Abstract. Agricultural activities are a major source contributing to NH3 emissions in Shanghai and most other regions of China; however, there is a long-standing and ongoing controversy regarding the contributions of vehicle-emitted NH3 to the urban atmosphere. From April 2014 to April 2015, we conducted measurements of a wide range of gases (including NH3) and the chemical properties of PM2.5 at hourly resolution at a Shanghai urban supersite. This large data set shows NH3 pollution events, lasting several hours with concentrations 4 times the annual average of 5.3 µg m−3, caused by the burning of crop residues in spring. There are also generally higher NH3 concentrations (mean ± 1 σ) in summer (7.3 ± 4.9 µg m−3; n = 2181) because of intensive emissions from temperature-dependent agricultural sources. However, the NH3 concentration in summer was only an average of 2.4 µg m−3 or 41 % higher than the average NH3 concentration of other seasons. Furthermore, the NH3 concentration in winter (5.0 ± 3.7 µg m−3; n = 2113) was similar to that in spring (5.1 ± 3.8 µg m−3; n = 2198) but slightly higher, on average, than that in autumn (4.5 ± 2.3 µg m−3; n = 1949). Moreover, other meteorological parameters like planetary boundary layer height and relative humidity were not major factors affecting seasonal NH3 concentrations. These findings suggest that there may be some climate-independent NH3 sources present in the Shanghai urban area. Independent of season, the concentrations of both NH3 and CO present a marked bimodal diurnal profile, with maxima in the morning and the evening. A spatial analysis suggests that elevated concentrations of NH3 are often associated with transport from regions west–northwest and east–southeast of the city, areas with dense road systems. The spatial origin of NH3 and the diurnal concentration profile together suggest the importance of vehicle-derived NH3 associated with daily commuting in the urban environment. To further examine vehicular NH3 emissions and transport, sampling of the NH3 concentration was performed in (from the entrance to the exit of the tunnel) and out (along a roadside transect spanning 310 m perpendicular to the tunnel) of a heavily trafficked urban tunnel during the spring of 2014. NH3 concentrations in the tunnel exit were over 5 and 11 times higher than those in the tunnel entrance and in the ambient air, respectively. Based on the derived mileage-based NH3 emission factor of 28 mg km−1, a population of 3.04 million vehicles in Shanghai produced around 1300 t NH3 in 2014, which accounts for 12 % of total NH3 emissions in the urban area. Collectively, our results clearly show that vehicle emissions associated with combustion are an important NH3 source in Shanghai urban areas and may have potential implications for PM2.5 pollution in the urban atmosphere.

PM (particulate matter less than 2.5 μm in diameter) is considered as a harmful carcinogen. Determining the precise relationship between the chemical constituents of PM in the air and cancer progression could aid the treatment of environment related disease and establishing risk reduction strategies. Herein, we used transcriptomics (RNA-seq) and an integrated microfluidic system to identify the global gene expression and differential target proteins expression induced by ambient fine particles collected from the heavy haze in China. The results clearly indicated that cancer related pathways exhibited the strongest dysregulation. The ambient fine particles could be uptaken into the cells by pinocytosis, mainly promoting the PI3K-Akt pathway, FGF/FGFR/MAPK/VEGF signaling, and the JAK-STAT pathway, leading to evading apoptosis, sustained angiogenesis, and cell proliferation, which are the most important hallmarks of cancer. And fine particles also have been demonstrated to create intracellular reactive oxygen species (ROS) and mitochondrial ROS, change intracellular free Ca, and induce apoptosis, which are all key players in mediating cancer progression. It was observed by transmission electron microscopy (TEM) that the particles from the haze could enter the mitochondria, resulting in disturbance of the mitochondrial membrane and disruption of the mitochondria, and these particles can even enter inside the nucleus. It was also found in our study of organics (OC, PAHs) and metals (Zn, As, V) that compounds of fine particles were more closely associated with the exacerbation of cancer and secondary aerosols generated by traffic had the largest impact on cancer related signal transductions.

No abstract

DNA double-strand breaks (DSBs) are highly toxic lesions that can drive genetic instability. These lesions also contribute to the efficacy of radiotherapy and many cancer chemotherapeutics. DNA repair efficiency is regulated by both intracellular and extracellular chemical signals. However, it is largely unknown whether this process is regulated by physical stimuli such as extracellular mechanical signals. Here, we report that DSB repair is regulated by extracellular mechanical signals. Low extracellular matrix (ECM) stiffness impairs DSB repair and renders cells sensitive to genotoxic agents. Mechanistically, we found that the MAP4K4/6/7 kinases are activated and phosphorylate ubiquitin in cells at low stiffness. Phosphorylated ubiquitin impairs RNF8-mediated ubiquitin signaling at DSB sites, leading to DSB repair deficiency. Our results thus demonstrate that ECM stiffness regulates DSB repair efficiency and genotoxic sensitivity through MAP4K4/6/7 kinase–mediated ubiquitin phosphorylation, providing a previously unidentified regulation in DSB-induced ubiquitin signaling.

No abstract