2 resultados para Atmospheric Chemistry, Ozone, Nitrogen oxides, Marine boundary layer, Photochemistry

em Massachusetts Institute of Technology


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Urban air pollution and climate are closely connected due to shared generating processes (e.g., combustion) for emissions of the driving gases and aerosols. They are also connected because the atmospheric lifecycles of common air pollutants such as CO, NOx and VOCs, and of the climatically important methane gas (CH4) and sulfate aerosols, both involve the fast photochemistry of the hydroxyl free radical (OH). Thus policies designed to address air pollution may impact climate and vice versa. We present calculations using a model coupling economics, atmospheric chemistry, climate and ecosystems to illustrate some effects of air pollution policy alone on global warming. We consider caps on emissions of NOx, CO, volatile organic carbon, and SOx both individually and combined in two ways. These caps can lower ozone causing less warming, lower sulfate aerosols yielding more warming, lower OH and thus increase CH4 giving more warming, and finally, allow more carbon uptake by ecosystems leading to less warming. Overall, these effects significantly offset each other suggesting that air pollution policy has a relatively small net effect on the global mean surface temperature and sea level rise. However, our study does not account for the effects of air pollution policies on overall demand for fossil fuels and on the choice of fuels (coal, oil, gas), nor have we considered the effects of caps on black carbon or organic carbon aerosols on climate. These effects, if included, could lead to more substantial impacts of capping pollutant emissions on global temperature and sea level than concluded here. Caps on aerosols in general could also yield impacts on other important aspects of climate beyond those addressed here, such as the regional patterns of cloudiness and precipitation.

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One of the major problems in the operations of mammalian cell bioreactors is the detrimental effect of gas sparging. Since the most convenient way to oxygenate any bioreactor is by gas sparging, this adverse effect has often been one of the limiting oxygen transport problems in both laboratory and industrial mammalian cell bioreactors. When one examines the literature on the effect of gas sparging on the death of mammalian cells, a great deal of confusions has been reported. It is not clear from the published literature as to the leading cause for gas-sparged related cell death. These confusions prevent the rational design and operations of mammalian cell bioreactors. In our laboratory, we have attempted to address this problem both fundamentally as well as attempt to obtain a general understanding on the adverse effect of gas sparging. Our analyses first examined the fluid shear associated with the various sections that the gas bubbles encounter during entrance, passage through the bioreactor and the final exit of the gas bubbles. Our analyses showed that the major damage of the mammalian cells by gas bubbles is due to the burst of the bubbles when exiting the bioreactor. It was also our hypothesis that the entrained cells in the liquid boundary layer of the gas bubble upon bursting is the major cause for cell death. We have corroborated this hypothesis by correlating the liquid entrainment with the cell death rate using results from our laboratory as well as other studies. Pluonic F-68, a weak surfactant, has routinely been used in laboratory and industrial bioreactors. In the past, the protective effect of Pluronic F-68 has never been shown as to why it is effective. In our research, we have data using microphotography which clearly demonstrated and corroborated our entrainment hypothesis is the major reason for the effectiveness of Pluronic F-68 in protecting the cells from gas-sparged related cell death.