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Ambient Particulate Matter (PM) has been shown to be associated with cardiopulmonary diseases and lung cancer. Several groups of investigators have shown that the size of the airborne particles and their surface area determine the potential to elicit inflammatory injury and other mechanisms of adverse cellular effects. Because traffic is an important source of PM, it seems obvious that physicochemical characterization of vehicles exhaust emission has an important impact on both quantitative and qualitative aspects of ambient PM. In the present study the exhaust emissions of 8 vehicles of different categories were analyzed to attempt to differentiate them. For such purpose the particulate was collected on SPME fibers exposed to the exhaust emission for 150 s. The particulate was first characterized by micro-Raman spectroscopy and then subjected to Fast Gas Chromatography-Mass Spectrometry analyses for the chemical identification of the Polycyclic Aromatic Hydrocarbons (PAHs) compounds, the organic fraction of particulate matter in air pollution with a major role in the toxicity, notably via its effects on inflammation. Both the particle count and the PAHs compositional data were assembled to be interpreted by Principal Components Analysis. This multivariate analysis grouped the data according mainly to the naphthalene amount, as well as the volume concentration of the particles smaller than 0.5 μm, suggesting that the different exhaust emissions could be easily differentiated. With this new methodology, future research should aim at establishing a mechanism of formation during internal engine combustion processes in order to obtain a clearer picture of the inflammatory and carcinogenic mechanisms of PM in the lungs.

The tumour growth paradox refers to the observation that incomplete treatment of cancers can enhance their growth. As shown here and elsewhere, the existence of cancer stem cells (CSCs) can explain this effect. CSC are less sensitive to treatments, hence any stress applied to the tumour selects for CSC, thereby increasing the fitness of the tumour. In this paper, we use a mathematical model to understand the role of CSC in the progression of cancer. Our model is a rather general system of integro-differential equations for tumour growth and tumour spread. Such a model has never been analysed, and we prove results on local and global existence of solutions, their uniqueness and their boundedness. We show numerically that this model exhibits the tumour growth paradox for all parameters tested. This effect becomes more relevant for small renewal rate of the CSC., (© The authors 2015. Published by Oxford University Press on behalf of the Institute of Mathematics and its Applications. All rights reserved.)