Diesel exhaust particles in blood trigger systemic and pulmonary morphological alterations

Short-term exposure to elevated levels of particulate matter is associated with increased respiratory and cardiovascular mortality and morbidity. However, the mechanisms underlying these effects are still unclear. Recent studies have suggested that inhaled ultrafine particles are able to translocate into the bloodstream. To gain more insight into this potential mechanism, we studied the effect of diesel exhaust particles (DEP, 0.02 and 0.1 mg/kg), 48 h following their intravenous administration, on systemic inflammation and both pulmonary and cardiac morphological alterations in rats. The intravenous administration of DEP (0.1 mg/kg) triggered systemic inflammation characterized by an increase of monocyte and granulocyte numbers. Both doses of DEP caused a reduction of the number of red blood cells (RBC) and haemoglobin concentration. Transmission electron microscopy analysis of RBC after in vitro incubation (5 μg/ml) or in vivo administration of DEP, revealed the presence of ultrafine-sized aggregates of DEP within the RBC. Larger aggregates were also taken up by the RBC. Moreover, while the myocardial morphology and capillary bed were not affected by DEP exposure, the lungs of rats exposed to DEP (0.02 and 0.1 mg/kg) showed clear evidence of inflammation, characterized by neutrophils infiltration. Stereological analysis revealed an increase in interalveolar wall thickness and a decrease in numbers of alveolar sacs per unit area of lung parenchyma of rat exposed to DEP. We conclude that 48 h after their systemic administration, DEP cause systemic and pulmonary morphological alterations.