Characterization and cytotoxicity of PM2.5 collected in Baton Rouge/Port Allen corridor of Louisiana.

摘要

The Environmental Protection Agency (EPA) defines particulate matter (PM) as particles in the air, including dust, soot, smoke and liquid droplets; and regulates PM concentration and exposure limits via the National Ambient Air Quality Standards (NAAQS). Both the chemical composition and size of PM are important characteristics that affect the impact of particles on human health. PM2.5 is transported deep into the lower pulmonary system where it can negatively influence or inhibit air exchange. Slow clearance rate from the pulmonary region means PM2.5 toxic particles are in contact with sensitive lung tissues exerting a more sustained and lethal damage to vital respiratory organs.;The most lethal toxins present in PM2.5 are believed to be the metals, the polycyclic aromatic hydrocarbons (PAHs), and the bacterial endotoxins. The work presents chemical analyses via Inductively Coupled Plasma Emission Spectrometry (ICP), to identify and quantify Fenton reactive metals present in an aqueous PM2.5 leachate, and Gas Chromatography -- Mass Spectrometry (GC-MS), to identify and quantify equally cytotoxic PAH compounds present in an organic (dichloromethane) PM2.5 fraction. The concentrations of cytotoxic endotoxins were quantified via standardized reagent kits.;PM2.5 induces a dose-dependent decrease in viability of A549 cells. PM2.5 at low concentrations induces the formation of reactive oxygen species (ROS). PM2.5 appeared to promote necrosis and apoptosis, with necrosis as a major mechanism in cell death as evidenced by acridine orange/ethidium bromide dual staining. Exposure of A549 cells to PM2.5 resulted in marked increases in Tumor Necrosis Factor-alpha (TNF-alpha), interleukin 8 (IL-8), and interleukin 6 (IL-6). Studies of quantitative gene expression in A549 cells indicated 31 pro-inflammatory genes were found to be differentially regulated out of which 27 were up-regulated and 4 were down-regulated relative to control after exposure to PM2.5 from the Baton Rouge capital site; also 25 pro-inflammatory genes were found to be differentially regulated out of which 22 were up-regulated and 3 were down-regulated relative to control after exposure to PM2.5 from the Port Allen site. Exposure of A549 cells to PM2.5 showed significant differential occurring in proteins involved in apoptosis, cell cycle, cytoskeleton, and signal transduction functional groups.