Research needs identified at the second PCB workshop in Brno,Czech Republic,May 7–11, 2002

More than 150 scientists from the Americas, Europe, and Asia met in Brno, Czech Republic, in May 2002 at the Second PCB Workshop, entitled “Recent Advances in the Environmental Toxicology and Health Effects of PCBs”. NIEHS/EPA-Superfund Basic Research Program, the Graduate Center for Toxicology at the University of Kentucky, and the Research Centre for Atmospheric and Environmental Chemistry and Ecotoxicology of Masaryk University, Brno, sponsored the Workshop. At six separate sessions (including posters) the origins, human residues and exposures, actions, biomarkers, risk and remediation issues relating to PCBs were discussed.     

Histopathology of cerebro neuronal cells in freshwater snail Bellamya bengalensis: impact on respiratory physiology,by acute poisoning of mercuric and zinc chloride

Mercuric (Hg) and zinc (Zn) chloride toxicity was investigated in cerebroneuronal cells and gills of Bellamya bengalensis using sublethal concentrations under lab conditions. Freshwater snail B. bengalensis was exposed to mean LC₅₀ concentration (1.56 ppm and 12.7 ppm) of Hg and Zn chloride, respectively. Bioaccumulation of Hg and Zn was observed in nervous and gill tissue in proportion to the time of exposure. Respiratory mechanisms and rate of oxygen consumption was depleted by both metals. Histopathological alterations in cerebro neuronal cells (giant, large, medium, and small) and gill filamental epithelia were apparent in Hg and Zn-exposed snails. Histopathology demonstrated increased cytoplasmic basophilia, extreme indentation of plasma membrane, karyolitic and eccentric nuclei, nuclear envelope with irregular size, and shrunken appearance of cerebroneuronal cells. Histologically, gill filamental epithelia showed hypertrophy, enlarged ciliated margins reduced length of cilia, nuclear dilations, thickening of basal lamina, and hemocytic accumulations in induced cells and severe loss of goblet mucus cells at the tip. Histopathology was accompanied by dysfunctioning cilia with decreased rate of respiration. Overall, neuronal impairment with damaged gill filament produced improper gaseous exchange leading to sluggish movement.     

Biomonitoring of oral epithelial cells in petrol station attendants: Comparison between buccal mucosa and lateral border of the tongue

Owing to the influence of geno- and cytotoxicity on chemical carcinogenesis, studies have demonstrated that petroleum derivatives are able to induce genetic damage and cellular death with conflicting results so far. The aim of the present study was to comparatively evaluate DNA damage (micronucleus) and cellular death (pyknosis, karyolysis and karyorrhexis) in exfoliated oral mucosa cells from gas petrol attendants using two different anatomic buccal sites: cheek mucosa and lateral border of the tongue. A total of 23 gas petrol attendants and 23 health controls (non-exposed individuals) were included in this setting. Individuals had epithelial cells from cheek and lateral border of the tongue mechanically exfoliated, placed in fixative and dropped in clean slides which were checked for the above nuclear phenotypes. The results pointed out significant statistical differences (p < 0.05) of micronucleated oral mucosa cells from gas petrol attendants for both oral sites evaluated. In the same way, petroleum derivate exposure was able to increase other nuclear alterations closely related to cytotoxicity such as karyorrhexis, pyknosis and karyolysis, being the most pronunciated effects as those found in the lateral border of the tongue. No interaction was observed between smoking and petroleum exposure. In summary, these data indicate that gas petrol attendants comprise a high risk group for DNA damage and cellular death. It seems that the lateral border of the tongue is a more sensitive site to geno- and cytotoxic insult induced by petroleum derivates.     

PCDD, PCDF, PCB and PBDE concentrations in breast milk of mothers residing in selected areas of Slovakia

The concentrations of polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), dioxin-like polychlorinated biphenyls (dl-PCBs) and polybrominated diphenylethers (PBDEs) in 33 breast milk samples collected in 2006-2007 from primipara mothers close to four industrial areas of Slovak Republic were determined. The total PCDDs/PCDFs and dl-PCBs expressed as TEQ based on WHO TEFs 1998 in breast milk samples varied from 5.0 to 51.8 pg g⁻¹ fat (median: 13.1 pg g⁻¹ fat; mean: 18.0 pg g⁻¹ fat). The measurements of seven PBDE congeners (IUPAC No. 28, 47, 99, 100, 153, 154, and 183) were performed for the first time in human milk from Slovakia. PBDE levels ranged between 0.22 and 1.62 ng g⁻¹ fat, with median and mean value of 0.43 ng g⁻¹ fat and 0.57 ng g⁻¹ fat respectively. No statistically significant differences were observed between studied areas in total PBDE concentrations.Furthermore, this study presents first results concerning the daily intake (DI) of PCDDs/PCDFs and dioxin-like compounds for the most vulnerable breast-fed infant population in Slovakia. The total PCDD/PCDF and dl-PCB DI for an infant during the first 2 months of life was estimated in a range from 14.4 to 230 pg TEQ kg⁻¹ b.w., with a median value of 58.9 pg TEQ kg⁻¹ b.w.. The DI values substantially exceeded the tolerable daily intake (TDI) 1-4 pg TEQ kg⁻¹ b.w. recommended by WHO. The dietary infant intake concerning PBDEs was estimated to be between 0.69 and 7.1 ng kg⁻¹ b.w. d⁻¹, with median value of 1.7 ng kg⁻¹ b.w. d⁻¹.     

PCDD/Fs and dioxin-like PCBs in human milk and estimation of infants' daily intake: a review

This paper reviews the recent scientific literature on PCDDs, PCDFs and dioxin-like PCBs in human milk. All the papers reporting levels of these contaminants in human breast milk published from January 2000 to January 2009 and available on the www.sciencedirect.com web site were identified and included. The aim was (1) to study levels of PCDDs, PCDFs and PCBs in human milk in mothers from different geographical areas and assess infant exposure to these contaminants; (2) to study the effect of variables such as the mother’s age, number of deliveries, dietary and smoking habits and her own nutrition in infancy, and the environment, on levels of the contaminants in breast milk; (3) to study time patterns, and (4) to identify data gaps.     

高等植物细胞中的钙通道

钙通道在高等植物细胞中参与众多的信号转导过程,对钙通道的研究最近几年获得长足的进步：不仅在质膜中直接发现了电位依赖性的钙通道、牵张刺激激活的机械敏感性钙通道等,而且在液泡膜中发现了众多具有不同开放调控机制的钙通道：受化学信使控制的钙释放通道、电位依赖性钙通道、钙离子诱导的钙释放通道．本文对高等植物细胞中钙通道的研究进行了综述     

稀土矿城市不同季节大气可吸入颗粒物中稀土含量特征及颗粒物细胞毒性

为探讨典型稀土矿城市不同季节大气可吸入颗粒物(inhalable particulate matter,PM10)中稀土元素污染特征及其细胞毒性响应,将前期采集于包头市的PM10颗粒物进行提取,检测PM10中的稀土元素(rare earth elements,REEs)含量,并将人肺上皮细胞(A549)暴露于不同浓度水平(25,50,100μg·m L-1)的PM10样品和标准颗粒物1649b(standard reference material,SRM1649b)暴露液,用WST-1法测定暴露24 h后的细胞活性,用2’7’二氯荧光素二醋酸盐(2’7’-dichlorofluorescein diacetate,DCFH-DA)荧光探针法和彗星实验分别测定暴露3 h后的细胞内活性氧(reactive oxygen species,ROS)产生水平和DNA双链损伤程度。结果表明,包头春、夏季大气PM10和SRM1649b均引起A549细胞活性下降,并诱导细胞内ROS生成量增加,造成显著的细胞内DNA损伤,含REEs的大气颗粒物毒性显著高于标准颗粒物。与春季相比,包头夏季PM10对细胞活性的抑制程度更高,造成更多的DNA双链损伤,从而表现出更强的细胞毒性和遗传毒性。包头PM10呈现明显的轻稀土元素(light rare earth elements,LREEs)富集,铈(Ce)、钷(Pm)、镧(La)和钕(Nd)含量占稀土总量的50%以上。LREEs均与细胞活性和细胞内ROS产生水平呈负相关性,包头春季和夏季PM10中稀土元素含量的差异是导致包头PM10细胞毒性效应不同于标准颗粒物且具有季节性差异的原因之一。