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To improve the knowledge of the underlying mechanisms of action involved in air pollution Particulate Matter (PM)-induced toxicity in human lungs, with a particular interest of the crucial role played by coated-organic chemicals, we were interested in the metabolic activation of Polycyclic Aromatic Hydrocarbons (PAH)-coated onto air pollution PM, and, thereafter, the formation of PAH-DNA adducts in a human lung epithelial cell model (A549 cell line). Cells were exposed to Dunkerque city's PM(2.5) at its Lethal Concentrations at 10% and 50% (i.e. LC(10)=23.72 microg/mL or 6.33 microg/cm2, and LC(50)=118.60 microg/mL or 31.63 microg/cm2), and the study of Cytochrome P450 (CYP) 1A1 gene expression (i.e. RT-PCR) and protein activity (i.e. EROD activity), and the formation of PAH-DNA adducts (i.e. 32P-postlabeling), were investigated after 24, 48, and/or 72 h. PAH, PolyChlorinated Dibenzo-p-Dioxins and -Furans (PCDD/F), Dioxin-Like PolyChlorinated Biphenyls (DLPCB), and PolyChlorinated Biphenyls (PCB)-coated onto collected PM were determined (i.e. GC/MS and HRGC/HRMS, respectively), Negative (i.e. TiO2 or desorbed PM, dPM; EqLC10=19.42 microg/mL or 5.18 microg/cm2, and EqLC50=97.13 microg/mL or 25.90 microg/cm2), and positive (i.e. benzo(a)pyrene; 1 microM) controls were included in the experimental design. Statistically significant increases of CYP1A1 gene expression and protein activity were observed in A549 cells, 24, 48 and 72 h after their exposure to dPM, suggesting thereby that the employed outgassing method was not efficient enough to remove total PAH. Both the CYP1A1 gene expression and EROD activity were highly induced 24, 48 and 72 h after cell exposure to PM. However, only very low levels of PAH-DNA adducts, also not reliably quantifiable, were reported 72 h after cell exposure to dPM, and, particularly, PM. The relatively low levels of PAH together with the presence of PCDD/F, DLPCB, and PCB-coated onto Dunkerque City's PM 2.5 could notably contribute to explain the borderline detection of PAH-DNA adducts in dPM and/or PM-exposed A549 cells. Hence, remaining very low doses of PAH in dPM or relatively low doses of PAH-coated onto PM were involved in enzymatic induction, a key feature in PAH-toxicity, but failed to show a clear genotoxicity in this in vitro study. We also concluded that, in the human lung epithelial cell model we used, and in the experimental conditions we chose, bulky-DNA adduct formation was apparently not a major factor involved in the Dunkerque City's PM 2.5-induced toxicity.

Polycyclic aromatic hydrocarbons (PAHs), mainly formed by incomplete anthropogenic organic matter combustion, are ubiquitous in the environment. To assess milk PAH contamination sources, milk samples were collected from the tank milk at farms located near potential contaminating emission sources such as cementworks, steelworks, and motorways. PAH analyses were carried out by gas chromatography coupled to mass spectrometry. Eight PAHs were identified in milk: naphthalene, acenaphthylene, acenaphthene, fluorene, anthracene, fluoranthene, pyrene, and benzo[a]anthracene. For all potential contaminating sources, these eight PAHs were detected with similar profiles and at low concentrations except for fluorene and naphthalene, for which source-molecule interaction is pointed out.

Polychlorodibenzo-para-dioxins (PCDDs) and Polychlorodibenzofurans (PCDFs) are ubiquitous in the environment. They are mainly formed as unwanted byproducts during various chemical, industrial, and combustion processes. Thus, these pollutants can be found in the food chain. The aim of this experiment was to study the transfer of PCDD/Fs from spiked milk to arterial blood in pigs, which are considered as valid models for humans. Pigs were fed with 900 mL of milk spiked with a mixture of 17 dioxins. The levels of PCDD/Fs in the serum extracts were determined using HRGC/HRMS prior to consumption of the milk, and at 3, 5, and 7 h after milk ingestion. Concentrations of PCDD/Fs in arterial plasma increased from 3 h to 5 h and decreased at 7 h. At time point 5 h, concentrations were found between 500 and 10000 pg x g(-1) fat. The transfer ratio <> was usually found between 0.7 and 3%. Related to the different milk concentrations, results of this study indicate a similar behavior of the studied molecules.