California Wildfires of 2008: Coarse and Fine Particulate Matter Toxicity

Background During the last week of June 2008, central and northern California experienced thousands of forest and brush fires, giving rise to a week of severe fire-related particulate air pollution throughout the region. California experienced PM10–2.5 (particulate matter with mass median aerodynamic diameter > 2.5 μm to < 10 μm; coarse ) and PM2.5 (particulate matter with mass median aerodynamic diameter < 2.5 μm; fine) concentrations greatly in excess of the air quality standards and among the highest values reported at these stations since data have been collected. Objectives These observations prompt a number of questions about the health impact of exposure to elevated levels of PM10–2.5 and PM2.5 and about the specific toxicity of PM arising from wildfires in this region. Methods Toxicity of PM10–2.5 and PM2.5 obtained during the time of peak concentrations of smoke in the air was determined with a mouse bioassay and compared with PM samples collected under normal conditions from the region during the month of June 2007. Results Concentrations of PM were not only higher during the wildfire episodes, but the PM was much more toxic to the lung on an equal weight basis than was PM collected from normal ambient air in the region. Toxicity was manifested as increased neutrophils and protein in lung lavage and by histologic indicators of increased cell influx and edema in the lung. Conclusions We conclude that the wildfire PM contains chemical components toxic to the lung, especially to alveolar macrophages, and they are more toxic to the lung than equal doses of PM collected from ambient air from the same region during a comparable season.

[1]  K. Akakura [Inflammatory cytokines]. , 2011, Nihon rinsho. Japanese journal of clinical medicine.

[2]  Lars Barregard,et al.  Population exposure to fine particles and estimated excess mortality in Finland from an East European wildfire episode , 2009, Journal of Exposure Science and Environmental Epidemiology.

[3]  J. Last,et al.  Lung response to coarse PM: bioassay in mice. , 2008, Toxicology and applied pharmacology.

[4]  W. Zin,et al.  Composition of Diesel Particles Influences Acute Pulmonary Toxicity: An Experimental Study in MICE , 2008, Inhalation toxicology.

[5]  W. Zin,et al.  Composition of diesel particles influences acute pulmonary toxicity: an experimental study in mice. , 2008, Inhalation toxicology.

[6]  Chris Piacitelli,et al.  Particle size-dependent radical generation from wildland fire smoke. , 2007, Toxicology.

[7]  M. Brauer,et al.  Woodsmoke Health Effects: A Review , 2007, Inhalation toxicology.

[8]  R. Hillamo,et al.  In vitro inflammatory and cytotoxic effects of size-segregated particulate samples collected during long-range transport of wildfire smoke to Helsinki. , 2006, Toxicology and applied pharmacology.

[9]  A. Ledbetter,et al.  Comparative pulmonary toxicological assessment of oil combustion particles following inhalation or instillation exposure. , 2006, Toxicological sciences : an official journal of the Society of Toxicology.

[10]  K. Donaldson,et al.  Explorer In vivo and in vitro proinflammatory effects of particulate air pollution ( PM 10 ) , 2006 .

[11]  David L. Crow San Joaquin Valley Air Pollution Control District Air Pollution Control Officer’s Determination of VOC Emission Factors for Dairies , 2005 .

[12]  J. Veranth,et al.  Inflammatory cytokines and cell death in BEAS-2B lung cells treated with soil dust, lipopolysaccharide, and surface-modified particles. , 2004, Toxicological sciences : an official journal of the Society of Toxicology.

[13]  J. Weiss,et al.  Quinones and Aromatic Chemical Compounds in Particulate Matter Induce Mitochondrial Dysfunction: Implications for Ultrafine Particle Toxicity , 2004, Environmental health perspectives.

[14]  F. Cassee,et al.  Ambient fine and coarse particle suppression of alveolar macrophage functions. , 2003, Toxicology letters.

[15]  J. Antonini,et al.  Residual oil fly ash increases the susceptibility to infection and severely damages the lungs after pulmonary challenge with a bacterial pathogen. , 2002, Toxicological sciences : an official journal of the Society of Toxicology.

[16]  B. Jordan,et al.  Indices of antioxidant status in rats subjected to wood smoke inhalation and/or thermal injury. , 2002, Toxicology.

[17]  J. Zelikoff,et al.  THE TOXICOLOGY OF INHALED WOODSMOKE , 2002, Journal of toxicology and environmental health. Part B, Critical reviews.

[18]  Irfan Rahman,et al.  PM10-exposed macrophages stimulate a proinflammatory response in lung epithelial cells via TNF-α , 2002 .

[19]  W. MacNee,et al.  PM(10)-exposed macrophages stimulate a proinflammatory response in lung epithelial cells via TNF-alpha. , 2002, American journal of physiology. Lung cellular and molecular physiology.

[20]  Jerold A. Last,et al.  TOXIC RESPONSES OF THE RESPIRATORY SYSTEM , 2001 .

[21]  Xianglin Shi,et al.  Wood smoke particles generate free radicals and cause lipid peroxidation, DNA damage, NFκB activation and TNF-α release in macrophages , 2000 .

[22]  A. Imrich,et al.  Insoluble components of concentrated air particles mediate alveolar macrophage responses in vitro. , 2000, Toxicology and applied pharmacology.

[23]  B. Jordan,et al.  Wood smoke particles generate free radicals and cause lipid peroxidation, DNA damage, NFkappaB activation and TNF-alpha release in macrophages. , 2000, Toxicology.

[24]  N. Urosevic,et al.  Variations in LPS responsiveness among different mouse substrains of C3H lineage and their congenic derivative sublines , 1999, Immunogenetics.

[25]  I. Adamson,et al.  Pulmonary toxicity of an atmospheric particulate sample is due to the soluble fraction. , 1999, Toxicology and applied pharmacology.

[26]  C. Monn,et al.  Cytotoxicity and induction of proinflammatory cytokines from human monocytes exposed to fine (PM2.5) and coarse particles (PM10-2.5) in outdoor and indoor air. , 1999, Toxicology and applied pharmacology.

[27]  J. Carter,et al.  Cytokine production by human airway epithelial cells after exposure to an air pollution particle is metal-dependent. , 1997, Toxicology and applied pharmacology.

[28]  W. MacNee,et al.  In vivo and in vitro proinflammatory effects of particulate air pollution (PM10). , 1997, Environmental health perspectives.

[29]  C. Sioutas,et al.  Alveolar macrophage interaction with air pollution particulates. , 1997, Environmental health perspectives.

[30]  J. Timbrell Casarett and Doull's Toxicology: The Basic Science of Poisons , 1981 .