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Project ID: 14-1-04-16

Year: 2014

Date Started: 09/01/2014

Ending Date:  01/30/2018

Title: The role of composition and particle size on the toxicity of wildfire emissions

Project Proposal Abstract: Short-term exposures to ambient particulate matter (PM) are associated with increased morbidity and mortality in the exposed population, and these same patterns have been noted during wildland fire episodes. Since the scale and frequency of wildfires are expected to increase because of climate change, hospital admissions for respiratory infections, asthma, and cardiovascular disease will rise in urban areas impacted by such events. It is also possible that cancer rates may increase. Despite the public health threat from exposure to wildland fire emissions, little is known about the relative toxicity of these aerosols from different combustion conditions and fuels, or if there are common bioactive components that are, on a mass basis, more or less harmful than constituents from regional and point source pollutants. We recently demonstrated that coarse particles obtained during the 2008 Pocosin Lakes National Wildlife Refuge peat fire in Eastern North Carolina were more toxic than PM samples collected after the fire was controlled, and this effect was associated with a 70% increase in lipopolysaccharide (LPS, endotoxin) levels. Furthermore, we have reported that coarse particles from a near road environment invoke strong pulmonary responses in mice, while ultrafine particles affected the heart. Based on these findings we hypothesize that the toxicity of smoke emissions from wildfires varies, depending on the type of fuel, combustion conditions, and resultant particle size and chemistry. We will test this hypothesis with the following objectives: a) Compare the relative cardiopulmonary toxicity and mutagenicity of coarse and fine emissions from four distinct fuel types (oak, pine, peat and mixed biomass) obtained from both smoldering and active flame phases, b) Provide a ranking of effects in the pulmonary, cardiac and mutagenic assessments and compare responses to size-fractionated ambient PM samples collected from urban and rural sites. c) Determine the role of lipopolysaccharide (LPS) and organic components on the relative potency of each sample. To achieve these objectives, we will use a multi-stage cryotrap system designed to collect large amounts of size-fractionated smoke particles and condensates from flaming and smoldering stages of controlled burns. Samples will be extensively analyzed to provide a comprehensive mass balance of elemental, organic and ionic species. The cardiopulmonary toxicity of the samples will then be assessed in mice, and mutagenic profiles will be ranked in various strains of Salmonella Spp. We will also utilize mouse lung tissue slices from LPS resistant and susceptible mice to further investigate the role of endotoxin in the pulmonary responses. Results from this proposal will address the first three questions in task statement 4 in the following ways: 1) The data generated will greatly expand the knowledge of the relative toxicity of different smoke emissions and provide a systematic comparison to ambient PM samples. 2) Information on the relative toxicity of the different size fractions of the smoke could influence understanding of the hazards attributed to coarse versus fine particles, which do not necessarily track together and are regulated separately. 3) Potency values will be created to help regulators decide whether to adhere to the NAAQS standards already in place, or possibly tighten or relax these values depending on the obtained data. This could be of particular value if we observe dramatic differences in toxicity between different fuel types or combustion conditions. Taken together, this research will provide new insight into health impacts of wildfire smoke from different fuel types and combustion conditions. Knowledge of the causal components of the smoke and the mechanisms of effect will aid in the specificity of regional public health alerts, and may also provide strategies for chemo-prevention in first responders and the population at risk.

Principal Investigator: Ian M. Gilmour

Agency/Organization: EPA-Environmental Protection Agency

Branch or Dept: Environmental Public Health Division

Other Project Collaborators




Branch or Dept

Agreements Contact

Larry L. Hodgson

EPA-Environmental Protection Agency

Office of Research and Development

Budget Contact

Amy O. Driggers

EPA-Environmental Protection Agency

Office of Research and Development

Co-Principal Investigator

Janice A. Dye PhD

EPA-Environmental Protection Agency

Office of Research and Development

Co-Principal Investigator

Michael D. Hays

EPA-Environmental Protection Agency

National Risk Management Research Laboratory

Co-Principal Investigator

Mehdi S. Hazari

EPA-Environmental Protection Agency

Office of Research and Development

Co-Principal Investigator

Mark A. Higuchi

EPA-Environmental Protection Agency

Environmental Public Health Division

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