Cytotoxic responses and potential respiratory health effects of carbon and carbonaceous nanoparticulates in the Paso del Norte airshed environment.

We have utilized a range of manufactured or commercial nanoparticulate materials, including surrogate carbon nano-PM along with combustion-generated carbonaceous (soot) nano-PM characteristic of environmental nano- PM (both indoor and outdoor) to investigate and compare their cytotoxic response in vitro with an immortalized human epithelial (lung model) cell line (A549). These have included nano-Ag, Al2O3, TiO2, Fe2O3, ZrO2, Si3N4, chrysotile asbestos, BC, 2 types of MWCNT-aggregate PM (MWCNT-R and MWCNT-N), and high-volume glass fiber collected soots: candle, wood, diesel (truck), tire, and 3-types of natural gas kitchen burner-generated soots: yellow (fuel-rich) flame, low-flow blue flame, and normal flow blue flame soot PM. These carbonaceous nano-PM species can be found in either the indoor and outdoor environments or microenvironments. Two-day and two-week in-vitro cultures of A549 showed cell death (or decreased cell viability) for all nanoparticulate materials, but especially significant for all but the TiO2 and candle, wood, and diesel PM. The natural gas kitchen burner combustion PM cell death response was characteristic of BC and MWCNT PM. There was no correlation with total PAH content of the soot PM. Cytokine release (IL-6, IL-8) was detected for the Ag, Fe2 O3, asbestos, BC and the MWCNT PM. Reactive oxygen species (ROS) production was also detected for Ag, Fe2 O3, ZrO2, asbestos, BC, and the MWCNT aggregate PM, as well as the natural gas kitchen burner combustion PM. TEM, FESEM, and optical microscopy examination of these nanomaterials illustrate the wide range in PM morphologies and crystallinities as well as cell morphologies. Taken together, these results illustrate proinflammatory and related respiratory health issues in relation to environmental nanoparticulates.