No abstract

Future energy technologies will be key for a successful reduction of man-made greenhouse gas emissions. With demand for electricity projected to increase significantly in the future, climate policy goals of limiting the effects of global atmospheric warming can only be achieved if power generation processes are profoundly decarbonized. Energy models, however, have ignored the fact that upstream emissions are associated with any energy technology. In this work we explore methodological options for hybrid life cycle assessment (hybrid LCA) to account for the indirect greenhouse gas (GHG) emissions of energy technologies using wind power generation in the UK as a case study. We develop and compare two different approaches using a multiregion input-output modeling framework - Input-Output-based Hybrid LCA and Integrated Hybrid LCA. The latter utilizes the full-sized Ecoinvent process database. We discuss significance and reliability of the results and suggest ways to improve the accuracy of the calculations. The comparison of hybrid LCA methodologies provides valuable insight into the availability and robustness of approaches for informing energy and environmental policy.

Global GHG emissions continue to rise, with nearly a quarter of it due to trade that is not currently captured within global climate policy. In the context of current trade patterns and limited global cooperation on climate change, the feasibility of consumptionbased emissions accounting to contribute to a more comprehensive (national) policy framework in the UK is investigated. Consumption-based emissions results for the UK from a range of models are presented, their technical robustness is assessed, and their potential application in national climate policy is examined using examples of policies designed to reduce carbon leakage and to address high levels of consumption. It is shown that there is a need to include consumption-based emissions as a complementary indicator to the current approach of measuring territorial emissions. Methods are shown to be robust enough to measure progress on climate change and develop and inform mitigation policy. Finally, some suggestions are made for future policy-oriented research in the area of consumption-based accounting that will facilitate its application to policy. Policy relevanceEmissions embodied in trade are rapidly increasing and there is thus a growing gap between production emissions and the emissions associated with consumption. This is a growing concern due to the absence of a global cap and significant variation in country-level mitigation ambitions. Robust measurements of consumption-based emissions are possible and provide new insights into policy options. This includes trade-related policy (e.g. border carbon adjustments) and domestic policies (e.g. resource efficiency strategies). As climate policy targets deepen, there is a need for a broad range of policy options in addition to production and technological solutions. Consumption-based emissions are complementary to production-based emissions inventories, which are still the most accurate estimate for aggregated emissions at the global level. However, without consumption-based approaches, territorial emissions alone will not provide a complete picture of progress in regional and national emissions reduction.

Keratinocyte-derived TNF-a acts as an endogenous tumour promoter and can also regulate AP-1 activity in mouse epidermis. To gain further insight into TNF-a signalling during skin tumour formation, mice deficient in TNFR1 (TNFR1 À/À mice) or TNFR2 (TNFR2 À/À mice) were subjected to chemical carcinogenesis. Tumour multiplicity was significantly reduced in TNFR1 À/À and TNFR2 À/À mice compared to wild-type (wt) mice, suggesting that both receptors have protumour activity. However, TNFR1 À/À mice were markedly more resistant to tumour development than TNFR2 À/À mice indicating that TNFR1 is the major mediator of TNF-a-induced tumour formation. TNFR1 and TNFR2 were both expressed in wt epidermis during tumour promotion and by primary keratinocytes in vitro. TPA-induced c-Jun expression was transient in TNFR1 À/À and TNFR2 À/À compared to wt epidermis and this was reflected by reduced induction of the AP-1-responsive genes granulocyte/macrophage-colony stimulating factor, matrix metalloproteinase-9 and matrix metalloproteinase-3. These genes were differentially regulated in TNFR1 À/À compared to TNFR2 À/À epidermis, suggesting that the TNF-a receptors act independently via different AP-1 complexes to transduce TNF-a signals during tumour promotion. In addition, TNFR2 cooperated with TNFR1 to optimise TNFR1-mediated TNF-a bioactivity on keratinocytes in vitro. Our data provide further insight into TNF-a signalling in malignancy and provide some rationale for the use of TNF-a antagonists in the treatment of cancer.