Abstract
Background: Exposure to airborne particulate matter (PM) has long been associated with adverse health problems. These fine PM particles can penetrate the distal regions of the lung causing severe respiratory problems.
Objectives: As relatively little information of indoor fine PM is available to evaluate the actual risks, we will focus our examination on lung injuries caused by fine indoor PM, by investigating the mechanism of the cell injury using primary culture of alveolar type II cells.
Method: Indoor PM was collected in Nara prefecture, Japan using an Andersen sampler by the impact cascade method. Particle samples of PM were collected on five Teflon filters in accordance with the diameter of particles (diameter: >11μm, 2.1-11 μm, 1.1-2.1 μm, 0.4-1.1 μm, <0.4 μm). Alveolar type II cells from rats were exposed to PM at the concentration of 500 μg/ml for 24 hrs respectively. At the end of the experiment, lactate dehydrogenase (LDH) activity released into the culture medium was determined and the percentage of LDH leakage was then calculated to reflect the cytotoxicity of PM.
Results: In relation to the control cells, the PM-induced LDH leakage was more significant among the smaller fine particles of indoor PM than the larger ones. However this did not occur with the above mentioned 1.1 μm diameter size of PM. Superoxide dismutase (SOD) significantly reduced LDH leakage-induced indoor PM. In the analysis of the elements in indoor PM, the most abundant element was iron (Fe).
Conclusions: Indoor PM causes oxidative cellular damage, which may be closely associated with a transition metal, Fe in rat alveolar epithelial cells.
- © 2011 ERS