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    The partitioning behavior of per- and polyfluoroalkyl compounds (PFCs) between pore water and sediment in two sediment cores collected from Tokyo Bay, Japan, was investigated. In addition, the fluxes and temporal trends in one dated... more
    The partitioning behavior of per- and polyfluoroalkyl compounds (PFCs) between pore water and sediment in two sediment cores collected from Tokyo Bay, Japan, was investigated. In addition, the fluxes and temporal trends in one dated sediment core were studied. Short-chain perfluoroalkyl carboxylic acids (PFCAs) (C < or = 7) were found exclusively in pore water, while long-chain PFCAs (C > or = 11) were found only in sediment The perfluoroalkyl sulfonates (PFSAs), n-ethylperfluoro-1-octanesulfonamidoacetic acid (N-EtFOSAA), and perfluorooctane sulfonamide (PFOSA) seemed to bind more strongly to sediment than PFCAs. The enrichment of PFCs on sediment increased with increasing organic matter and decreasing pH. The perfluorocarbon chain length and functional group were identified as the dominating parameters that had an influence on the partitioning behavior of the PFCs in sediment The maximum SigmaPFC contamination in sediment was observed in 2001-2002 to be a flux of 197 pg cm(-2) yr(-1). Statistically significant increased concentrations in Tokyo Bay were found for perfluorooctanesulfonate (PFOS) (1956-2008), perfluorononanoic acid (PFNA) (1990-2008), and perfluoroundecanoic acid (PFUnDA) (1990-2008). Concentrations of PFOSA and N-EtFOSAA increased between 1985 and 2001, but after 2001, the concentration decreased significantly, which corresponded with the phase out of perfluorooctyl sulfonyl fluoride-based compounds by the 3M Company in 2000.
    Polybrominated diphenyl ethers (PBDEs) are used extensively as flame-retardants and are ubiquitous in the environment and in wildlife and human tissue. Recent studies have shown that PBDEs induce neurotoxic effects in vivo and apoptosis... more
    Polybrominated diphenyl ethers (PBDEs) are used extensively as flame-retardants and are ubiquitous in the environment and in wildlife and human tissue. Recent studies have shown that PBDEs induce neurotoxic effects in vivo and apoptosis in vitro. However, the signaling mechanisms responsible for these events are still unclear. In this study, we investigated the action of a commercial mixture of PBDEs (pentabrominated diphenyl ether, DE-71) on a human neuroblastoma cell line, SK-N-SH. A cell viability test showed a dose-dependent increase in lactate dehydrogenase leakage and 3-(4,5-dimethylthia-zol-2-yl)-2,5-diphenyl-tetrazolium bromide reduction. Cell apoptosis was observed through morphological examination, and DNA degradation in the cell cycle and cell apoptosis were demonstrated using flow cytometry and DNA laddering. The formation of reactive oxygen species was not observed, but DE-71 was found to significantly induce caspase-3, -8, and -9 activity, which suggests that apoptosis is not induced by oxidative stress but via a caspase-dependent pathway. We further investigated the intracellular calcium ([Ca(2+)](i)) levels using flow cytometry and observed an increase in the intracellular Ca(2+) concentration with a time-dependent trend. We also found that the N-methyl d-aspartate (NMDA) receptor antagonist MK801 (3 microM) significantly reduced DE-71-induced cell apoptosis. The results of a Western blotting test demonstrated that DE-71 treatment increases the level of Bax translocation to the mitochondria in a dose-dependent fashion and stimulates the release of cytochrome c (Cyt c) from the mitochondria into the cytoplasm. Overall, our results indicate that DE-71 induces the apoptosis of [Ca(2+)](i) in SK-N-SH cells via Bax insertion, Cyt c release in the mitochondria, and the caspase activation pathway.
    To our knowledge, this is the first study reporting concentrations of perfluorinated compounds (PFCs) in waterbird eggs in south China. Concentrations of 11 PFCs (PFOS, PFHxS, PFBS, PFOSA, PFDoDA, PFUnDA, PFDA, PFNA, PFOA, PFHpA, PFHxA)... more
    To our knowledge, this is the first study reporting concentrations of perfluorinated compounds (PFCs) in waterbird eggs in south China. Concentrations of 11 PFCs (PFOS, PFHxS, PFBS, PFOSA, PFDoDA, PFUnDA, PFDA, PFNA, PFOA, PFHpA, PFHxA) were measured in night heron, great egret, and little egret eggs from south China (Hong Kong, Xiamen, Quanzhou). PFOS was found to be the dominant PFC in the waterbird eggs. Total concentrations of the 11 PFCs in waterbird eggs ranged from 27.0 ng/g ww (great egret from Hong Kong) to 160 ng/g ww (night heron from Quanzhou). Significant differences in PFOS concentrations were found among species, but not among locations. The composition profiles of the individual PFCs among egg samples were generally similar. Positive correlations were found between PFOS and some of the PFCAs in the egg samples from Hong Kong. Concentrations of some of the PFCs were significantly correlated with total PCB concentrations reported in a previous study in the night heron egg samples, but not in the great egret samples. Preliminary risk assessment suggests that there is no immediate risk of a reduction in offspring survival in waterbirds in south China due to PFOS, but more information is needed on the potential effects of PFCs in waterbirds.
    Recent studies showed that perfluorooctane sulfonate (PFOS) affects the mammalian immune system at levels reportedly found in the general human population. It has been demonstrated that exposure to immunotoxic chemicals may diminish the... more
    Recent studies showed that perfluorooctane sulfonate (PFOS) affects the mammalian immune system at levels reportedly found in the general human population. It has been demonstrated that exposure to immunotoxic chemicals may diminish the host resistance of animals to various pathogenic challenges and enhance mortality. Therefore, the current study was carried out to characterize the effect of a 21 day pre-administration of zero, 5, or 25 microg PFOS/kg bw/day in female B6C3F1 mice on host resistance to influenza A virus infection. At the end of PFOS exposure, body/organ weights did not significantly change whereas PFOS distribution in blood plasma, spleen, thymus and lung was dose-dependently increased. PFOS exposure in mice resulted a significant increase in emaciation and mortality in response to influenza A virus. The effective plasma concentrations in female mice were at least several fold lower than reported mean blood PFOS levels from occupationally exposed humans, and fell in the upper range of blood concentrations of PFOS in the normal human population and in a wide range of wild animals. Hence, it should be important to clarify the precise mechanism(s) for excess mortality observed in the high dose group.