Abstract
Abstract Epidemiological studies conducted first in the USA and later in the UK, suggest that a relationship exists between increased cardio-respiratory hospital admissions, morbidity and mortality rates and increases in PM10 concentrations. In urban environments, ultrafine diesel exhaust particles (DEP), accounts for 20-80 % by mass of the airborne PM10 arising from vehicular activities. In previous work, we used well characterised DEP as a surrogate for PM10 and examined its bioreactivity in vivo by assessing lung permeability, inflammation and epithelial cell markers in lavage fluid. Delivery of a single instillate of l mg DEP into the rat lung was not found to cause progressive damage but did produce a transient change in lung permeability. In the experiment described here, we instilled two different doses (control [NaCl], 0.25 and 1.25 mg) of DEP into the rat lung and assessed the responses using the methods described above with the addition of a new technique known as gene expression profiling.
Published Version
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