Identifying Ammonia Hotspots in China Using a National Observation Network.

The limited availability of ammonia (NH3) measurements is currently a barrier to understanding the vital role of NH3 in secondary aerosol formation during haze pollution events and prevents a full assessment of the atmospheric deposition of reactive nitrogen. The observational gaps motivated us to design this study to investigate the spatial distributions and seasonal variations in atmospheric NH3 on a national scale in China. On the basis of a 1-year observational campaign at 53 sites with uniform protocols, we confirm that abundant concentrations of NH3 [1 to 23.9 µg m-3] were identified in typical agricultural regions, especially over the North China Plain (NCP). The spatial pattern of the NH3 surface concentration was generally similar to those of the satellite column concentrations as well as a bottom-up agriculture NH3 emission inventory. However, the observed NH3 concentrations at urban and desert sites were comparable with those from agricultural sites and 2-3 times those of mountainous/forest/grassland/waterbody sites. We also found that NH3 deposition fluxes at urban sites account for only half of the emissions in the NCP, suggesting the transport of urban NH3 emissions to downwind areas. This finding provides policy makers with insights into the potential mitigation of nonagricultural NH3 sources in developed regions.

Fossil Fuel Combustion-Related Emissions Dominate Atmospheric Ammonia Sources during Severe Haze Episodes: Evidence from (15)N-Stable Isotope in Size-Resolved Aerosol Ammonium.

The reduction of ammonia (NH3) emissions is urgently needed due to its role in aerosol nucleation and growth causing haze formation during its conversion into ammonium (NH4(+)). However, the relative contributions of individual NH3 sources are unclear, and debate remains over whether agricultural emissions dominate atmospheric NH3 in urban areas. Based on the chemical and isotopic measurements of size-resolved aerosols in urban Beijing, China, we find that the natural abundance of (15)N (expressed using δ(15)N values) of NH4(+) in fine particles varies with the development of haze episodes, ranging from -37.1‰ to -21.7‰ during clean/dusty days (relative humidity: ∼ 40%), to -13.1‰ to +5.8‰ during hazy days (relative humidity: 70-90%). After accounting for the isotope exchange between NH3 gas and aerosol NH4(+), the δ(15)N value of the initial NH3 during hazy days is found to be -14.5‰ to -1.6‰, which indicates fossil fuel-based emissions. These emissions contribute 90% of the total NH3 during hazy days in urban Beijing. This work demonstrates the analysis of δ(15)N values of aerosol NH4(+) to be a promising new tool for partitioning atmospheric NH3 sources, providing policy makers with insights into NH3 emissions and secondary aerosols for regulation in urban environments.

Isotopic evidence for enhanced fossil fuel sources of aerosol ammonium in the urban atmosphere.

The sources of aerosol ammonium (NH4+) are of interest because of the potential of NH4+ to impact the Earth's radiative balance, as well as human health and biological diversity. Isotopic source apportionment of aerosol NH4+ is challenging in the urban atmosphere, which has excess ammonia (NH3) and where nitrogen isotopic fractionation commonly occurs. Based on year-round isotopic measurements in urban Beijing, we show the source dependence of the isotopic abundance of aerosol NH4+, with isotopically light (-33.8‰) and heavy (0 to +12.0‰) NH4+ associated with strong northerly winds and sustained southerly winds, respectively. On an annual basis, 37-52% of the initial NH3 concentrations in urban Beijing arises from fossil fuel emissions, which are episodically enhanced by air mass stagnation preceding the passage of cold fronts. These results provide strong evidence for the contribution of non-agricultural sources to NH3 in urban regions and suggest that priority should be given to controlling these emissions for haze regulation. This study presents a carefully executed application of existing stable nitrogen isotope measurement and mass-balance techniques to a very important problem: understanding source contributions to atmospheric NH3 in Beijing. This question is crucial to informing environmental policy on reducing particulate matter concentrations, which are some of the highest in the world. However, the isotopic source attribution results presented here still involve a number of uncertain assumptions and they are limited by the incomplete set of chemical and isotopic measurements of gas NH3 and aerosol NH4+. Further field work and lab experiments are required to adequately characterize endmember isotopic signatures and the subsequent isotopic fractionation process under different air pollution and meteorological conditions.

Spinal cord dynorphin expression increases, but does not drive microglial prostaglandin production or mechanical hypersensitivity after incisional surgery in rats.

Spinally released dynorphin contributes to hypersensitivity from nerve injury, inflammation, and sustained morphine treatment, but its role in post-operative pain has not been tested. Intrathecal injection of dynorphin activates cyclooxygenase (COX)-1 and -2 to induce hypersensitivity. Spinal COX-1 expression and activity increase following incisional paw surgery in rats, although the stimulus for this increase is not known. In the current study we tested whether spinal dynorphin expression increases after incisional surgery and induces hypersensitivity in this setting, and whether dynorphin stimulates COX-1 activity in spinal cord microglia. Paw incision resulted in increased prodynorphin immunoreactivity in laminae I, IIo, and V in the L4-L6 spinal cord dorsal horn ipsilateral to surgery. Change in prodynorphin expression did not parallel that of mechanical hypersensitivity. Repeated intrathecal dynorphin A antiserum injection failed to alter mechanical hypersensitivity after incisional surgery, although it was effective against mechanical hypersensitivity following spinal nerve ligation. Paw incision increased COX-1 immunoreactivity in the L4-L6 ipsilateral spinal cord, and these cells were confirmed to be microglia by co-localization with OX-42. Spinal cord microglia in culture expressed COX-1 immunoreactivity and released PGE2, but dynorphin A failed to increase release of PGE2 in these cultures. These results suggest that increased COX-1 expression occurs in spinal cord microglia following incisional surgery. Although prodynorphin immunoreactivity also increases, it likely does not drive COX-1 expression or mechanical hypersensitivity in this setting.