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Abstract. Emissions from mobile sources are important contributors to both primary and secondary organic aerosols (POA and SOA) in urban environments. We compiled recently published data to create comprehensive model-ready organic emission profiles for on- and off-road gasoline, gas-turbine, and diesel engines. The profiles span the entire volatility range, including volatile organic compounds (VOCs, effective saturation concentration C*=107–1011 µg m−3), intermediate-volatile organic compounds (IVOCs, C*=103–106 µg m−3), semi-volatile organic compounds (SVOCs, C*=1–102 µg m−3), low-volatile organic compounds (LVOCs, C*≤0.1 µg m−3) and non-volatile organic compounds (NVOCs). Although our profiles are comprehensive, this paper focuses on the IVOC and SVOC fractions to improve predictions of SOA formation. Organic emissions from all three source categories feature tri-modal volatility distributions (“by-product” mode, “fuel” mode, and “lubricant oil” mode). Despite wide variations in emission factors for total organics, the mass fractions of IVOCs and SVOCs are relatively consistent across sources using the same fuel type, for example, contributing 4.5 % (2.4 %–9.6 % as 10th to 90th percentiles) and 1.1 % (0.4 %–3.6 %) for a diverse fleet of light duty gasoline vehicles tested over the cold-start unified cycle, respectively. This consistency indicates that a limited number of profiles are needed to construct emissions inventories. We define five distinct profiles: (i) cold-start and off-road gasoline, (ii) hot-operation gasoline, (iii) gas-turbine, (iv) traditional diesel and (v) diesel-particulate-filter equipped diesel. These profiles are designed to be directly implemented into chemical transport models and inventories. We compare emissions to unburned fuel; gasoline and gas-turbine emissions are enriched in IVOCs relative to unburned fuel. The new profiles predict that IVOCs and SVOC vapour will contribute significantly to SOA production. We compare our new profiles to traditional source profiles and various scaling approaches used previously to estimate IVOC emissions. These comparisons reveal large errors in these different approaches, ranging from failure to account for IVOC emissions (traditional source profiles) to assuming source-invariant scaling ratios (most IVOC scaling approaches).

Consumer, industrial, and commercial product usage is a source of exposure to potentially hazardous chemicals. In addition, cleaning agents, personal care products, coatings, and other volatile chemical products (VCPs), evaporate and react in the atmosphere producing secondary pollutants. Here, we show high air emissions from VCP usage (≥ 14 kg person −1 yr −1 , at least 1.7× higher than current operational estimates) are supported by multiple estimation methods and constraints imposed by ambient levels of ozone, hydroxyl radical (OH) reactivity, and the organic component of fine particulate matter (PM 2.5 ) in Pasadena, California. A near-field model, which estimates human chemical exposure during or in the vicinity of product use, indicates these high air emissions are consistent with organic product usage up to ~75 kg person −1 yr −1 , and inhalation of consumer products could be a non-negligible exposure pathway. After constraining the PM 2.5 yield to 5% by mass, VCPs produce ~41% of the photochemical organic PM 2.5 (1.1 ± 0.3 μ g m −3 ) and ~17% of maximum daily 8-hr average ozone (9 ± 2 ppb) in summer Los Angeles. Therefore, both toxicity and ambient criteria pollutant formation should be considered when organic substituents are developed for VCPs in pursuit of safer and sustainable products and cleaner air.

Tumor-associated macrophages (TAMs) are major components of the tumor microenvironment. Although a role for TAMs in promoting tumor progression has been revealed, the differentiation mechanisms and intrinsic signals of TAMs regulated by the tumor microenvironment remain unclear. Here we constructed an in vitro TAMs cell model, TES-TAMs, which is from tumor-extract-stimulated bone-marrow-derived macrophages. We performed a comparative proteomics analysis of bone-marrow-derived macrophages and TES-TAMs, which indicated that TES-TAMs possessed characteristic molecular expression of TAMs. Intriguingly, the signal pathways enriched in up-regulated differentially expressed proteins of TAMs demonstrated that glycolysis metabolism reprogramming may play an important role in TAM differentiation. We found that hexokinase-2, a key mediator of aerobic glycolysis, and the downstream proteins PFKL and ENO1 were remarkably increased in both TES-TAMs and primary TAMs from our MMTV-PyMT mice model. This phenomenon was then verified in human THP-1 cell lines stimulated by tumor extract solution from breast cancer patient. Taken together, our study provides insight into the induction of TAM differentiation by the tumor microenvironment through metabolic reprogramming.