Abstract
The mechanisms by which elevated levels of particulate air pollution increase the risk of cardiovascular (CV)-related deaths remain unclear. A role for plasma fibrinogen has been proposed with the suggestion that particle induced inflammation in the lung may stimulate an hepatic acute phase response and thereby increase plasma fibrinogen concentration, a known risk factor for CV disease. Human alveolar epithelial cells have been reported to synthesize fibrinogen and we therefore investigated the possibility that particle deposition may, through direct and indirect mechanisms, induce local alveolar production of fibrinogen. Here we present data to suggest that PM 10 exposure could stimulate alveolar epithelial cell synthesis of fibrinogen indirectly, through the induction of inflammatory cytokines such as interleukin-6. Locally produced fibrinogen may exacerbate pulmonary inflammation and potentially contribute to systemic levels of plasma fibrinogen, thereby increasing the risk of CV responses in susceptible, PM 10 exposed individuals.
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