Why is particulate matter produced by wildfires toxic to lung macrophages?

Lisa M. Franzi, Jennifer M. Bratt, Keisha M. Williams, Jerold A Last

Research output: Contribution to journalArticle

21 Scopus citations

Abstract

The mechanistic basis of the high toxicity to lung macrophages of coarse PM from the California wildfires of 2008 was examined in cell culture experiments with mouse macrophages. Wildfire PM directly killed macrophages very rapidly in cell culture at relatively low doses. The wildfire coarse PM is about four times more toxic to macrophages on an equal weight basis than the same sized PM collected from normal ambient air (no wildfires) from the same region and season. There was a good correlation between the extent of cytotoxicity and the amount of oxidative stress observed at a given dose of wildfire PM in vitro. Our data implicate NF-κB signaling in the response of macrophages to wildfire PM, and suggest that most, if not all, of the cytotoxicity of wildfire PM to lung macrophages is the result of oxidative stress. The relative ratio of toxicity and of expression of biomarkers of oxidant stress between wildfire PM and "normal" PM collected from ambient air is consistent with our previous results in mice in vivo, also suggesting that most, if not all, of the cytotoxicity of wildfire PM to lung macrophages is the result of oxidative stress. Our findings from this and earlier studies suggest that the active components of coarse PM from the wildfire are heat-labile organic compounds. While we cannot rule out a minor role for endotoxin in coarse PM preparations from the collected wildfire PM in our observed results both in vitro and in vivo, based on experiments using the inhibitor Polymyxin B most of the oxidant stress and pro-inflammatory activity observed was not due to endotoxin.

Original languageEnglish (US)
Pages (from-to)182-188
Number of pages7
JournalToxicology and Applied Pharmacology
Volume257
Issue number2
DOIs
StatePublished - Dec 1 2011

Keywords

  • Air pollution
  • Coarse PM
  • Cytotoxicity
  • Oxidative stress

ASJC Scopus subject areas

  • Pharmacology
  • Toxicology

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