The goal of the Tropospheric Ozone Assessment Report (TOAR) is to provide the research community with an up-to-date scientific assessment of tropospheric ozone, from the surface to the tropopause. While a suite of observations provides significant information on the spatial and temporal distribution of tropospheric ozone, observational gaps make it necessary to use global atmospheric chemistry models to synthesize our understanding of the processes and variables that control tropospheric ozone abundance and its variability. Models facilitate the interpretation of the observations and allow us to make projections of future tropospheric ozone and trace gas distributions for different anthropogenic or natural perturbations. This paper assesses the skill of current-generation global atmospheric chemistry models in simulating the observed present-day tropospheric ozone distribution, variability, and trends. Drawing upon the results of recent international multi-model intercomparisons and using a range of model evaluation techniques, we demonstrate that global chemistry models are broadly skillful in capturing the spatio-temporal variations of tropospheric ozone over the seasonal cycle, for extreme pollution episodes, and changes over interannual to decadal periods. However, models are consistently biased high in the northern hemisphere and biased low in the southern hemisphere, throughout the depth of the troposphere, and are unable to replicate particular metrics that define the longer term trends in tropospheric ozone as derived from some background sites. When the models compare unfavorably against observations, we discuss the potential causes of model biases and propose directions for future developments, including improved evaluations that may be able to better diagnose the root cause of the model-observation disparity. Overall, model results should be approached critically, including determining whether the model performance is acceptable for the problem being addressed, whether biases can be tolerated or corrected, whether the model is appropriately constituted, and whether there is a way to satisfactorily quantify the uncertainty.

The evolution of organic aerosol (OA) and brown carbon (BrC) in wildfire plumes, including the relative contributions of primary versus secondary sources, has been uncertain in part because of limited knowledge of the precursor emissions and the chemical environment of smoke plumes. We made airborne measurements of a suite of reactive trace gases, particle composition, and optical properties in fresh western US wildfire smoke in July through August 2018. We use these observations to quantify primary versus secondary sources of biomass-burning OA (BBPOA versus BBSOA) and BrC in wildfire plumes. When a daytime wildfire plume dilutes by a factor of 5 to 10, we estimate that up to one-third of the primary OA has evaporated and subsequently reacted to form BBSOA with near unit yield. The reactions of measured BBSOA precursors contribute only 13 ± 3% of the total BBSOA source, with evaporated BBPOA comprising the rest. We find that oxidation of phenolic compounds contributes the majority of BBSOA from emitted vapors. The corresponding particulate nitrophenolic compounds are estimated to explain 29 ± 15% of average BrC light absorption at 405 nm (BrC Abs405) measured in the first few hours of plume evolution, despite accounting for just 4 ± 2% of average OA mass. These measurements provide quantitative constraints on the role of dilution-driven evaporation of OA and subsequent radical-driven oxidation on the fate of biomass-burning OA and BrC in daytime wildfire plumes and point to the need to understand how processing of nighttime emissions differs.

Wildfires are an important source of nitrous acid (HONO), a photolabile radical precursor, yet in situ measurements and quantification of primary HONO emissions from open wildfires have been scarce. We present airborne observations of HONO within wildfire plumes sampled during the Western Wildfire Experiment for Cloud chemistry, Aerosol absorption and Nitrogen (WE-CAN) campaign. ΔHONO/ΔCO close to the fire locations ranged from 0.7 to 17 pptv ppbv–1 using a maximum enhancement method, with the median similar to previous observations of temperate forest fire plumes. Measured HONO to NO x enhancement ratios were generally factors of 2, or higher, at early plume ages than previous studies. Enhancement ratios scale with modified combustion efficiency and certain nitrogenous trace gases, which may be useful to estimate HONO release when HONO observations are lacking or plumes have photochemical exposures exceeding an hour as emitted HONO is rapidly photolyzed. We find that HONO photolysis is the dominant contributor to hydrogen oxide radicals (HO x = OH + HO2) in early stage (<3 h) wildfire plume evolution. These results highlight the role of HONO as a major component of reactive nitrogen emissions from wildfires and the main driver of initial photochemical oxidation.

Wildfires have a significant adverse impact on air quality in the United States (US). To understand the potential health impacts of wildfire smoke, many epidemiology studies rely on concentrations of fine particulate matter (PM) as a smoke tracer. However, there are many gas-phase hazardous air pollutants (HAPs) identified by the Environmental Protection Agency (EPA) that are also present in wildfire smoke plumes. Using observations from the Western Wildfire Experiment for Cloud Chemistry, Aerosol Absorption, and Nitrogen (WE-CAN), a 2018 aircraft-based field campaign that measured HAPs and PM in western US wildfire smoke plumes, we identify the relationships between HAPs and associated health risks, PM, and smoke age. We find the ratios between acute, chronic noncancer, and chronic cancer HAPs health risk and PM in smoke decrease as a function of smoke age by up to 72% from fresh (<1 day of aging) to old (>3 days of aging) smoke. We show that acrolein, formaldehyde, benzene, and hydrogen cyanide are the dominant contributors to gas-phase HAPs risk in smoke plumes. Finally, we use ratios of HAPs to PM along with annual average smoke-specific PM to estimate current and potential future smoke HAPs risks.

Reactive nitrogen (N r) within smoke plumes plays important roles in the production of ozone, the formation of secondary aerosols, and deposition of fixed N to ecosystems. The Western Wildfire Experiment for Cloud Chemistry, Aerosol Absorption, and Nitrogen (WE-CAN) field campaign sampled smoke from 23 wildfires throughout the western U.S. during summer 2018 using the NSF/NCAR C-130 research aircraft. We empirically estimate N r normalized excess mixing ratios and emission factors from fires sampled within 80 min of estimated emission and explore variability in the dominant forms of N r between these fires. We find that reduced N compounds comprise a majority (39%-80%; median = 66%) of total measured reactive nitrogen (ΣN r) emissions. The smoke plumes sampled during WE-CAN feature rapid chemical transformations after emission. As a result, within minutes after emission total measured oxidized nitrogen (ΣNO y) and measured total ΣNH x (NH 3 + pNH 4) are more robustly correlated with modified combustion efficiency (MCE) than NO x and NH 3 by themselves. The ratio of ΣNH x /ΣNO y displays a negative relationship with MCE, consistent with previous studies. A positive relationship with total measured ΣN r suggests that both burn conditions and fuel N content/volatilization differences contribute to the observed variability in the distribution of reduced and oxidized N r. Additionally, we compare our in situ field estimates of N r EFs to previous lab and field studies. For similar fuel types, we find ΣNH x EFs are of the same magnitude or larger than lab-based NH 3 EF estimates, and ΣNO y EFs are smaller than lab NO x EFs. Plain Language Summary Smoke from large wildfires in the western U.S. degrades air quality across the whole U.S. Smoke contains a mixture of many different gases and particles, including carbon compounds like carbon dioxide and carbon monoxide, as well as nitrogen compounds such as ammonia and nitrogen oxides. Gases containing nitrogen are important for the production of ozone and the formation of more or larger particles as the smoke moves downwind. During the summer of 2018, we used the National Science Foundation/National Center for Atmospheric Research C130 research aircraft to fly through smoke across the western U.S. and measure many of the most abundant nitrogen compounds. We find that the smoke plumes we sampled emitted more nitrogen in a reduced form than in an oxidized form, and chemical reactions change the form and phase of nitrogen very quickly in the smoke. We compare our field measurements with laboratory measurements with the goal of using them together to improve our forecasts of how and where wildfire smoke will impact air quality. LINDAAS ET AL.

Satellite observations of formaldehyde (HCHO) columns provide top‐down information on emissions of highly reactive volatile organic compounds (VOCs). We examine the long‐term trends in HCHO columns observed by the Ozone Monitoring Instrument from 2005 to 2014 across North America. Biogenic isoprene is the dominant source of HCHO, and its emission has a large temperature dependence. After correcting for this dependence, we find a general pattern of increases in much of North America but decreases in the southeastern U.S. Over the Houston‐Galveston‐Brazoria industrial area, HCHO columns decreased by 2.2% a−1 from 2005 to 2014, consistent with trends in emissions of anthropogenic VOCs. Over the Cold Lake Oil Sands in the southern Alberta in Canada, HCHO columns increased by 3.8% a−1, consistent with the increase in crude oil production there. HCHO variability in the northwestern U.S. and Midwest could be related to afforestation and corn silage production. Although NOx levels can affect the HCHO yield from isoprene oxidation, we find that decreases in anthropogenic NOx emissions made only a small contribution to the observed HCHO trends.

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Objective-In vitro studies implicate that the low-density lipoprotein receptor (LDLR)-related protein (LRP) in macrophages has a pro-atherogenic potential. In the present study, we investigated the in vivo role of macrophage specific LRP in atherogenesis independent of its role in the uptake of lipoproteins. Methods and Results-We generated macrophage-specific LRP-deficient mice on an apoE/LDLR double-deficient background. Macrophage LRP deletion did not affect plasma cholesterol and triglyceride levels, lipoprotein distribution, and blood monocyte counts. Nevertheless, macrophage LRP deficiency resulted in a 1.8-fold increase in total atherosclerotic lesion area in the aortic root of 18-week-old mice. Moreover, LRP deficiency also resulted in a relatively higher number of advanced lesions. Whereas macrophage and smooth muscle cell content did not differ between LRP-deficient mice and control littermates, a 1.7-fold increase in collagen content and 2.3-fold decrease in relative number of CD3ϩ T cells were observed in lesions from macrophage specific LRP-deficient mice. Conclusions-Our data demonstrate that independent of its role in lipoprotein uptake, absence of LRP in macrophages resulted in more advanced atherosclerosis and in lesions that contained more collagen and less CD3ϩ T cells. In contrast to previous in vitro studies, we conclude that macrophage LRP has an atheroprotective potential and may modulate the extracellular matrix in the atherosclerotic lesions. Key Words: atherosclerosis Ⅲ collagen Ⅲ genetically altered mice Ⅲ LRP Ⅲ macrophage C ardiovascular diseases are the leading cause of morbidity and mortality in the Western world. The primary cause of cardiovascular diseases is atherosclerosis, which is characterized by lipid accumulation and inflammation in the vascular wall. 1,2 Macrophages play a central role in the pathogenesis of atherosclerosis by internalizing modified low-density lipoprotein (LDL), production of cytokines and growth factors, and thus stimulate migration and proliferation of smooth muscle cells (SMCs), and plaque development and progression. 1 The LDL receptor (LDLR)-related protein (LRP) is a large-cell-surface multi-ligand endocytic clearance and signaling receptor of the LDLR gene family. [3][4][5][6][7][8] LRP is known to recognize Ͼ50 structurally and functionally different ligands. 9,10 It is expressed in a variety of cell types including hepatocytes, SMCs, and macrophages. 11 The hepatic LRP was originally identified as an endocytic receptor for apolipoprotein E (apoE)-rich lipoproteins. 4 Recently, we showed that hepatic LRP deficiency in mice increased atherosclerosis independent of plasma lipoproteins. 12 Similarly, SMCspecific LRP-deficient mice display impaired vessel wall integrity and have increased susceptibility to cholesterol-diet induced atherosclerosis. 7 These data show that LRP protects against the development of atherosclerosis at the level of the liver and the SMCs, independent of its role in the removal of plasma lipoproteins.In contrast, several lines...