Stephen P. Faux

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Parental smoking data have been reabstracted from the interview records of the Oxford Survey of Childhood Cancers (deaths from 1971 to 1976). Reported smoking habits for the parents of 2587 children who died with cancer were compared with similar information for the parents of 2587 healthy controls (matched pairs analysis). Maternal daily consumption of(More)
This review focuses on the potential role that oxidative stress plays in the adverse effects of PM(10). The central hypothesis is that the ability of PM(10) to cause oxidative stress underlies the association between increased exposure to PM(10) and both exacerbations of lung disease and lung cancer. Pulmonary inflammation may also underlie the(More)
Ultrafine particles have been shown to induce pro-inflammatory effects both in vivo and in vitro. Increased expression of pro-inflammatory genes probably requires the activation of specific transcription factors such as nuclear factor kappa B (NF-kappaB) via a number of possible pathways including Ca2+ and reactive oxygen species. The fluorescent dye fura(More)
Respired ultrafine particles induce a greater inflammation in rat lungs than fine particles; we have hypothesized that this is due to their comparatively huge number and surface area for the production of free radicals. We tested this hypothesis by studying the effects of fine and ultrafine (uf) carbon black (CB) particles in comparison with quartz on A549(More)
Cardiovascular disease is the most common cause of mortality in the Western world and accounts for up to a third of all deaths worldwide. Cardiovascular disease is multifactorial and involves complex interplay between lifestyle (diet, smoking, exercise, ethanol consumption) and fixed (genotype, age, menopausal status, gender) causative factors. The(More)
Asbestos fibers cause persistent induction of the oxidative stress sensitive transcription factors nuclear factor kappa-B (NF-kappa B) and activator protein-1 (AP-1) in mammalian cells. These transcription factors play an important role in the regulation of cellular activity. Lipid peroxidation, mediated by reactive oxygen species, is thought to be a(More)
The mechanism(s) by which cigarette smoke contributes to lung diseases, such as cancer, remains unclear. Recent developments in our knowledge of cell signalling events suggest that cigarette smoke causes oxidative stress and proinflammatory responses in cells of the lung. Cigarette smoke is a complex mixture of over 4000 compounds and high levels of(More)
Emphysema is characterized by enlargement of the distal airspaces in the lungs due to destruction of alveolar walls. Alveolar endothelial and epithelial cell apoptosis induced by cigarette smoke is thought to be a possible mechanism for this cell loss. In contrast, our studies show that cigarette smoke condensate (CSC) induces necrosis in alveolar(More)
In recent years, it has become apparent that minerals can trigger alterations in gene expression by initiating signaling events upstream of gene transactivation. These cascades may be initiated at the cell surface after interaction of minerals with the plasma membrane either through receptorlike mechanisms or integrins. Alternatively, signaling pathways may(More)
Chemical carcinogens are generally classified as genotoxic or non-genotoxic. However, weak genotoxicity at high concentrations is sometimes observed and interpretation is often problematic. In addition, certain rodent carcinogens exert their effects at doses associated with cytotoxicity and compensatory hyperplasia may be a contributing factor to(More)