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Exposure to urban airborne particulate matter (PM) has been associated with adverse health effects. The majority of research articles published on air pollution PM relate to PM10. However, increasing emphasis and stringent regulations have been placed on PM2.5. The mechanisms for PM-induced adverse health effects are not well understood, but inflammation seems to be of importance. We focused our attention also on the capacity of air pollution PM2.5 to induce cytotoxic and inflammatory responses in human epithelial lung cells (L132) in culture. Particulate matter was collected in Dunkerque, a French seaside city characterized by the proximity of industrial activity and heavy motor vehicle traffic. Size distribution results showed that the cumulative frequency of PM2.5 was 92.15% and their specific surface area was 1 m2 g-1. Inorganic and organic chemicals usually associated with the natural environment but also so-called anthropogenic elements were found in PM, suggesting that much of the PM was derived from wind-borne dust from the industrial complex and the heavy diesel motor vehicle. We observed PM concentration-dependent cytotoxic effects in L132 cells (lc10 = 18.84 g PM ml-1; lc50 = 75.36 g PM ml-1). We showed that exposure to Dunkerque City's PM2.5 induced significant increases (in a concentration- and time-dependent manner) in protein secretion and[sol ]or gene expression of inflammatory cytokines (i.e. TNF-a, IL-1, IL-8, GM-CSF, IL-6, TGF-1). We hypothesized also that the occurrence of the acute inflammatory response might rely on the capacity of such air pollutants to generate oxidative species, which have been implicated in the stringent regulation of the cytokine network. Hence, we suggest that the development of inflammatory effects that worsen over time stems from the cytotoxicity in Dunkerque City's PM2.5-exposed L132 cells in culture. Copyright 2005 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Any influence of iron in polycyclic aromatic hydrocarbon (PAH)/iron oxide mixtures on the capacity of PAHs to induce metabolizing enzymes will be one of the ways that iron oxides can affect PAH carcinogenicity. Because cytochromes P450 (CYPs) are haemoproteins, it will be of interest to investigate the possible involvement of Fe2O3 in benzo[a]pyrene (BaP)/Fe2O3 mixtures on the induction of CYP1A1 enzymes in the lung. Male Sprague‐Dawley rats were instilled intratracheally with haematite (56Fe2O3 or 54Fe2O3, 3 mg), BaP (3 mg) or BaP (3 mg) coated onto haematite (56Fe2O3 or 54Fe2O3) particles (3 mg). Firstly, mRNA expressions of cyp1a1 were studied. Secondly, protein concentrations and catalytic activities (7‐ethoxyresorufin O‐deethylase: EROD) of CYP1A1 were determined. Thirdly, 54Fe from BaP/54Fe2O3 mixtures in microsomal proteins was studied using time‐of‐flight laser microprobe mass spectrometry (ToF‐LMMS). Statistically significant increases in mRNA expressions, protein concentrations and catalytic activities of CYP1A1 were observed in animals exposed to BaP, to BaP coated onto 56Fe2O3 particles or to BaP coated onto 54Fe2O3 particles versus controls. Both of the BaP/Fe2O3 mixtures induced higher CYP1A1 protein levels and EROD activities than BaP alone. Iron oxide particles per se did not affect mRNA levels of cyp1a1 but only enhanced BaP‐mediated increases of CYP1A1 protein levels and activity. The ToF‐LMMS spectrum profiles showed that the 54Fe/56Fe ratio in the microsomes of BaP coated onto 54Fe2O3 particle‐instilled animals was 1.3 instead of the theoretical ratio (i.e. 0.063) observed in BaP coated onto 56Fe2O3 particle‐instilled animals. Taken together, these novel data support the hypothesis that the Fe2O3‐induced increases of the metabolic activation of BaP might rely on the property of Fe2O3 particles to enhance the BaP‐induced translation rate of the cyp1a1 gene into functional haemoproteins. Copyright © 2004 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]