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This paper presents the results of a geotechnical investigation regarding the slope stability in a pit lake, emphasizing the impact of water level variations. Advanced analysis techniques were utilized for this study. The research was performed by using fully coupled flow-deformation analyses. For the fully coupled approach, Bishop’s effective-stress equation was used, and for the description of soil hydraulic behavior, the Van Genuchten’s model was applied. The analysis of slope stability associated with reservoir water level changes revealed that the slope tended to become unstable as the water level decreased; the stability factor was negatively related to the rate of water level reduction. Concerning the water level fluctuations, the analyses revealed that the soil mass seemed to become less stable as the rate of water level change increased. Under a specific range of rates of water level variation, the safety factor became higher as the number of fluctuations increased. Additionally, the simulation results concerning the water level rising indicate that the pressure due to the external water level acts on the slope surface with a positive impact on the stability factor. The results obtained reflect the effects under a specific site condition, but they can be used as a reference for evaluating slope stability in a pit lake design.

BackgroundAssociation of particulate matter with adverse health effects has been established in epidemiological studies and animal experiments. Epidemiological studies are difficult to undertake while animal studies are impractical for high-throughput toxicity testing. The ease and rapidity of in vitro tests emphasizes their potential for use in risk assessment of chemicals and particles. We examined the association between in vitro and in vivo responses to ambient particles, to determine the potential of cell-based assays as standalone toxicity screening tools.MethodsAssays of cytotoxicity and key inflammatory mediators were applied to determine the in vitro biological potency of a panel of urban and mineral particles in J774A.1 macrophages and A549 lung epithelial cells. The particles were also screened for the presence of AhR agonists using the Ah receptor-dependent gene induction assay and for endotoxin using the Limulus amebocyte lysate assay. A subset of the particles with a contrasting in vitro toxicity profile was delivered intratracheally in BALB/c mice to assess their in vivo biological potency. Results from various bioassays were combined within the in vitro and in vivo models. The combined potency measures were examined for associations.ResultsOverall, J774A.1 cells were more sensitive to particle effects than A549 cells. Whereas the combined cytotoxicity estimates were highly correlated between the two cell lines, the combined in vitro inflammatory potency estimates were not, emphasizing functional differences of the two cell types. Secretion of inflammatory markers by J774A.1 cells was correlated with AhR ligand binding profile and endotoxin levels of particles. Particle instillation led to an acute toxicity response in BALB/c mice, with neutrophilia and release of inflammatory mediators. While the combined toxicity estimates were not correlated between in vitro and in vivo models, the combined inflammatory and integrated potency estimates (toxicity and inflammation) approached the threshold for significance (p = 0.052) in a correlation within in vitro and in vivo models, with a ranking of fine particle (DWR1), minerals (TiO2, CRI) and coarse particles (SRM-, EHC-type) from low to high potency.ConclusionIntegration of in vitro endpoints shows promise in determining adverse outcomes of particle exposures in vivo. The devised data reduction and computational approach will prove useful in the development of models for assessment of hazard potential of particles; however, distinct models may be needed for particles of different type, such as urban particles vs. mineral particles, nanomaterials.

BackgroundAssociation of particulate matter with adverse health effects has been established in epidemiological studies and animal experiments. Epidemiological studies are difficult to undertake while animal studies are impractical for high-throughput toxicity testing. The ease and rapidity of in vitro tests emphasizes their potential for use in risk assessment of chemicals and particles. We examined the association between in vitro and in vivo responses to ambient particles, to determine the potential of cell-based assays as standalone toxicity screening tools.MethodsAssays of cytotoxicity and key inflammatory mediators were applied to determine the in vitro biological potency of a panel of urban and mineral particles in J774A.1 macrophages and A549 lung epithelial cells. The particles were also screened for the presence of AhR agonists using the Ah receptor-dependent gene induction assay and for endotoxin using the Limulus amebocyte lysate assay. A subset of the particles with a contrasting in vitro toxicity profile was delivered intratracheally in BALB/c mice to assess their in vivo biological potency. Results from various bioassays were combined within the in vitro and in vivo models. The combined potency measures were examined for associations.ResultsOverall, J774A.1 cells were more sensitive to particle effects than A549 cells. Whereas the combined cytotoxicity estimates were highly correlated between the two cell lines, the combined in vitro inflammatory potency estimates were not, emphasizing functional differences of the two cell types. Secretion of inflammatory markers by J774A.1 cells was correlated with AhR ligand binding profile and endotoxin levels of particles. Particle instillation led to an acute toxicity response in BALB/c mice, with neutrophilia and release of inflammatory mediators. While the combined toxicity estimates were not correlated between in vitro and in vivo models, the combined inflammatory and integrated potency estimates (toxicity and inflammation) approached the threshold for significance (p = 0.052) in a correlation within in vitro and in vivo models, with a ranking of fine particle (DWR1), minerals (TiO2, CRI) and coarse particles (SRM-, EHC-type) from low to high potency.ConclusionIntegration of in vitro endpoints shows promise in determining adverse outcomes of particle exposures in vivo. The devised data reduction and computational approach will prove useful in the development of models for assessment of hazard potential of particles; however, distinct models may be needed for particles of different type, such as urban particles vs. mineral particles, nanomaterials.

Almost all post exploitation open pit mines in the world are shaped as a final reservoir intended to be filled with water. In Europe, the creation of water lakes is the most common way of reclaiming post open pit mines. The safety and the security of mine lakes is one of the priorities of mine regions. One of the main hazards identified is the slope stability of lake banks. To develop a reliability methodology for assessing the long-term stability of flooded open pit mines, a large-scale numerical model of the lake was carried out and was applied on Lake Most, which is one of the largest mining lakes in Europe (Czech Republic). The large-scale numerical model was built, based on the site observations, large scale LiDAR data and geotechnical data. The results highlighted the reliability of the methodology to combine the geometric model with the geological model to create a large-scale numerical model, and to identify local and potentially instable zones.

Epidemiologic studies have shown an association between exposure to ambient particulate air pollution atherosclerosis; adhesion molecules

BACKGROUND: Controlled exposures of animals and humans to particulate matter (PM) or ozone air pollution cause an increase in plasma levels of endothelin-1, a potent vasoconstrictor that regulates pulmonary arterial pressure. OBJECTIVES: The primary objective of this field study was to determine whether Mexico City children, who are chronically exposed to levels of PM and [O.sub.3] that exceed the United States air quality standards, have elevated plasma endothelin-1 levels and pulmonary arterial pressures. METHODS: We conducted a study of 81 children, 7.9 [+ or -] 1.3 years of age, lifelong residents of either northeast (n = 19) or southwest (n = 40) Mexico City or Polotitlan (n = 22), a control city with PM and [O.sub.3] levels below the U.S. air quality standards. Clinical histories, physical examinations, and complete blood counts were done. Plasma endothelin-1 concentrations were determined by immunoassay, and pulmonary arterial pressures were measured by Doppler echocardiography. RESULTS: Mexico City children had higher plasma endothelin-1 concentrations compared with controls (p < 0.001). Mean pulmonary arterial pressure was elevated in children from both northeast (p < 0.001) and southwest (p < 0.05) Mexico City compared with controls. Endothelin-1 levels in Mexico City children were positively correlated with daily outdoor hours (p = 0.012), and 7-day cumulative levels of PM air pollution < 2.5 [micro]m in aerodynamic diameter ([PM.sub.2.5]) before endothelin1 measurement (p = 0.03). CONCLUSIONS: Chronic exposure of children to [PM.sub.2.5] is associated with increased levels of circulating endothelin-1 and elevated mean pulmonary arterial pressure. KEY WORDS: air pollution, endothelial dysfunction, endothelin-1, children, particulate matter, pulmonary arterial pressure. Environ Health Perspect 115:1248-1253 (2007). doi:10.1289/ehp.9641 available via http://dx.doi.org/ [Online 27 April 2007], Activation of the endothelin system and vasoconstriction h1as been reported in animal models (Bouthillier et al. 1998; Kang et al. 2002; Thomson et al. 2004, 2005; Vincent et al. 2001a) [...]

Alveolar macrophages (AM) play a key role in clearing atmospheric particulates from the lung surface and stimulating epithelial cells to produce proinflammatory mediators. The present study examines the role of 'acute response' cytokines TNF-[alpha] and IL-1[beta] released by AM exposed to ambient particulate matter with a diameter of 0.05), and the combination of the two antibodies most effective. When HBEC were treated similarly, anti-TNF-[alpha] antibodies had the greatest effect. In A549 cells P[M.sub.10]-exposed AM supernatants increased NF-[kappa]B, activator protein (AP)-1 and specificity protein 1 binding, while anti-TNF-[alpha] and anti-IL-1[beta] antibodies reduced NF-[kappa]B and AP-1 binding. We conclude that AM-derived TNF-[alpha] and IL-1[beta] provide a major stimulus for the production of proinflammatory mediators by lung epithelial cells and that their relative importance may depend on the type of epithelial cell target. ribonuclease protection assay; transcription factors; enzyme-linked immunosorbent assay; proinflammatory mediators; particulate matter with diameter < 10 [micro]m

Exposure to air pollution [particulate matter, particles air pollution; alveolar macrophages; atherosclerosis; inflammation; leukocytes

We examined the hypothesis that ambient particulate matter with a diameter of interleukin-8; monocyte chemoattractant protein-1; intercellular adhesion molecule-1; nuclear factor-[kappa]B; transcription factor specificity protein 1; particulate matter

The pharmacokinetics of salicylate and the concentration of hydroxylated plasma and lung metabolites were analyzed in juvenile, adult and senescent rats after exposure to ozone. Analysis of Fischer 344 rat lungs indicated a significant increase in 2,3-dihydroxybenzoic acid (DHBA) metabolites in senescent rats due to higher basal rate of .OH production and sensitivity to oxidants compared to juvenile rats. However, the levels of 2,3-DHBA, 2,5-DHBA and salicylate in the plasma and lungs were similar in juvenile, adult and senescent Fischer 344 rats after acute ozone exposure.

Bronchoalveolar lavage fluid in Fischer 344 rat models was analyzed after exposure to 04-08 parts per million of ozone to determine the toxicodynamics of the pollutant to age-related lung sensitivity. Senescent F344 rats exhibited higher increase in N-acetyl-beta-D-glucosaminidase activity and liberation of interleukin-6 after exposure to ozone compared to juvenile rats. The alterations in the bronchoalveolar lavage fluids of aging rats were also different from the oxidant-mediated lung injury of juveniles.