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Comparative toxicity of air pollution particulate matter (PM2.5) sampled under urban, industrial or rural influence in human bronchial epithelial lung cells (BEAS-2B)
Abstracts / Toxicology Letters 205S (2011) S36–S59
risk to observe ED accesses for venous thromboembolism (OR 1.69 with 95% CI 1.13–2.53). No significant association was found with cardiovascular or cerebrovascular disease. As regards venous thrombosis risk, interestingly, in a subgroup of subjects without active thrombosis and without anticoagulant therapy (n = 103) an inverse correlation between PM10-2.5 and prothrombin time was found (R = −0.226; P = 0.022).
S53
OS9-4 From cell to man: evaluation of a possible biomarker of uranium exposure O. Prat 1,∗ , E. Ansoborlo 1 , N. Sage 1 , D. Cavadore 1 , J. Lecoix 1 , P. Kurttio 2 , E. Quemeneur 1 1
doi:10.1016/j.toxlet.2011.05.204
OS9-3 Comparative toxicity of air pollution particulate matter (PM2.5 ) sampled under urban, industrial or rural influence in human bronchial epithelial lung cells (BEAS-2B) G. Garcon 1,∗ , M. Dergham 1 , S. Billet 1 , C. Lepers 1 , A. Verdin 1 , D. Courcot 1 , F. Cazier 2 , P. Shirali 1 1
Unité De Chimie Environnementale Et Interactions Sur Le Vivant, Ea 4492, Université du Littoral Côte d’Opale, Dunkerque, France, 2 Centre Commun De Mesures, Université du Littoral-Côte d’Opale, Dunkerque, France Purpose: A growing body of evidence has shown a correlation between the exposure to air pollution particulate matter (PM) and the acute exacerbation of morbidity and mortality. Atmospheric aerosols are generally heterogeneous mixtures that greatly vary in constituent, particle size and chemical composition. The underlying mechanisms for PM-induced adverse health effects are still not totally understood, but oxidative stress and inflammatory response seem to be of importance. Air pollution PM2.5 samples were also collected in spring–summer (2008) and autumn–winter (2008–2009) under urban and/or industrial influence (Dunkerque, France), or under rural influence (Rubrouck, France). Their most toxicologically relevant physicochemical characteristics were determined. Thereafter, the occurrence of oxidative damage (MalonDiAldehyde, MDA; glutathione; SuperOxide Dismutase, SOD; 8-Hydroxy-2 deoxyGuanosine, 8-OHdG) and inflammatory response (Tumor Necrosis Factor-alpha, TNF-␣; InterLeukin-1, IL-1; InterLeukin6; InterLeukin-8, IL-8) were studied in PM2.5 -exposed human bronchial epithelial cells (BEAS-2B). Methods: Physicochemical characterization of the air pollution PM2.5 samples referred to: size distribution (SEM), specific surface area (BET method), inorganic elements (ICP-MS), ionic species (IC), and organic chemicals (GC–MS). Oxidative damage and inflammatory response were considered 24–72 h after BEAS-2B cell exposure to air pollution PM2.5 (3.75 or 15 g/cm2 ) by studying MDA and glutathione (HPLC-Fluorescence), SOD (colorimetry), 8-OHdG (ELISA), and TNF-␣, IL-1, IL-6, and IL-8 gene expression (RT-qPCR) and protein secretion (ELISA). Results of the study: Physicochemical characteristics of the air pollution PM2.5 samples confirmed their high heterogeneity depending upon their respective emission sources. Their toxicity in BEAS-2B cells might rely on both the occurrence of oxidative damage and inflammatory response. doi:10.1016/j.toxlet.2011.05.205
site De Marcoule, Cea, Bagnols Sur Ceze, France, 2 Stuk, Laippatie, Finland Purpose: Ore workers are conventionally monitored for exposure by measuring the uranium in their urine, but specific biomarkers of kidney damage still remain to be discovered. A recent toxicogenomics study allowed us to focus on osteopontin (OSTP) normally excreted in human urine and linked to mineral metabolism. We examined the association between osteopontin and uranium exposure both in vitro, in a human kidney cell model, and in the urine of exposed individuals. Methods: OSTP was measured in supernatants of uraniumexposed HK2 cells to establish a dose–response curve and a time course experiment. Its role was studied through a gene extinction experiment. Uranium and OSTP were then monitored in the urine of exposed nuclear fuel industry workers and a chronically exposed population. These levels were compared with those found in a non-exposed population. Results: The study of HK2 cells indicated that OSTP secretion decreased after uranium exposure in a concentration and time dependent manner, but its suppression does not affect cell sensitivity to uranium. In spite of wide inter-individual variability, this parameter decreases also in human urine when urinary uranium exceeds 30 g/L after an acute exposure, a value considered to be critical for kidney damage. This study reports how toxicogenomics can highlight putative toxicity biomarkers in an easy to access biological fluid. The decrease of urinary osteopontin in response to uranium exposure suggests kidney damage and would thus be complementary to current markers. doi:10.1016/j.toxlet.2011.05.1042
OS9-5 Protocol sC-II of subClinical investigations for the presence of occupational environmental toxins, engineered nanoparticles, irritants and allergens as triggers and causative agents of toxic, allergic and immune responses in individuals within human habitations J. Dumanov Dir. Clinical Environmental Toxicology, subClinical Research Group US EU, Sparta, USA Purpose: subClinical protocol sC II (NEURO-TOXO) is a comprehensive differential diagnostic system of the indoor environment that was designed and aims to investigate the presence and quantity of toxins, allergens and inhabitant exposure to potentially dangerous agents and carcinogens. Methods: The (sC-2) protocol was tested 42 human environments including 26 households, 8 medical offices and 8 administrative offices (government and non-manufacturing/production business) of those patients clinically diagnosed as having possible toxic exposure, fatigue syndrome or neurosis. This protocol used air pump sampling, TO-15 summa type canisters with Gas Chromatography/Mass Spectroscopy (GC/MS) and selective ion monitoring (SIM) to collect ambient samples at the sampling sites where were detected significant amount of CO2 , CO, polycyclic hydrocarbons
risk to observe ED accesses for venous thromboembolism (OR 1.69 with 95% CI 1.13–2.53). No significant association was found with cardiovascular or cerebrovascular disease. As regards venous thrombosis risk, interestingly, in a subgroup of subjects without active thrombosis and without anticoagulant therapy (n = 103) an inverse correlation between PM10-2.5 and prothrombin time was found (R = −0.226; P = 0.022).
S53
OS9-4 From cell to man: evaluation of a possible biomarker of uranium exposure O. Prat 1,∗ , E. Ansoborlo 1 , N. Sage 1 , D. Cavadore 1 , J. Lecoix 1 , P. Kurttio 2 , E. Quemeneur 1 1
doi:10.1016/j.toxlet.2011.05.204
OS9-3 Comparative toxicity of air pollution particulate matter (PM2.5 ) sampled under urban, industrial or rural influence in human bronchial epithelial lung cells (BEAS-2B) G. Garcon 1,∗ , M. Dergham 1 , S. Billet 1 , C. Lepers 1 , A. Verdin 1 , D. Courcot 1 , F. Cazier 2 , P. Shirali 1 1
Unité De Chimie Environnementale Et Interactions Sur Le Vivant, Ea 4492, Université du Littoral Côte d’Opale, Dunkerque, France, 2 Centre Commun De Mesures, Université du Littoral-Côte d’Opale, Dunkerque, France Purpose: A growing body of evidence has shown a correlation between the exposure to air pollution particulate matter (PM) and the acute exacerbation of morbidity and mortality. Atmospheric aerosols are generally heterogeneous mixtures that greatly vary in constituent, particle size and chemical composition. The underlying mechanisms for PM-induced adverse health effects are still not totally understood, but oxidative stress and inflammatory response seem to be of importance. Air pollution PM2.5 samples were also collected in spring–summer (2008) and autumn–winter (2008–2009) under urban and/or industrial influence (Dunkerque, France), or under rural influence (Rubrouck, France). Their most toxicologically relevant physicochemical characteristics were determined. Thereafter, the occurrence of oxidative damage (MalonDiAldehyde, MDA; glutathione; SuperOxide Dismutase, SOD; 8-Hydroxy-2 deoxyGuanosine, 8-OHdG) and inflammatory response (Tumor Necrosis Factor-alpha, TNF-␣; InterLeukin-1, IL-1; InterLeukin6; InterLeukin-8, IL-8) were studied in PM2.5 -exposed human bronchial epithelial cells (BEAS-2B). Methods: Physicochemical characterization of the air pollution PM2.5 samples referred to: size distribution (SEM), specific surface area (BET method), inorganic elements (ICP-MS), ionic species (IC), and organic chemicals (GC–MS). Oxidative damage and inflammatory response were considered 24–72 h after BEAS-2B cell exposure to air pollution PM2.5 (3.75 or 15 g/cm2 ) by studying MDA and glutathione (HPLC-Fluorescence), SOD (colorimetry), 8-OHdG (ELISA), and TNF-␣, IL-1, IL-6, and IL-8 gene expression (RT-qPCR) and protein secretion (ELISA). Results of the study: Physicochemical characteristics of the air pollution PM2.5 samples confirmed their high heterogeneity depending upon their respective emission sources. Their toxicity in BEAS-2B cells might rely on both the occurrence of oxidative damage and inflammatory response. doi:10.1016/j.toxlet.2011.05.205
site De Marcoule, Cea, Bagnols Sur Ceze, France, 2 Stuk, Laippatie, Finland Purpose: Ore workers are conventionally monitored for exposure by measuring the uranium in their urine, but specific biomarkers of kidney damage still remain to be discovered. A recent toxicogenomics study allowed us to focus on osteopontin (OSTP) normally excreted in human urine and linked to mineral metabolism. We examined the association between osteopontin and uranium exposure both in vitro, in a human kidney cell model, and in the urine of exposed individuals. Methods: OSTP was measured in supernatants of uraniumexposed HK2 cells to establish a dose–response curve and a time course experiment. Its role was studied through a gene extinction experiment. Uranium and OSTP were then monitored in the urine of exposed nuclear fuel industry workers and a chronically exposed population. These levels were compared with those found in a non-exposed population. Results: The study of HK2 cells indicated that OSTP secretion decreased after uranium exposure in a concentration and time dependent manner, but its suppression does not affect cell sensitivity to uranium. In spite of wide inter-individual variability, this parameter decreases also in human urine when urinary uranium exceeds 30 g/L after an acute exposure, a value considered to be critical for kidney damage. This study reports how toxicogenomics can highlight putative toxicity biomarkers in an easy to access biological fluid. The decrease of urinary osteopontin in response to uranium exposure suggests kidney damage and would thus be complementary to current markers. doi:10.1016/j.toxlet.2011.05.1042
OS9-5 Protocol sC-II of subClinical investigations for the presence of occupational environmental toxins, engineered nanoparticles, irritants and allergens as triggers and causative agents of toxic, allergic and immune responses in individuals within human habitations J. Dumanov Dir. Clinical Environmental Toxicology, subClinical Research Group US EU, Sparta, USA Purpose: subClinical protocol sC II (NEURO-TOXO) is a comprehensive differential diagnostic system of the indoor environment that was designed and aims to investigate the presence and quantity of toxins, allergens and inhabitant exposure to potentially dangerous agents and carcinogens. Methods: The (sC-2) protocol was tested 42 human environments including 26 households, 8 medical offices and 8 administrative offices (government and non-manufacturing/production business) of those patients clinically diagnosed as having possible toxic exposure, fatigue syndrome or neurosis. This protocol used air pump sampling, TO-15 summa type canisters with Gas Chromatography/Mass Spectroscopy (GC/MS) and selective ion monitoring (SIM) to collect ambient samples at the sampling sites where were detected significant amount of CO2 , CO, polycyclic hydrocarbons