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The impacts of wildfires along the wildland urban interface (WUI) on atmospheric particulate concentrations and composition are an understudied source of air pollution exposure. To assess the residual impacts of the 2021 Marshall Fire (Colorado), a wildfire that predominantly burned homes and other human-made materials, on homes within the fire perimeter that escaped the fire, we performed a combination of fine particulate matter (PM2.5) filter sampling and chemical analysis, indoor dust collection and chemical analysis, community scale PurpleAir PM2.5 analysis, and indoor particle number concentration measurements. Following the fire, the chemical speciation of dust collected in smoke-affected homes in the burned zone showed elevated concentrations of the biomass burning marker levoglucosan (medianlevo = 4147 ng g−1), EPA priority toxic polycyclic aromatic hydrocarbons (median Σ16PAH = 1859.3 ng g−1), and metals (median Σ20Metals = 34.6 mg g−1) when compared to samples collected in homes outside of the burn zone 6 months after the fire. As indoor dust particles are often resuspended and can become airborne, the enhanced concentration of hazardous metals and organics within dust samples may pose a threat to human health. Indoor airborne particulate organic carbon (median = 1.91 μg m−3), particulate elemental carbon (median = .02 μg m−3), and quantified semi-volatile organic species in PM2.5 were found in concentrations comparable to ambient air in urban areas across the USA. Particle number and size distribution analysis at a heavily instrumented supersite home located immediately next to the burned area showed indoor particulates in low concentrations (below 10 μg m−3) across various sizes of PM (12 nm–20 μm), but were elevated by resuspension from human activity, including cleaning. 

Abstract. Anthropogenic secondary organic aerosol (ASOA), formed from anthropogenicemissions of organic compounds, constitutes a substantial fraction of themass of submicron aerosol in populated areas around the world andcontributes to poor air quality and premature mortality. However, theprecursor sources of ASOA are poorly understood, and there are largeuncertainties in the health benefits that might accrue from reducinganthropogenic organic emissions. We show that the production of ASOA in 11urban areas on three continents is strongly correlated with the reactivityof specific anthropogenic volatile organic compounds. The differences inASOA production across different cities can be explained by differences inthe emissions of aromatics and intermediate- and semi-volatile organiccompounds, indicating the importance of controlling these ASOA precursors.With an improved model representation of ASOA driven by the observations,we attribute 340 000 PM2.5-related premature deaths per year to ASOA, which isover an order of magnitude higher than prior studies. A sensitivity casewith a more recently proposed model for attributing mortality to PM2.5(the Global Exposure Mortality Model) results in up to 900 000 deaths. Alimitation of this study is the extrapolation from cities with detailedstudies and regions where detailed emission inventories are available toother regions where uncertainties in emissions are larger. In addition tofurther development of institutional air quality management infrastructure,comprehensive air quality campaigns in the countries in South and CentralAmerica, Africa, South Asia, and the Middle East are needed for furtherprogress in this area. 

We use a 0-D photochemical box model and a 3-D global chemistry-climate model, combined with observations from the NOAA Southeast Nexus (SENEX) aircraft campaign, to understand the sources and sinks of glyoxal over the Southeast United States. Box model simulations suggest a large difference in glyoxal production among three isoprene oxidation mechanisms (AM3ST, AM3B, and MCM v3.3.1). These mechanisms are then implemented into a 3-D global chemistry-climate model. Comparison with field observations shows that the average vertical profile of glyoxal is best reproduced by AM3ST with an effective reactive uptake coefficient γglyx of 2 × 10-3, and AM3B without heterogeneous loss of glyoxal. The two mechanisms lead to 0-0.8 µg m-3 secondary organic aerosol (SOA) from glyoxal in the boundary layer of the Southeast U.S. in summer. We consider this to be the lower limit for the contribution of glyoxal to SOA, as other sources of glyoxal other than isoprene are not included in our model. In addition, we find that AM3B shows better agreement on both formaldehyde and the correlation between glyoxal and formaldehyde (RGF = [GLYX]/[HCHO]), resulting from the suppression of δ-isoprene peroxy radicals (δ-ISOPO2). We also find that MCM v3.3.1 may underestimate glyoxal production from isoprene oxidation, in part due to an underestimated yield from the reaction of IEPOX peroxy radicals (IEPOXOO) with HO2. Our work highlights that the gas-phase production of glyoxal represents a large uncertainty in quantifying its contribution to SOA.