Aggregates of ultrafine particles modulate lipid peroxidation and bacterial killing by alveolar macrophages.

We hypothesized that aggregates of ultrafine carbon and washed diesel particles impair the ability of alveolar macrophages (AM) to kill bacteria and enhance the AM lipid peroxidation (LPO) of lung surfactant. Rat AM were exposed, 5h, to particles 20 microg/ml. The AM, containing carbon or washed diesel particles, were incubated 2h, with Streptococcus pneumoniae, an American Type Culture Collection (ATCC) strain or clinical isolates. Surviving bacteria were quantified. Surfactant was incubated, 5h, with carbon or washed diesel loaded AM and LPO was measured. The particle load was approximately 1 microg/10(6) AM, representing accepted exposure to ambient particles in Europe. Metal concentrations were 10 to 100 fold higher in washed diesel--than in carbon particles. There was a dose dependent increase in bacterial survival with carbon-loaded macrophages, but not with washed diesel-loaded AM. Clinical isolates had a higher survival rate with carbon-loaded macrophages than the ATCC strain. Surfactant LPO was increased with washed diesel-loaded macrophages (95%) and with carbon-loaded macrophages (55%) compared to controls. High LPO caused by washed diesel-loaded AM reflects their increased oxidative metabolism, probably caused by particle metals. The additional oxygen metabolites maintained bactericidal activity of AM, while corresponding activity was decreased in carbon-loaded AM. Altered functions of AM may explain health problems related to air pollution.