This study examines potential changes in car and truck powertrain technology and fuel mix that could enable a transition to low carbon futures, out to 2050, in California. We consider combinations of battery-electric and plug-in hybrid electric vehicles, hydrogen fuel cells, and advanced biofuels, including ethanol, diesel biofuels, and renewable natural gas, for internal combustion engines that could lead to 80% GHG reductions compared to 1990. We consider two main low-carbon scenarios—a high ZEV adoption case (ZEV) and a mixed (ZEV and Biofuel) adoption case (ZEV+B)—both relative to a business-as-usual (BAU) case. We find that achieving an 80% reduction in CO₂ from cars and trucks (separately and together) appears feasible at relatively low cumulative cost, and with eventual likely net savings (as fuel savings exceed vehicle cost, mostly after 2030). However, the required rates of increase in sales of ZEV cars and trucks, and production volumes of advanced, low-carbon biofuels, will be quite challenging. Regarding ZEVs, we expect the greatest challenge to be for long-haul trucks, and we reduce the rate of sales increase for these as a result. In the ZEV scenario, all vehicle types reach 100% ZEV sales shares by 2050 (except long-haul trucks, which reach 80%). In the ZEV+B scenario, these targets are lower, but a strong ramp-up in advanced biofuel use is needed to achieve the 80% target, with commercial scale cellulosic production of ethanol and renewable diesel dominant by 2050. The net costs or savings of the scenarios are relatively low—on the order of ±$10-50 billion over the next 30 years—in relation to $4 trillion total spending in the BAU scenario. However, the additional costs of vehicle purchase run as high as $110 billion in the ZEV scenario, which will likely require substantial purchase incentives to overcome. Future research should examine how costs translate into policy needs (including generalized cost factors such as driving range) and the potential role, sourcing, and cost of advanced biofuels.

To achieve California’s ambitious climate goals, a shift to hydrogen fuel for some transportation sectors may be essential.In this report, we explore the build-out of a hydrogen fuel distribution system including uptake of light-, medium-, and heavy-duty fuel cell electric vehicles. Our analysis of Base and High Case scenarios includes costs of building and operating a hydrogen vehicle and fuel system and estimates workforce impacts. We consider scenarios with about 125,000 vehicles by 2030 in the Base Case and 250,000 in the high case. This increases by an order of magnitude to 2045. Vehicle and station investment costs associated with the Base Case reach anywhere from $4 to 12 billion USD by 2030 and increase by a factor of eight by 2045. Costs per kg of hydrogen, including fuel transmission to stations and station costs delivered to vehicles, could be in the range of $4 to 8 per kg. This becomes $6 to 10/kg as a final delivered cost, if production of hydrogen were to cost $2/kg. Workforce impacts in the Base Case include 600 to 2,200 jobs created by 2030, rising rapidly thereafter. This report was prepared by the ITS-UC Davis Energy Futures Hydrogen Program in partnership with the UCLA Luskin Center for Innovation.

The significance of intracellular Ap4A levels over immune activity of dendritic cells (DCs) has been studied in Nudt2fl/fl/CD11c-cre mice. The transgenic mice have been generated by crossing floxed NUDT2 gene mice with DC marker CD11c recombinase (cre) mice. The DCs derived from these mice have higher levels of Ap4A (≈30-fold) compared with those derived from Nudt2+/+ mice. Interestingly, the elevated Ap4A in DCs has led them to possess higher motility and lower directional variability. In addition, the DCs are able to enhance immune protection indicated by the higher cross-presentation of antigen and priming of CD8+ OT-I T cells. Overall, the study denotes prominent impact of Ap4A over the functionality of DCs. The Nudt2fl/fl/CD11c-cre mice could serve as a useful tool to study the influence of Ap4A in the critical immune mechanisms of DCs.