Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 5 de 5
Filter
Add more filters











Database
Language
Publication year range
1.
Chemosphere ; 287(Pt 1): 131989, 2022 Jan.
Article in English | MEDLINE | ID: mdl-34450366

ABSTRACT

Thermally enhanced bioremediation is a promising approach to shorten the bioremediation period of tetrachloroethene (PCE) and trichloroethene (TCE). To clarify the influence that temperature has on stepwise PCE dechlorination and associated microorganisms, this study conducted dechlorination experiments using contaminated soil and groundwater under five distinct temperature conditions (i.e., 15, 20, 25, 30, and 35 °C). PCE and TCE were dechlorinated most rapidly at 25-35 °C, whereas the preferable temperatures for the dechlorination of cis-1,2- dichloroethene (cis-1,2-DCE) and vinyl chloride (VC) were 25-30 °C and 25 °C, respectively. Microbial community analysis revealed that Sulfurospirillum and Geobacter may have a dominant contribution to the dechlorination of PCE to cis-1,2-DCE, whereas Dehalococcoides harboring VC reductase genes are likely major contributors to the dechlorination of cis-1,2-DCE and VC. These results suggest that temperature influences various microbial groups, including major dechlorinating microorganisms, resulting in the different extent of PCE dechlorination. In addition, the microbial community structure greatly changed after the onset of the experiment, whereas the temperature influence of 15-30 °C on the microbial community structure was minor; however, the microbial community was significantly impacted at 35 °C. Collectively, these results suggest that thermally enhanced anaerobic dechlorination at 25 °C is useful for successful dechlorination of chlorinated ethenes in a short period.


Subject(s)
Tetrachloroethylene , Trichloroethylene , Vinyl Chloride , Ethylenes , Temperature
2.
Environ Pollut ; 235: 223-234, 2018 Apr.
Article in English | MEDLINE | ID: mdl-29291522

ABSTRACT

Particulate matter with diameters <2.5 µm (i.e., PM2.5) has multiple natural and anthropological sources. The association between PM2.5 and the exacerbation of respiratory allergy and asthma has been well studied, but the components of PM2.5 that are responsible for allergies have not yet been determined. Here, we elucidated the effects of aqueous and organic extract of PM2.5 collected during four seasons in November 2014-December 2015 in two cities (Kawasaki, an industrial area and Fukuoka, an urban area affected by transboundary pollution matter) of Japan on respiratory health. Ambient PM2.5 was collected by high-volume air samplers and extracted into water soluble and lipid soluble components. Human airway epithelial cells, murine bone marrow-derived antigen-presenting cells (APC) and splenocytes were exposed to PM2.5 extracts. We measured the cell viability and release of interleukin (IL)-6 and IL-8 from airway epithelial cells, the DEC205 and CD86 expressions on APCs and cell proliferation, and TCR and CD19 expression on splenocytes. The water-soluble or aqueous extracts, especially those from Kawasaki in fall, had a greater cytotoxic effect than the lipid-soluble or organic extracts in airway epithelial cells, but they caused almost no pro-inflammatory response. Extract of fall, especially the aqueous extract from Fukuoka, increased the DEC205 and CD86 expressions on APC. Moreover, aqueous extracts of fall, summer, and spring from Fukuoka significantly increased proliferation of splenocytes. Organic extract of spring and summer from Kawasaki significantly elevated the TCR expression, and organic extract of summer from Kawasaki decreased the CD19 expression. These results suggest that PM2.5 extract samples are responsible for cytotoxicity in airway epithelial cells and for activating APCs and T-cells, which can contribute to the exacerbation of respiratory diseases such as asthma. These effects can differ by PM2.5 components, collection areas and seasons.


Subject(s)
Air Pollutants/analysis , Environmental Exposure/statistics & numerical data , Particulate Matter/analysis , Air Pollutants/toxicity , Asthma/metabolism , Cell Survival/drug effects , Cities , Environmental Monitoring/methods , Epithelial Cells/drug effects , Humans , Immune System/drug effects , Interleukin-6/metabolism , Japan , Particulate Matter/toxicity , Seasons
3.
Environ Toxicol ; 32(9): 2172-2181, 2017 Sep.
Article in English | MEDLINE | ID: mdl-28444933

ABSTRACT

Particulate matter with aerodynamic diameter ≤2.5 µm (PM2.5 ) is generally composed of carbon nuclei associated with various organic carbons, metals, ions and biological materials. Among these components, polyaromatic hydrocarbons (PAHs) such as benzo(a)pyrene (BaP) and quinones have detrimental effects on airway epithelial cells and immunodisrupting effects, which leads to the exacerbation of respiratory allergies. The effects of PAHs and the carbon nuclei, separately as well as in combination, remain to be established. We investigated the effects of BaP, 9,10-phenanthroquinone (9,10-PQ), and 1,2-napthoquinone (1,2-NQ) and their combined effects with heated diesel exhaust particle (H-DEP) as carbon nuclei of typical PM2.5 . We exposed human airway epithelial cells (BEAS-2B), murine bone marrow-derived antigen-presenting cells (APCs), and murine splenocytes to BaP, 9,10-PQ, or 1,2-NQ in the presence and absence of H-DEP. Several important inflammatory cytokines and cell surface molecules were measured. PAHs alone did not have apparent cytotoxic effects on BEAS-2B, whereas combined exposure with H-DEP induced noticeable detrimental effects which mainly reflected the action of H-DEP itself. BaP increased CD86 expression as an APC surface molecule regardless of the presence or absence of H-DEP. None of the BaP, 9,10-PQ, or 1,2-NQ exposure alone or their combined exposure with H-DEP resulted in any significant activation of splenocytes. These results suggest that PAHs and carbon nuclei show additive effects, and that BaP with the carbon nuclei may contribute to exacerbations of allergic respiratory diseases including asthma by PM2.5 , especially via antigen-presenting cell activation.


Subject(s)
Carbon/chemistry , Lymphocytes/drug effects , Particulate Matter/toxicity , Polycyclic Aromatic Hydrocarbons/toxicity , Respiratory Mucosa/drug effects , Vehicle Emissions/toxicity , Animals , Antigen-Presenting Cells/drug effects , Antigen-Presenting Cells/metabolism , Benzo(a)pyrene/toxicity , Bone Marrow Cells/drug effects , Bone Marrow Cells/metabolism , Cytokines/metabolism , Epithelial Cells/drug effects , Epithelial Cells/metabolism , Humans , Lymphocytes/metabolism , Mice , Naphthoquinones/toxicity , Phenanthrenes/toxicity , Respiratory Mucosa/cytology , Respiratory Mucosa/metabolism , Spleen/cytology , Spleen/drug effects , Spleen/metabolism
4.
J Appl Toxicol ; 37(5): 583-590, 2017 05.
Article in English | MEDLINE | ID: mdl-27714829

ABSTRACT

Epidemiologic studies have revealed that Asian sand dust particles (ASDs) can affect respiratory and immune health represented by asthma. Factors responsible for the exacerbation of asthma remain unclear. The fungus Bjerkandera adusta (B.ad) and polycyclic aromatic hydrocarbons such as benzo[a]pyrene (BaP) have been identified in ASDs collected from the atmosphere when an ASD event occurred. We investigated the effects of B.ad and BaP related to ASDs on respiratory and immune systems. Bone marrow-derived antigen-presenting cells (APCs) and splenocytes from atopic prone NC/Nga mice and human airway epithelial cells were exposed to the B.ad or to BaP in the presence and absence of heated-ASDs (H-ASDs). B.ad and BaP in both the presence and absence of H-ASDs increased the expression of cell surface molecules on APCs. H-ASDs alone slightly activated APCs. The expressions induced by B.ad were higher than those induced by BaP in the presence and absence of H-ASDs. There were no remarkable effects on the activation of splenocytes or the proinflammatory responses in airway epithelial cells. These results suggest that B.ad rather than BaP contributes to the exacerbation of asthma regardless of the presence or absence of sand particles, particularly by the activation of the immune system via APCs. Copyright © 2016 John Wiley & Sons, Ltd.


Subject(s)
Asthma/physiopathology , Dust , Silicon Dioxide/toxicity , Animals , Antigen-Presenting Cells/drug effects , Asia , Benzo(a)pyrene/toxicity , Cell Proliferation/drug effects , Coriolaceae/chemistry , Cytokines/biosynthesis , Epithelial Cells/drug effects , Humans , Male , Mice , Polycyclic Aromatic Hydrocarbons/toxicity , Spleen/drug effects , Spleen/immunology
5.
Appl Environ Microbiol ; 80(24): 7505-11, 2014 Dec.
Article in English | MEDLINE | ID: mdl-25261510

ABSTRACT

To secure food and water safety, quantitative information on multiple pathogens is important. In this study, we developed a microfluidic quantitative PCR (MFQPCR) system to simultaneously quantify 11 major human viral pathogens, including adenovirus, Aichi virus, astrovirus, enterovirus, human norovirus, rotavirus, sapovirus, and hepatitis A and E viruses. Murine norovirus and mengovirus were also quantified in our MFQPCR system as a sample processing control and an internal amplification control, respectively. River water contaminated with effluents from a wastewater treatment plant in Sapporo, Japan, was collected and used to validate our MFQPCR system for multiple viruses. High-throughput quantitative information was obtained with a quantification limit of 2 copies/µl of cDNA/DNA. Using this MFQPCR system, we could simultaneously quantify multiple viral pathogens in environmental water samples. The viral quantities obtained using MFQPCR were similar to those determined by conventional quantitative PCR. Thus, the MFQPCR system developed in this study can provide direct and quantitative information for viral pathogens, which is essential for risk assessments.


Subject(s)
Microfluidics/methods , Polymerase Chain Reaction/methods , Rivers/virology , Viruses/isolation & purification , Japan , Molecular Sequence Data , Phylogeny , Viruses/classification , Viruses/genetics , Wastewater/virology
SELECTION OF CITATIONS
SEARCH DETAIL