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Compelling evidence indicates that exposure to air pollutionparticulate matter (PM) affects human health. However, how PM compositioninteracts with PM-size to cause adverse health effects needs elucidation.In this study, we were also interested in the physicochemical characteristicsand toxicological end points of PM2.5–0.3samplesproduced in rural, urban, or industrial surroundings, thereby expectingto differentiate their respective in vitroadversehealth effects in human bronchial epithelial cells (BEAS-2B). Physicochemicalcharacteristics of the three PM2.5–0.3samples,notably their inorganic and organic components, were closely relatedto their respective emission sources. Referring also to the dose/responserelationships of the three PM2.5–0.3samples, themost toxicologically relevant exposure times (i.e., 24, 48, and 72h) and doses (i.e., 3.75 μg PM/cm2and 15 μgPM/cm2) to use to study the underlying mechanisms of actioninvolved in PM-induced lung toxicity were chosen. Organic chemicalsadsorbed on the three PM2.5–0.3samples (i.e., polycyclicaromatic hydrocarbons) were able to induce the gene expression ofxenobiotic-metabolizing enzymes (i.e., Cytochrome P4501A1 and 1B1,and, to a lesser extent, NADPH-quinone oxidoreductase-1). Moreover,intracellular reactive oxygen species within BEAS-2B cells exposedto the three PM2.5–0.3samples induced oxidativedamage (i.e., 8-hydroxy-2′-deoxyguanosine formation, malondialdehydeproduction and/or glutathione status alteration). There were alsostatistically significant increases of the gene expression and/orprotein secretion of inflammatory mediators (i.e., notably IL-6 andIL-8) in BEAS-2B cells after their exposure to the three PM2.5–0.3samples. Taken together, the present findings indicated that oxidativedamage and inflammatory response preceeded cytotoxicity in air pollutionPM2.5–0.3-exposed BEAS-2B cells and supported theidea that PM-size, composition, and origin could interact in a complexmanner to determine the in vitroresponsiveness toPM. [ABSTRACT FROM AUTHOR]

Background Classified as carcinogenic to humans by the IARC in 2013, fine air particulate matter (PM 2.5 ) can be inhaled and retained into the lung or reach the systemic circulation. This can cause or exacerbate numerous pathologies to which the elderly are often more sensitive. Methods In order to estimate the influence of age on the development of early cellular epigenetic alterations involved in carcinogenesis, peripheral blood mononuclear cells sampled from 90 patients from three age classes (25–30, 50–55 and 75–80 years old) were ex vivo exposed to urban PM 2.5 . Results Particles exposure led to variations in telomerase activity and telomeres length in all age groups without any influence of age. Conversely, P16 INK4A gene expression increased significantly with age after exposure to PM 2.5 . Age could enhance MGMT gene expression after exposure to particles, by decreasing the level of promoter methylation in the oldest people. Conclusion Hence, our results demonstrated several tendencies in cells modification depending on age, even if all epigenetic assays were carried out after a limited exposure time allowing only one or two cell cycles. Since lung cancer symptoms appear only at an advanced stage, our results underline the needs for further investigation on the studied biomarkers for early diagnosis of carcinogenesis to improve survival. [ABSTRACT FROM AUTHOR]