Generation of oxidatively damaged DNA by particulate matter (PM) is hypothesized to occur via production of reactive oxygen species (ROS) and inflammation. We investigated this hypothesis by comparing ROS production, inflammation and oxidatively damaged DNA in different experimental systems investigating air pollution particles. There is substantial evidence indicating that exposure to air pollution particles was associated with elevated levels of oxidatively damaged nucleobases in circulating blood cells and urine from humans, which is supported by observations of elevated levels of genotoxicity in cultured cells exposed to similar PM. Inflammation is most pronounced in cultured cells and animal models, whereas an elevated level of oxidatively damaged DNA is more pronounced than inflammation in humans. There is non-congruent data showing corresponding variability in effect related to PM sampled at different locations (spatial variability), times (temporal variability) or particle size fraction across different experimental systems of acellular conditions, cultured cells, animals and humans. Nevertheless, there is substantial variation in the genotoxic, inflammation and oxidative stress potential of PM sampled at different locations or times. Small air pollution particles did not appear more hazardous than larger particles, which is consistent with the notion that constituents such as metals and organic compounds also are important determinants for PM-generated oxidative stress and inflammation. In addition, the results indicate that PM-mediated ROS production is involved in the generation of inflammation and activated inflammatory cells can increase their ROS production. The observations indicate that air pollution particles generate oxidatively damaged DNA by promoting a milieu of oxidative stress and inflammation.

Oxidative stress and inflammation generated DNA damage by exposure to air pollution particles

The current global gold rush, driven by increasing consumption in developing countries and uncertainty in financial markets, is an increasing threat for tropical ecosystems. Gold mining causes significant alteration to the environment, yet mining is often overlooked in deforestation analyses because it occupies relatively small areas. As a result, we lack a comprehensive assessment of the spatial extent of gold mining impacts on tropical forests. In this study, we provide a regional assessment of gold mining deforestation in the tropical moist forest biome of South America. Specifically, we analyzed the patterns of forest change in gold mining sites between 2001 and 2013, and evaluated the proximity of gold mining deforestation to protected areas (PAs). The forest cover maps were produced using the Land Mapper web application and images from the MODIS satellite MOD13Q1 vegetation indices 250 m product. Annual maps of forest cover were used to model the incremental change in forest in ?1600 potential gold mining sites between 2001?2006 and 2007?2013. Approximately 1680 km2 of tropical moist forest was lost in these mining sites between 2001 and 2013. Deforestation was significantly higher during the 2007?2013 period, and this was associated with the increase in global demand for gold after the international financial crisis. More than 90% of the deforestation occurred in four major hotspots: Guianan moist forest ecoregion (41%), Southwest Amazon moist forest ecoregion (28%), Tapaj?s?Xing? moist forest ecoregion (11%), and Magdalena Valley montane forest and Magdalena?Urab? moist forest ecoregions (9%). In addition, some of the more active zones of gold mining deforestation occurred inside or within 10 km of ?32 PAs. There is an urgent need to understand the ecological and social impacts of gold mining because it is an important cause of deforestation in the most remote forests in South America, and the impacts, particularly in aquatic systems, spread well beyond the actual mining sites.

/pdf/global-demand-for-gold-is-another-threat-for-tropical-1wkecgavg9.pdf

Global demand for gold is another threat for tropical forests

Recently, we used cell-free assays to demonstrate the toxic effects of complex mixtures of organic extracts from urban air particles (PM2.5) collected in four localities of the Czech Republic (Ostrava-Bartovice, Ostrava-Poruba, Karvina and Trebon) which differed in the extent and sources of air pollution. To obtain further insight into the biological mechanisms of action of the extractable organic matter (EOM) from ambient air particles, human embryonic lung fibroblasts (HEL12469) were treated with the same four EOMs to assess changes in the genome-wide expression profiles compared to DMSO treated controls. For this purpose, HEL cells were incubated with subtoxic EOM concentrations of 10, 30, and 60 μg EOM/ml for 24 hours and global gene expression changes were analyzed using human whole genome microarrays (Illumina). The expression of selected genes was verified by quantitative real-time PCR. Dose-dependent increases in the number of significantly deregulated transcripts as well as dose-response relationships in the levels of individual transcripts were observed. The transcriptomic data did not differ substantially between the localities, suggesting that the air pollution originating mainly from various sources may have similar biological effects. This was further confirmed by the analysis of deregulated pathways and by identification of the most contributing gene modulations. The number of significantly deregulated KEGG pathways, as identified by Goeman's global test, varied, depending on the locality, between 12 to 29. The Metabolism of xenobiotics by cytochrome P450 exhibited the strongest upregulation in all 4 localities and CYP1B1 had a major contribution to the upregulation of this pathway. Other important deregulated pathways in all 4 localities were ABC transporters (involved in the translocation of exogenous and endogenous metabolites across membranes and DNA repair), the Wnt and TGF-β signaling pathways (associated particularly with tumor promotion and progression), Steroid hormone biosynthesis (involved in the endocrine-disrupting activity of chemicals), and Glycerolipid metabolism (pathways involving the lipids with a glycerol backbone including lipid signaling molecules). The microarray data suggested a prominent role of activation of aryl hydrocarbon receptor-dependent gene expression.

/pdf/global-gene-expression-changes-in-human-embryonic-lung-4yaow6hcxa.pdf

Global gene expression changes in human embryonic lung fibroblasts induced by organic extracts from respirable air particles

Even though clean air is considered as a basic requirement for the maintenance of human health, air pollution continues to pose a significant health threat in developed and developing countries alike. Monitoring and modeling of classic and emerging pollutants is vital to our knowledge of health outcomes in exposed subjects and to our ability to predict them. The ability to anticipate and manage changes in atmospheric pollutant concentrations relies on an accurate representation of the chemical state of the atmosphere. The task of providing the best possible analysis of air pollution thus requires efficient computational tools enabling efficient integration of observational data into models. A number of air quality models have been developed and play an important role in air quality management. Even though a large number of air quality models have been discussed or applied, their heterogeneity makes it difficult to select one approach above the others. This paper provides a brief review on air quality models with respect to several aspects such as prediction of health effects.

A review of AirQ Models and their applications for forecasting the air pollution health outcomes

Epidemiological and toxicological studies have suggested that the health effects associated with exposure to particulate matter (PM) are related to the different physicochemical properties of PM. These effects occur through the initiation of differential cellular responses including: the induction of antioxidant defenses, proinflammatory responses, and ultimately cell death. The main objective of this study was to investigate the effects of size-fractionated ambient PM on epithelial cells in relation to their physicochemical properties. Concentrated ambient PM was collected on filters for three size fractions: coarse (aerodynamic diameter [AD] 2.5-10 μm), fine (0.15-2.5 μm), and quasi-ultrafine (<0.2 μm), near a busy street in Toronto, Ontario, Canada. Filters were extracted and analyzed for chemical composition and redox activity. Chemical analyses showed that the coarse, fine, and quasi-ultrafine particles were comprised primarily of metals, water-soluble species, and organic compounds, respectively. The highest redox activity was observed for fine PM. After exposure of A549 cells to PM (10-100 μg/ml) for 4 h, activation of antioxidant, proinflammatory and cytotoxic responses were assessed by determining the expression of heme oxygenase (HMOX-1, mRNA), interleukin-8 (IL-8, mRNA), and metabolic activity of the cells, respectively. All three size fractions induced mass-dependent antioxidant, proinflammatory, and cytotoxic responses to different degrees. Quasi-ultrafine PM caused significant induction of HMOX-1 at the lowest exposure dose. Correlation analyses with chemical components suggested that the biological responses correlated mainly with transition metals and organic compounds for coarse and fine PM and with organic compounds for quasi-ultrafine PM. Overall, the observed biological responses appeared to be related to the combined effects of size and chemical composition and thus both of these physicochemical properties should be considered when explaining PM toxicity.

The combined effects of physicochemical properties of size-fractionated ambient particulate matter on in vitro toxicity in human A549 lung epithelial cells

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

The bilinear receptor model positive matrix factorization (PMF) was used to apportion particulate matter with an aerodynamic diameter of 1-10 microm (PM1-10) sources in a village, Brezno, situated in an industrial region of northern Bohemia in Central Europe. The receptor model analyzed the data sets of 90- and 60-min integrations of PM1-10 mass concentrations and elemental composition for 27 elements. The 14-day sampling campaigns were conducted in the village in summer 2008 and winter 2010. Also, to ensure seasonal and regional representativeness of the data sets recorded in the village, the spatial-temporal variability of the 24-hr PM10 and PM1-10 within 2008-2010 in winter and summer across the multiple sites was evaluated. There were statistically significant interseasonal differences of the 24-hr PM data, but not intrasummer or intrawinter differences of the 24-hr PM1-10 data across the multiple sites. PMF resolved seven sources of PM1-10. They were high-temperature coal combustion; combustion in local heating boilers; marine aerosol; mineral dust; primary biological/wood burning; road dust, car brakes; and gypsum. The main summer factors were assigned to mineral dust (38.2%) and primary biological/wood burning (33.1%). In winter, combustion factors dominated (80%) contribution to PM1-10. The conditional probability function (CPF) helped to identified local sources of PM1-10. The source of marine aerosol from the North Sea and English Channel was indicated by the Hybrid Single Particle Lagrangian Integrated Trajectory Model (HYSPLIT).

https://www.tandfonline.com/doi/pdf/10.1080/10962247.2013.825215

Particulate matter source apportionment in a village situated in industrial region of Central Europe.

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<dae<10μm), upper (05<dae<1μm), and lower (017<dae<05μm) accumulation aerosol particles and ultrafine particles (dae<017) High-volume aerosol samples were collected consecutively in four localities that differed in the level of environmental pollution The genotoxicity of EOMs was measured by analysis of DNA adducts induced in an a cellular assay consisting of calf thymus DNA with/without rat liver microsomal S9 fraction coupled with (32)P-postlabelling The upper accumulation fraction was the major size fraction in all four localities, forming 37-46% of the total PM mass Per m(3) of sampled air, this fraction also bound the largest amount of c-PAHs Correspondingly, the upper accumulation fraction induced the highest DNA-adduct levels Per PM mass itself, the lower accumulation fraction is seen to be the most efficient in binding DNA-reactive organic compounds Interestingly, the results suggest that the fraction of ultrafine particles of various ambient-air samples is neither a major carrier of c-PAHs, nor a major inducer of their genotoxicity, which is an important finding that is relevant to the toxicity and health effects of ultrafine particles, which are so extensively discussed these days

http://konsys-t.tanger.cz/files/proceedings/14/reports/2051.pdf

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

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

Jiri Krouzek

Papers

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

Particulate matter source apportionment in a village situated in industrial region of Central Europe.

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

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