Contamination of tea leaves by anthraquinone: The atmosphere as a possible source.

The detection of anthraquinone in tea leaves has raised concerns due to a potential health risk associated with this species. This led the European Union to impose a maximum residue limit (MRL) of 0.02 mg/kg for anthraquinone in dried tea leaves. As atmospheric contamination has been identified as one of the possible sources of anthraquinone residue, this study investigates the contamination resulting from the deposition of atmospheric anthraquinone using a global chemical transport model that accounts for the emission, atmospheric transport, chemical transformation, and deposition of anthraquinone on the surface. The largest contribution to the global atmospheric budget of anthraquinone is from residential combustion followed by the secondary formation from oxidation of anthracene. Simulations suggest that atmospheric anthraquinone deposition could be a substantial source of the anthraquinone found on tea leaves in several tea-producing regions, especially near highly industrialized and populated areas of southern and eastern Asia. The high level of anthraquinone deposition in these areas may result in residues in tea products exceeding the EU MRL. Additional contamination could also result from local tea production operations.

Evaluating the Impact of Chemical Complexity and Horizontal Resolution on Tropospheric Ozone Over the Conterminous US With a Global Variable Resolution Chemistry Model.

A new configuration of the Community Earth System Model (CESM)/Community Atmosphere Model with full chemistry (CAM-chem) supporting the capability of horizontal mesh refinement through the use of the spectral element (SE) dynamical core is developed and called CESM/CAM-chem-SE. Horizontal mesh refinement in CESM/CAM-chem-SE is unique and novel in that pollutants such as ozone are accurately represented at human exposure relevant scales while also directly including global feedbacks. CESM/CAM-chem-SE with mesh refinement down to ∼14 km over the conterminous US (CONUS) is the beginning of the Multi-Scale Infrastructure for Chemistry and Aerosols (MUSICAv0). Here, MUSICAv0 is evaluated and used to better understand how horizontal resolution and chemical complexity impact ozone and ozone precursors over CONUS as compared to measurements from five aircraft campaigns, which occurred in 2013. This field campaign analysis demonstrates the importance of using finer horizontal resolution to accurately simulate ozone precursors such as nitrogen oxides and carbon monoxide. In general, the impact of using more complex chemistry on ozone and other oxidation products is more pronounced when using finer horizontal resolution where a larger number of chemical regimes are resolved. Large model biases for ozone near the surface remain in the Southeast US as compared to the aircraft observations even with updated chemistry and finer horizontal resolution. This suggests a need for adding the capability of replacing sections of global emission inventories with regional inventories, increasing the vertical resolution in the planetary boundary layer, and reducing model biases in meteorological variables such as temperature and clouds.

Direct Radiative Effect and Public Health Implications of Aerosol Emissions Associated with Shifting to Gasoline Direct Injection (GDI) Technologies in Light-Duty Vehicles in the United States.

Due to their enhanced fuel economy, the market share of gasoline direct injection (GDI) vehicles has increased significantly over the past decade. However, GDI engines emit higher levels of black carbon (BC) aerosols compared to traditional port fuel injection (PFI) engines. Here, we performed coupled chemical transport and radiative transfer simulations to estimate the aerosol-induced public health and direct radiative effects of shifting the U.S. fleet from PFI to GDI technology. By comparing simulations with current emission profiles and emission profiles modified to reflect a shift from PFI to GDI, we calculated the change in aerosol (mostly BC) concentrations associated with the fleet change. Standard concentration-response calculations indicated that the total annual deaths in the U.S. attributed to particulate gasoline-vehicle emissions would increase from 855 to 1599 due to shifting from PFI to GDI. Furthermore, the increase in BC associated with the shift would lead to an annual average positive radiative effect over the U.S. of approximately +0.075 W/m2, with values as large as +0.45 W/m2 over urban regions. On the other hand, the reduction in CO2 emissions associated with the enhanced fuel economy of GDI vehicles would yield a globally uniform negative radiative effect, estimated to be -0.013 W/m2 over a 20 year time horizon. Therefore, the climate burden of the increase in BC emissions dominates over the U.S., especially over source regions.

Nuclear factor-kappaB regulates beta-cell death: a critical role for A20 in beta-cell protection.

Apoptotic beta-cell death is central to the pathogenesis of type 1 diabetes and may be important in islet graft rejection. Despite this, genetic control of beta-cell apoptosis is only poorly understood. We report that inhibition of gene transcription sensitized beta-cells to tumor necrosis factor (TNF)-alpha-induced apoptosis, indicating the presence of a regulated antiapoptotic response. Using oligonucleotide microarrays and real-time PCR, we identified TNFAIP3/A20 as the most highly regulated antiapoptotic gene expressed in cytokine-stimulated human and mouse islets. Cytokine induction of A20 mRNA in primary islets and insulinoma cells was rapid and observed within 1 h, consistent with A20 being an immediate early response gene in beta-cells. Regulation of A20 was nuclear factor-kappaB (NF-kappaB)-dependent, two NF-kappaB sites within the A20 promoter were found to be necessary and sufficient for A20 expression in beta-cells. Activation of NF-kappaB by TNF receptor-associated factor (TRAF) 2, TRAF6, NF-kappaB-inducing kinase, or protein kinase D, which transduce signals downstream of Toll-like receptors, TNF receptors, and free radicals, respectively, were all potent activators of the A20 promoter. Moreover, A20 expression was induced in transplanted islets in vivo. Finally, A20 expression was sufficient to protect beta-cells from TNF-induced apoptosis. These data demonstrate that A20 is the cardinal antiapoptotic gene in beta-cells. Further, A20 expression is NF-kappaB dependent, thus linking islet proinflammatory gene responses with protection from apoptosis.