Labile Iron Concentrations in Ambient Ultrafine Particles May Affect Mitochondrial Toxicity

ANNE M. JOHANSEN (1), Celia L. Faiola (2), Sara Rybka (1), Carin Thomas (1), Justin Johnston (1), Stephanie Bryner (1)

(1) Central Washington University, Ellensburg, WA, (1) Washington State University, Pullman, WA

     Abstract Number: 331
     Last modified: November 9, 2009

Abstract
The ultrafine size fraction of ambient particles (ultrafine particles, UFP, diameter < 100 nm) has been identified as being far more potent in their adverse health effects than their larger counterparts. Despite a spur of diverse studies on this topic, the detailed mechanisms for why UFP display such distinctive toxicity are not well understood. In the present study, ambient UFP were exposed to mitochondria, while monitoring electron transport chain (ETC) activity. UFP samples were collected in rural (Ellensburg) and urban (Seattle) Washington State. UFP chemical characterization and quantification for comparison with the biochemical toxic effects included trace metals with strong-acid digestion, ferrous iron (Fe(II)) with long pathlength spectroscopy, polycyclic aromatic hydrocarbons with GC-MS, and surface analyses of carbon functional groups with XPS. Low doses of UFP (8 micro-gram/mL) caused a decrease in mitochondrial ETC function compared to controls, and generally, inhibition of electron transport peaked after 20 min of exposure. A weak correlation (R2=0.23, P=0.09, N=14) is observed between UFP Fe(II) content and ETC activity during the initial 0-10 min exposure of mitochondria to UFPs. No such correlation exists with total Fe or other trace metals. Results from this study indicate that the redox active fraction of Fe and not the total Fe concentration contributes to the potential detrimental behavior of UFP, and while Fe in combustion derived UFP is known to stem from engine wear, lube oil and/or fuel additives, the processes that determine iron speciation, and thus, in part, UFP biochemical reactivity, remain elusive.