞的毒性作用阈值可能为1nmol·L-1或更低.TCDD的生殖毒性作用可能与直接对卵巢颗粒细胞的毒性作用和抑制甾体激素的生物合成以及分泌有关.     

Dioxin alters inflammatory responses to lipopolysaccharide

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) has well characterized effects on specific immune responses, but the effects on the innate immune system are less understood. The effect of TCDD on inflammatory responses induced by lipopolysaccharide (LPS) was evaluated in C57BL/6J female mice. Mice were treated with 30?µg?kg^?1 TCDD or vehicle once, p.o., and 4 days later, animals received LPS (0.05?×?10⁷?EU?kg^?1, i.p.) or vehicle. Inflammatory mediators and the liver injury marker, alanine aminotransferase (ALT), were measured, and liver histology was evaluated. TCDD-treated animals had higher plasma ALT activity than vehicle-treated animals, but the effect was mild and time-dependent. Few changes in liver histopathology were observed, mainly represented in greater steatosis in TCDD/LPS-treated mice compared to mice treated with LPS or TCDD alone. LPS produced a time-dependent increase in the plasma concentrations of interleukins (IL)-6, -10, and -12 and interferon (IFN)-γ, tumor necrosis factor (TNF)-α, and monocyte chemoattractant protein (MCP)-1. With the exception of IL-12, concentrations of each of these mediators were higher in plasma of mice co-treated with TCDD and LPS compared to either agent alone. The dose–response curve for the concentration of IL-6 in plasma suggested that dioxin increased the potency of LPS to cause the release of this cytokine but not the maximal response. Co-treatment with TCDD and LPS also led to greater expression of mRNA for IL-10 and IFN-γ compared to either TCDD or LPS alone. These results suggest that TCDD changes the inflammatory cytokine profile induced by LPS and that LPS enhances the hepatic steatotic response to TCDD.     

2,3,7,8-四氯二苯并二噁英和Aroclor 1254对大鼠睾丸的单独和联合毒性效应

为了探讨2,3,7,8-四氯二苯并二噁英(TCDD)和Aroclor1254对大鼠睾丸的单独和联合毒性效应,采用2×2析因设计将SD大鼠随机分为4组,即对照组、Aroclor1254单独染毒组(10mg·kg-1)、TCDD单独染毒组(10μg·kg-1)和联合染毒组(TCDD10μg·kg-1+Aroclor125410mg·kg-1),每组5只.灌胃染毒,每天1次,连续12d.染毒结束后处死大鼠,称睾丸湿重、检测睾丸组织病理学及睾丸组织脂质过氧化状况.结果表明,各染毒组大鼠的睾丸均呈现毒性效应,表现为睾丸湿重降低,睾丸组织出现明显的病理学改变,丙二醛(MDA)水平升高、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性降低,这些毒性效应多数在联合染毒组表现更为明显.析因分析结果表明TCDD与Aroclor1254对大鼠睾丸的联合毒性效应为相加作用.以上结果提示TCDD与Aroclor1254单独和联合染毒均具有睾丸毒性,且二者的联合效应为相加作用,在对二噁英和PCBs进行环境风险评价时应考虑这种联合作用.     

2,3,7,8-四氯苯并二噁英（TCDD）短期染毒可造成着床前胚胎丢失并伴随雌性生殖器官中毒物相关蛋白的诱导表达（Short Time Exposure of TCDD Causing Loss of Implantation Failure of Embryos and Its Associated with Induced Expression of Relevant Proteins）

为探明妊娠早期胚胎的丢失是否与卵巢、输卵管、子宫组织受到2,3,7,8-四氯苯并二噁英(TCDD)直接毒害有关,检测了NIH小鼠胚胎着床前期和后期TCDD暴露对胚胎毒性影响的敏感性,并利用免疫组化方法分析了模型动物肝脏、子宫、输卵管和卵巢组织中TCDD所引起的AhR、ARNT以及Cyp1a2分子标记物的变化.检测发现:妊娠第9d,100ng·kg-1·d-1剂量TCDD经口染毒,造成胚胎着床数量减少,且着床前期暴露的影响大于着床后期;子宫蜕膜反应受到明显抑制;胚胎迁移率没有明显变化,但胚胎数量减少.免疫组织化学分析发现正常组小鼠的肝脏、子宫、输卵管和卵巢组织中有AhR和Cyp1a2弱阳性信号表达,ARNT有细胞核的强阳性信号表达;妊娠第1～8d、第1～3d和第4～8d处理组小鼠肝脏、子宫、输卵管和卵巢组织中的AhR、Cyp1a2的阳性面积和光密度值均高于正常组;随处理时间和组织蓄积量的增加,ARNT在组织中的变化由胞核(妊娠第1～3d组)表达到胞浆(妊娠第4～8d组)表达,然后完全无表达(妊娠第1～8d组).以上研究结果表明:TCDD对早期妊娠小鼠子宫、输卵管和卵巢组织中的AhR、ARNT和Cyp1a2的激活和代谢方式与肝脏相同,说明雌性生殖系统中的组织有TCDD蓄积和代谢活性,这可能是导致早期胚胎迁移、着床等过程改变,造成胚胎丢失的重要原因.     

Abstracts to forthcoming papers

Soil and sediments collected at a former chlor‐alkali plant in coastal Georgia (United States), revealed the presence of PCDF concentrations as great as 82.3 ng/g, dry wt. PCDF congener profile in soil was typical of “chlorine pattern”; with elevated proportions of OCDF and HpCDF. Concentrations of PCDFs declined gradually by 44‐fold at a distance of about 500 m along the contamination gradient. Of PCDDs/DFs, 2,3,7,8‐substituted PCDFs accounted for 94–98% of the TCDD‐like activity, which declined by 25‐fold, corresponding with the reduction of total PCDF concentrations. Concentrations of PCDDs in sediments were as great as 17 ng/g, with an elevated contribution from OCDD. The magnitude of decline in PCDD concentrations with distance from the source was less pronounced than that for PCDFs. PBDDs and PBDFs were not detected. Polybrominated biphenyl ether (PBBE) and monobromo‐heptachloro dibenzo‐p‐dioxins and dibenzofurans (PXDDs/DFs) were found, though, at low concentrations. Their spatial distribution was similar to those of PCDDs.     

Bioavailability and metabolism of hexavalent chromium compounds †

Intratracheal instillation of ⁵¹CrCl₃ in anaesthetized rabbits resulted in partial absorption. In blood, the absorbed material was entirely confined to the plasma compartment. Only trace amounts were deposited in liver and kidney. By contrast, after similar application of Na, ⁵¹CrO₄ the bulk of blood radioactivity was present in red blood cells (RBC). Substantial deposition occurred in liver and kidneys. It is concluded that Cr(VI) may enter the body unreduced via the lung and is partially deposited in cells over a prolonged period of time.

Since chromium was accumulated in liver after administration of Cr(VI) we investigated the intracellular disposition of Cr(VI) in the isolated perfused liver. No significant sex differences in chromium distribution were observed. At the end of the experiments (1 h), 60% of the applied dose (312μg Cr/liver) was located in the cytosol, whilst 14% was in the mitochondria, 9% in the microsomal pellet and 2% was associated with the nuclei. Gel chromatography of the cytosolic compartment showed that the overwhelming part of chromium was eluted in fractions with an apparent molecular weight of 6,000 dalton. These fractions exhibited absorption maxima at 410nm and 548nm. It is concluded, that cytosolic reduction might be the main intracellular redox pathway for chromates. This view was confirmed by monitoring the reaction of Cr(VI) with GSH in vitro. GSH reduced Cr(VI) without further cofactors under formation of GSH‐chromium complexes, which possibly represent major intermediates in the metabolism of Cr(VI).     

Improvement of sampling and analytical methods for polychlorinated dibenzo‐p‐dioxins and dibenzofurans in environmental samples and its quantitative evaluation

Sampling of PCDDs/Fs in flue gas from a MSW incinerator was conducted using a modified apparatus of the 5 train method, which has been widely used for the sampling of PCDDs/Fs emission. In the atmosphere a high volume air sampler with special packings was used. Collection efficiencies of PCDDs/Fs were more than 98% for both samplers, using ¹³C₁₂—PCDD reference standard isomers. It was suggested that these sampling methods were adaptable for the measurements of PCDDs/Fs at sources and in the environment. To validate the applicability of existing methodologies on the PCDD/F determination, interlaboratory comparisons were undertaken. From high resolution GC/MS analysis, 2,3,7,8‐TCDD concentrations in reference ash samples were 0.052±0.013 ng/g as comparable results between the laboratories. In addition, the daily intakes of PCDDs/Fs for exposed persons in the MSW incineration facilities in Japan were estimated ranging of 0.053 to 0.28 pg/kg/day by the international toxic equivalent calculations.     

Relationships between exposure to polyhalogenated aromatic hydrocarbons and organochlorine pesticides and the risk for developing type 2 diabetes: a systematic review and a meta-analysis of exposures to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)

A systematic review was performed to evaluate the association between environmental exposures to polyhalogenated aromatic hydrocarbons (PHAHs) and organochlorine (OC) pesticides and the risk for type 2 diabetes (T2D). Searches of EMbase, Google Scholar, Medline, and Scopus were performed. Reports were included if they were original human studies whose design included a control group and if the sample size was larger than 10 participants per group. The articles were excluded if the type of diabetes was unknown or Type 1. Odds ratios (OR), 95% confidence intervals (CI), and modified Naranjo scores for the effects of environmental contaminants were determined for each study. Of the 35 eligible studies, six were included in the meta-analysis; these focused specifically on 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Meta-analysis of these studies showed no significant increased OR for the development of T2D from exposure to TCDD. However, subgroup analysis showed significant elevated OR for the development of T2D if exposure is repeated and accompanied by exposure to other persistent pesticides (OR?=?1.48; 1.10–1.90) but a decreased odds for T2D with exposure resulting from accidental exposure (OR?=?0.46; 0.39–0.52). Our results suggest that there are significant risks of developing T2D in populations with recurring exposures to TCDD in concert with other persistent chlorinated pesticides. A mean Naranjo score of 2.0 was determined for all 35 articles; this score was 2.5 when examining only TCDD studies and 2.1 when examining studies that looked only at T2D. Each of these Naranjo scores suggests a possible association between the prevalence of T2D and exposure to PHAHs or OC pesticides.     

2,3,7,8-四氯二苯并二噁英和β-萘黄酮暴露对斑马鱼肝和鳃MROD酶活性的影响

为了研究2,3,7,8-四氯二苯并二噁英(TCDD)和β-萘黄酮(β-NF)对斑马鱼(Danio rerio)肝脏和鳃CYP1A依赖性7-甲氧基-3-异酚噁唑酮-脱甲基酶(MROD)活性的影响,分别利用不同浓度的TCDD(0、0.05、0.1、0.2、0.4μg·L-1)和β-NF(0、25、50、100、200μg·L-1)对斑马鱼进行水浴暴露,48h后取样测定肝脏和腮MROD活性.结果表明,与对照组比较,TCDD暴露组和β-NF暴露组斑马鱼肝脏和鳃MROD活性均显著增强(p<0.01),且MROD活性的增加与TCDD或β-NF暴露浓度呈现明显的剂量-效应关系.初步推断斑马鱼肝脏和鳃CYP1A依赖性MROD酶活性可能能够作为TCDD或β-NF污染的生物标志物.