M. Alaghmand

Airborne particulate matter, hydroxyl radical production and cellular toxicity

Studies suggest that oxidative stress is a cause for the observed pathology in lung after exposures to air pollution. The aim of this study was to examine the effects of different airborne particulate matter (PM) on the survival of human bronchial epithelial cells immortalized with adenovirus-12 SV40 hybrid virus clone 2b (BEAS-2B cells, S6 subclone; BEAS). This was achieved by correlating cell survival directly with the flux of hydroxyl radicals (•OH) generated in a mixture of cells and particulates. A relatively new and highly sensitive fluorescence-based method was used to detect and quantify •OH. Two different toxicological methods were employed to test BEAS-2B cell survival in the presence of various types of airborne PM. Low •OH production was observed when this cell line was exposed to diesel particulate matter resulting in moderate toxicity. Urban dust (UD) which produced similar •OH flux in the presence of cells, resulted in protection from phosphate buffer saline toxicity, a required control. Amorphous silica which did not generate •OH radicals was the most toxic of all the particles tested. On the other hand, both cell death and hydroxyl radical formation were substantially enhanced when an external biological reductant, β-nicotinamide adenine dinucleotide phosphate, was added to a suspension of cells and UD. These results suggest that oxidants are crucial in generating high concentration of •OH and consequently cell death.