Lung antioxidant and cytokine responses to coarse and fine particulate matter from the great California wildfires of 2008

Abstract

The authors have previously demonstrated that wildfire-derived coarse or fine particulate matter (PM) intratracheally instilled into lungs of mice induce a strong inflammatory response. In the current study, the authors demonstrate that wildfire PM simultaneously cause major increases in oxidative stress in the mouse lungs as measured by decreased antioxidant content of the lung lavage supernatant fluid 6 and 24 h after PM administration. Concentrations of neutrophil chemokines/cytokines and of tumor necrosis factor (TNF)-α were elevated in the lung lavage fluid obtained 6 and 24 h after PM instillation, consistent with the strong neutrophilic inflammatory response observed in the lungs 24 h after PM administration, suggesting a relationship between the proinflammatory activity of the PM and the measured level of antioxidant capacity in the lung lavage fluid. Chemical analysis shows relatively low levels of polycyclic aromatic hydrocarbons compared to published results from typical urban PM. Coarse PM fraction is more active (proinflammatory activity and oxidative stress) on an equal-dose basis than the fine PM despite its lower content of polycyclic aromatic hydrocarbons. There does not seem to be any correlation between the content of any specific polycyclic aromatic hydrocarbon (or of total polycyclic aromatic hydrocarbon content) in the PM fraction and its toxicity. However, the concentrations of the oxidation products of phenanthrene and anthracene, phenanthraquinone and anthraquinone, were several-fold higher in the coarse PM than the fine fraction, suggesting a significant role for atmospheric photochemistry in the formation of secondary pollutants in the wildfire PM and the possibility that such secondary pollutants could be significant sources of toxicity in the wildfire PM.

Keywords::

• Air pollution
• antioxidant
• coarse PM
• fine PM
• lung inflammation
• mouse
• oxidative stress
• polycyclic aromatic hydrocarbon (PAH)
• source-specific particulate matter
• wildfire

Acknowledgments

We thank Dr. Steven Cliff for providing the high-volume PM sampler and cascade impactor used in these experiments, and Dr. Kent Pinkerton and Jennifer Bratt for many helpful discussions and suggestions.

Declaration of interest

This study was funded in part by a training grant, ES-07059, from the National Institute of Environmental Health Sciences, and by research grants U07/CCU906162 from the National Institute for Occupational Safety and Health, and RD-83241401 and RD-8324301 from the US Environmental Protection Agency. The authors have no conflicts of interest to declare related to this work.