Stabilisation/solidification of landfill leachate concentrate and its residue obtained by partial evaporation.

Landfilling of waste is inseparably linked to the production of landfill leachate, which is treated and processed by different procedures. One of the options according to technical and economic development is the application of pressure-driven membrane processes, where landfill leachate concentrate (LLC) is produced. This may be further subjected to a stabilisation/solidification process (S/S) as one of its possible processing methods that leads to limited re-introduction of undesirable substances into the landfill body. This paper presents the research of the S/S of LLC, investigates the effect of the waste/binder ratio, the influence of Portland cement substitution, the influence of the additional concentration of the concentrate by evaporation at different levels from the original LLC, and the use of an innovative special highly absorbing binder based on specifically treated fly ash for selected leachate characteristics and compressive strength of the test specimen. The S/S process in most cases met the legislative requirements for water leachate characteristics for non-hazardous waste. Additionally, the comparison of indicative expense for selected solidificate compositions and scenarios is involved. The results of the study serve as necessary basement for further development of treatment of LLC.

Ultrafine particles are not major carriers of carcinogenic PAHs and their genotoxicity in size-segregated aerosols.

Some studies suggest that genotoxic effects of combustion-related aerosols are induced by carcinogenic polycyclic aromatic hydrocarbons (c-PAHs) and their derivatives, which are part of the organic fraction of the particulate matter (PM) in ambient air. The proportion of the organic fraction in PM is known to vary with particle size. The ultrafine fraction is hypothesized to be the most important carrier of c-PAHs, since it possesses the highest specific surface area of PM. To test this hypothesis, the distribution of c-PAHs in organic extracts (EOMs) was compared for four size fractions of ambient-air aerosols: coarse (1

An acellular assay to assess the genotoxicity of complex mixtures of organic pollutants bound on size segregated aerosol. Part I: DNA adducts.

An acellular assay consisting of calf thymus DNA with/without rat liver microsomal S9 fraction was used to study the genotoxicity of complex mixtures of organic air pollutants bound to size segregated aerosols by means of DNA adduct analysis. We compared the genotoxicity of the organic extracts (EOMs) from three size fractions of aerosol ranging from 0.17µm to 10µm that were collected by high volume cascade impactors in four localities of the Czech Republic differing in the extent of the environmental pollution: (1) small village in proximity of a strip mine, (2) highway, (3) city center of Prague and (4) background station. The total DNA adduct levels induced by 100µg/ml of EOMs were analyzed by (32)P-postlabelling analysis with a nuclease P1 method for adduct enrichment. The main finding of the study was most of the observed genotoxicity was connected with a fine particulate matter fraction (<1µm). The concentrations of carcinogenic polycyclic aromatic hydrocarbons (c-PAHs) in EOMs indicate that fine fractions (0.5-1µm) bound the highest amount of c-PAHs in all aerosol sampling sites, which might be related to the higher specific surface of this fraction as compared with a course fraction (1-10µm) and higher mass as compared with a condensational fraction (0.17-0.5µm). As for aerosol mass, both fine and condensational fractions are effective carriers of c-PAHs. Similarly, the DNA adduct levels per m(3) of air were highest for the fine fraction, while the condensational fraction (strip mine site and city center) revealed the highest DNA adduct levels in cases where aerosol mass is taken into consideration. A strong correlation was found between the c-PAHs and DNA adduct levels induced by EOMs in all the localities and for various size fractions (R(2)=0.98, p<0.001). It may be concluded that the analysis of total DNA adducts induced in an acellular assay with/without metabolic activation represents a relatively simple method to assess the genotoxic potential of various complex mixtures.

An acellular assay to assess the genotoxicity of complex mixtures of organic pollutants bound on size segregated aerosol. Part II: oxidative damage to DNA.

Ambient air particulate matter (atmospheric aerosol; PM) is an important factor in the development of various diseases. Oxidative stress is believed to be one of the mechanisms of action of PM on the human organism. The aim of our study was to investigate the ability of organic extracts of size segregated aerosol particles (EOM; three fractions of aerodynamic diameter 1-10µm, 0.5-1µm and 0.17-0.5µm) to induce oxidative damage to DNA in an in vitro acellular system of calf thymus (CT) DNA with and without S9 metabolic activation. PM was collected in the Czech Republic at four places with different levels of air pollution. Levels of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) tended to increase with decreasing sizes of PM. S9 metabolic activation increased the oxidative capacity of PM; mean levels of 8-oxodG/10(5) dG per 1000m(3) of air for samples with and without metabolic activation were 0.093 and 0.067, respectively (p<0.05). When results of oxidative damage to DNA were normalized per microgram of aerosol mass, mean levels of 8-oxodG/10(5) dG were 0.265 and 0.191, for incubation with and without S9 fraction, respectively (p<0.05). We observed a significant positive association between concentrations of polycyclic aromatic hydrocarbons (c-PAHs) bound to PM and levels of 8-oxodG/10(5) dG per 1000m(3) of air after metabolic activation of EOM samples (R=0.695, p<0.05). The correlation was weaker and non-significant for samples without metabolic activation (R=0.523, p=0.08). In conclusion, we showed that organic extracts of PM were able to induce oxidative damage to DNA in vitro; this ability was increased after S9 metabolic activation of EOM and with decreasing sizes of PM.