Major histocompatibility complex (MHC) class I and class II molecules present antigens to CD8+ and CD4+ T cells respectively. Here we uncover a previously unrecognized role for MHC class I in modulating CD4+ T cell-mediated immunity. In allogeneic graft-versus-host disease and tumor models, we demonstrate that the absence of MHC class I on target cells significantly increases their susceptibility to CD4+ T cell cytotoxicity. Transcriptomic and functional studies suggest that this was because of heightened sensitivity to enhanced ferroptosis of the target cells. In large human transcriptomic and sequencing datasets, a role for CD4+ T cells in enhancing immune checkpoint blocker-mediated responses in persons with melanoma and mismatch-repair-deficient colon cancers that have downregulated MHC class I was suggested. These findings revise and expand the known role of MHC class I in CD8+ T cell and natural killer cell immunity and demonstrate a previously unrecognized role in CD4+ T cell-mediated cancer and alloimmunity.

China's rapid transition to vehicle electrification significantly increases the demand for critical minerals, thereby exacerbating supply risks. This study focuses on China's new energy vehicles, as well as the 3C battery (lithiumion batteries utilized in devices such as computers, communication equipment, and consumer electronics) and stainless steel industries, which involve critical metal resources. It sets up three scenarios to analyze future resource supply and demand risks, and develops eco-strategies to mitigate these risks. Results reveal that under the stated policy, medium-electrification, and deep-electrification scenarios, lithium demand is projected to reach 1,083.52 LCE (Lithium Carbonate Equivalent) kilotons (kt), 1,108.63 LCE kt, and 1,190.77 LCE kt, respectively. Nickel demand is estimated at 3,221.29 kt, 3,240.82 kt, and 3,272.90 kt, while cobalt demand is forecasted at 218.21 kt, 220.66 kt, and 224.69 kt in 2040. Before 2040, the external dependence on lithium, nickel, and cobalt consistently exceeds 40 %. Moreover, there is a risk of demand outpacing supply for lithium and cobalt by 2037 and 2027, respectively. Advancements in battery technologies, increased energy density, and enhanced metal recovery processes are essential to mitigating these supply risks.

The European Union (EU) has put forward a new regulatory framework for batteries through the EU Batteries Regulation (2023/1542), which sets a series of minimum thresholds of recycled materials for electric vehicle (EV) batteries sold on the EU market. Since the EU is the largest market for China’s EV export, compliance with the EU Batteries Regulation is a prerequisite for China’s EV export. To evaluate the feasibility of meeting these regulatory requirements, a future-oriented Chinese EV recycled materials use potential analysis model has been developed, forecasting the maximum proportion of recycled materials in China’s EV batteries from 2020 to 2035. To find out the risk factors, influencing aspects such as battery lifespan, demand, technology development, collection rate, and battery reshoring have been considered. The findings indicate that compared to other metals, the maximum proportion of recycled lithium is the lowest, forecast to be 21.2% in 2031, and increasing to 28.3% by 2035. Conversely, the maximum proportion of recycled graphite is the highest, at 28.9% in 2031 and reaching 41.3% in 2035. These results suggest that Chinese EV batteries could meet the targets set by the EU Batteries Regulation in most scenarios. Moreover, the analysis indicates that battery lifespan and collection rate constitute significant risk factors potentially influencing the recycled material content in Chinese EV batteries, which in turn impacts Chinese EV export to the EU. Finally, policy recommendations are proposed to enhance EV export and to bolster EV battery recycling industry development.

ABSTRACT:Microbial dysbiosis and metabolite changes in the gastrointestinal (GI) tract have been linked to pathogenesis and severity of many diseases, including graft-versus-host disease (GVHD), the major complication of allogeneic hematopoietic stem cell transplantation. However, published studies have only considered the microbiome and metabolome of excreted stool and do not provide insight into the variability of the microbial community and metabolite composition throughout the GI tract or the unique temporal dynamics associated with different gut locations. Because such geographical variations are known to influence disease processes, we used a multi-omics approach to characterize the microbiome and metabolite profiles of gut contents from different intestinal regions in well-characterized mouse models of GVHD. Our analysis validated analyses from excreted stool, but importantly, uncovered new biological insights from the microbial and metabolite changes between syngeneic and allogeneic hosts that varied by GI location and time after transplantation. Our integrated analysis confirmed the involvement of known metabolic pathways, including short-chain fatty acid synthesis and bile acid metabolism, and identified additional functional genes, pathways, and metabolites, such as amino acids, fatty acids, and sphingolipids, linked to GI GVHD. Finally, we validated a biological relevance for one such newly identified microbial metabolite, phenyl lactate, that heretofore had not been linked to GI GVHD. Thus, our analysis of the geographic variability in the intestinal microbiome and metabolome offers new insights into GI GVHD pathogenesis and potential for novel therapeutics.

ABSTRACT:Immunological memory in adaptive and innate immune cells is well characterized, enabling enhanced responses upon secondary challenges. However, it has only been recently appreciated that the nonimmune target cells of inflammation, particularly organ-specific stem cells (SCs), also exhibit memory of previous inflammatory exposures. Previous inflammation experience imprints on the SCs and influences their regenerative potential and responses to subsequent inflammatory insults. This phenomenon has been observed in hematopoietic, intestinal, and skin epithelial SCs, with profound implications for tissue homeostasis, disease progression, and therapeutic strategies. Herein, we expand and develop the notion of inflammatory memory of SCs and explore recent insights in the field. We discuss the emerging understanding of the molecular underpinnings and their potential clinical and biological implications. Inflammatory memory is driven by spatiotemporal changes in gene loci and transcription regulated by DNA and histones' epigenetic modifications, metabolic reprogramming, and chromatin accessibility changes. Understanding these mechanisms is critical for improving the outcomes of hematologic diseases, hematopoietic SC transplantation, and cellular immunotherapies.

Mitochondrial metabolism orchestrates T cell functions, yet the role of specific mitochondrial components in distinct T cell subsets remains poorly understood. Here, we explored the role of mitochondrial complex II (MC II), the only complex from the electron transport chain (ETC) that plays a role in both ETC and metabolism, in regulating T cell functions. Surprisingly, MC II exerts divergent effects on CD4+ and CD8+ T cell activation and function. Using T cell-specific MC II subunit, succinate dehydrogenase A-deficient (SDHA-deficient) mice, we integrated single-cell RNA-seq and metabolic profiling, with in vitro and in vivo T cell functional assays to illuminate these differences. SDHA deficiency induced metabolic changes and remodeled gene expression exclusively in activated T cells. In CD4+ T cells, SDHA loss dampened both oxidative phosphorylation (OXPHOS) and glycolysis, impaired cytokine production, proliferation, and reduced CD4+ T cell-mediated graft-versus-host disease after allogeneic stem cell transplantation (SCT). In contrast, SDHA deficiency in CD8+ T cells reduced OXPHOS but paradoxically upregulated glycolysis and demonstrated enhanced cytotoxic functions in vitro and in vivo. This metabolic reprogramming endowed SDHA-KO CD8+ T cells with superior in vivo antitumor efficacy after immune checkpoint inhibitor therapy and allogeneic SCT. These findings reveal MC II as a bifurcation point for metabolic and functional specialization in CD4+ and CD8+ T cells.

Hydrogen fuel cell is promising option for low-carbon transportation but poses concerns regarding potential emission increase in production activities. Limited by insufficient primary data, previous studies relied on incomplete material and energy inventory, leading to uncertain knowledge of life-cycle impacts of fuel cell. This study provided real-world data of material composition and in-plant energy demand for a refined evaluation of greenhouse gas (GHG) emissions and mitigation potentials of fuel cell. Result showed cradle-to-gate emissions of an 83.5 kW fuel cell applied to minivan were 5952 kg CO2-eq, equally contributed by upstream materials production and in-plant electricity and hydrogen consumptions. By 2030, proposed low-carbon strategies are expected to mitigate 66% emissions. The impacts assessed here were higher than preceding studies, which disregarded or underestimated manufacturing stage inputs. It emphasizes the necessity of large-scale field surveys and meta-analyses to maturate accounting standard and refine life-cycle assessment of fuel cell in the future.

Tissue-intrinsic mechanisms that regulate severity of systemic pathogenic immune-mediated diseases, such as acute graft-versus-host disease (GVHD), remain poorly understood. Following allogeneic hematopoietic stem cell transplantation, autophagy, a cellular stress protective response, is induced in host nonhematopoietic cells. To systematically address the role of autophagy in various host nonhematopoietic tissues, both specific classical target organs of acute GVHD (intestines, liver, and skin) and organs conventionally not known to be targets of GVHD (kidneys and heart), we generated mice with organ-specific knockout of autophagy related 5 (ATG5) to specifically and exclusively inhibit autophagy in the specific organs. When compared with wild-type recipients, animals that lacked ATG5 in the gastrointestinal tract or liver showed significantly greater tissue injury and mortality, while autophagy deficiency in the skin, kidneys, or heart did not affect mortality. Treatment with the systemic autophagy inducer sirolimus only partially mitigated GVHD mortality in intestine-specific autophagy-deficient hosts. Deficiency of autophagy increased MHC class I on the target intestinal epithelial cells, resulting in greater susceptibility to damage by alloreactive T cells. Thus, autophagy is a critical cell-intrinsic protective response that promotes tissue tolerance and regulates GVHD severity.

It remains unknown whether and how intestinal stem cells (ISCs) adapt to inflammatory exposure and whether the adaptation leaves scars that will affect their subsequent regeneration. We investigated the consequences of inflammation on Lgr5+ ISCs in well-defined clinically relevant models of acute gastrointestinal graft-versus-host disease (GI GVHD). Utilizing single-cell transcriptomics, as well as organoid, metabolic, epigenomic, and in vivo models, we found that Lgr5+ ISCs undergo metabolic changes that lead to the accumulation of succinate, which reprograms their epigenome. These changes reduced the ability of ISCs to differentiate and regenerate ex vivo in serial organoid cultures and also in vivo following serial transplantation. Furthermore, ISCs demonstrated a reduced capacity for in vivo regeneration despite resolution of the initial inflammatory exposure, demonstrating the persistence of the maladaptive impact induced by the inflammatory encounter. Thus, inflammation imprints the epigenome of ISCs in a manner that persists and affects their sensitivity to adapt to future stress or challenges.

The truck electrical highway technology has advantages in energy saving, carbon reduction and freight cost reduction in specific scenarios, and has been listed as an important forward-looking direction by many countries. the progress of different technical routes of freight commercial vehicles are investigated.The cost economy, the environmental and social benefits of carbon reduction and emission reduction of different technical routes of freight commercial vehicles are analyzed to provides a reference for enterprises to look forward to the technical layout, and to support the formulation of relevant policies and standards in the future.

China has pledged to peak its CO2 emissions by 2030 and achieve carbon neutrality by 2060. To meet these goals, China needs to accelerate the electrification of passenger vehicles. However, the rapid development of electric vehicles may impact the supply of critical raw materials, which may hinder the low-carbon transition. Therefore, the impact of vehicle electrification on CO2 emissions and the corresponding bottlenecks in the supply of critical raw materials should be systematically considered. In this study, we developed the China Automotive Fleet CO2 Model (CAFCM) to simulate a mixed-technology passenger vehicle fleet evolution. We further assessed the impact of energy and CO2 emissions and evaluated the demand for critical battery materials. We designed three scenarios with different powertrain type penetration rates to depict the potential uncertainty. The results showed that (1) the CO2 emissions of passenger vehicles in both the operation stage and the fuel cycle can peak before 2030; (2) achieving the dual carbon goals will lead to a rapid increase in the demand for critical raw materials for batteries and lead to potential supply risks, especially for cobalt, with the cumulative demand for cobalt for new energy passenger vehicles in China being 5.7 to 7.3 times larger than China’s total cobalt reserves; and (3) the potential amount of critical material recycled from retired power batteries will rapidly increase but will not be able to substantially alleviate the demand for critical materials before 2035. China’s new energy vehicle promotion policies and key resource supply risks must be systematically coordinated under the dual carbon goals.

Introduction: Little is known about the target-cell intrinsic features that affect tissue susceptibility to T-cell mediated cell death. The major histocompatibility complex (MHC) Class I presents antigens to CD8+ T cells, while MHC class II presents antigens to CD4+ T cells, and this process is critical for infectious, tumor, auto- and allo -immunity. However, MHC Class I has been suggested to have a non-canonical role iron metabolism, but whether it plays a role in tissue tolerance to CD4+ T cell mediated damage is not known. Herein, we investigated the role of MHC Class I on target cells in CD4+ T-cell mediated damage to intestinal epithelial cells (IECs) utilizing clinically relevant models of T-cell mediated gastrointestinal damage from Graft-versus-Host Disease (GVHD), a major complication of allogeneic stem cell transplantation. Methods: Because MHC class I is expressed on all nucleated cells, to specifically assess the role of MHC Class I on IECs, we generated and utilized intestine-specific MHC Class I knockout mice (B2m∆IEC) as recipients for MHC Class II-disparate bm12–>B2m∆IEC allogeneic stem cell transplant (allo-SCT). We utilized flow cytometry, immunological, molecular and biochemical assays to assess cell death pathways and tissue damage in IECs. We performed mechanistic studies to assess the role of iron and utilized clinically relevant iron chelation treatment to assess survival after treatment. Results: Here, we demonstrate that absence of MHC Class I on target cells exacerbates CD4+ T cell mediated killing of IECs leading to greater mortality in the KO animals than WT recipients (P<0.01) (Fig.1). Compared with wild-type (WT) mice, B2m∆IEC mice, despite an increase in mortality following MHC II disparate allo-SCT, did not demonstrate significant changes in T cell activation, or antigen presentation. In vitro co-culture cell killing assays demonstrate that B2m knockout cells have increased cell death compared with WT cells when co-cultured with activated bm12 CD4+ T cells. Because B2m knockout mice have increased liver iron deposition, we hypothesized that the increase in GI damage might be a consequence of iron related cell death in the IECs in B2m∆IEC mice. We demonstrate that absence of B2m on the intestine is sufficient to drive an increase in tissue iron levels in the liver and intestine. Furthermore, B2m∆IEC allo-recipient mice demonstrated increased intracellular labile iron in IECs. Given the increased mortality in B2m∆IEC allo-recipient mice and the increase in intracellular iron in IECs, we investigated the role of iron-dependent cell death, ferroptosis. We show that IECs from B2m∆IEC allo-recipient mice have increased ferroptosis compared with WT animals (P<0.05). Finally, chelation of iron with administration of clinically utilized iron chelator (Deferasirox) ameliorated excess mortality from GVHD in the B2m∆IEC mice. Conclusion: Absence of MHC Class I expression on target cells exacerbates CD4+ T cell mediated killing by enhancing iron dependent ferroptosis. These data demonstrate that in contrast to immunological paradigm, class I regulates CD4+ T cell mediated cytotoxicity even as it is essential for CD8+ T cell immunity.

Intestinal stem cells (ISC) encounter inflammatory insults in immune mediated gastro-intestinal (GI) diseases. It remains unknown whether, and how, they adapt, and if the adaptation leaves scars on the ISCs that affects their subsequent regeneration capacity. We investigated the consequences of inflammation on Lgr5+ISCs in well-defined clinically relevant models of gastro-intestinal acute graft-versus-host disease (GI GVHD). Utilizing single cell transcriptomics, organoid, metabolic, epigenomic and in vivo models we found that Lgr5+ISCs undergo metabolic changes that lead to accumulation of succinate, which reprograms its epigenome. These changes reduced the ability of ISCs to differentiate and regenerate ex vivo in serial organoid cultures demonstrating the persistence of the maladaptive impact of an in vivo inflammatory encounter by the ISCs. Thus, inflammation from GI GVHD leaves a memory of its effects on ISCs that persist and are likely to affect their sensitivity to adapt to future stress or challenges.

Although battery electric vehicles (BEVs) are climate-friendly alternatives to internal combustion engine vehicles (ICEVs), an important but often ignored fact is that the climate mitigation benefits of BEVs are usually delayed. The manufacture of BEVs is more carbon-intensive than that of ICEVs, leaving a greenhouse gas (GHG) debt to be paid back in the future use phase. Here we analyze millions of vehicle data from the Chinese market and show that the GHG break-even time (GBET) of China's BEVs ranges from zero (i.e., the production year) to over 11 years, with an average of 4.5 years. 8% of China's BEVs produced and sold between 2016 and 2018 cannot pay back their GHG debt within the eight-year battery warranty. We suggest enhancing the share of BEVs reaching the GBET by promoting the effective substitution of BEVs for ICEVs instead of the single-minded pursuit of speeding up the BEV deployment race.

China’s automotive industry has been dedicated to a series of carbon-reduction efforts and has strived for comprehensive green and low-carbon transformation in order to achieve carbon peaking and carbon neutrality goals. On the basis of automobiles’ whole life-cycle (WLC) carbon emission accounting, this paper calculates life-cycle carbon emissions per vehicle, proposes green and low-carbon development path for China’s automotive industry, quantifies and analyzes implicated carbon-reduction potential, and puts forth suggestions for high-quality green and low-carbon development of China’s automotive industry. The first is to establish a sound standard and data management system; the second is to promote research, development and application of low-carbon materials and low-carbon technologies; the third is to accelerate the pace of fostering a new consumption model in the automotive industry. The research results can further support national policy-making regarding carbon emissions, promote corporations’ research, development and application of low-carbon technologies, encourage green and low-carbon consumption, and lead the automotive industry to achieve WLC neutrality.

Introduction: Intestinal stem cells (ISCs) are responsible for the remarkable ability to maintain intestinal epithelium homeostasis and regeneration throughout life. Inflammatory damage of ISCs underpins injury caused by graft-versus-host disease (GVHD), inflammatory bowel diseases (IBD) and immune check-point blocker mediated colitis. However, it remains unknown whether the ISCs that survive or tolerate inflammation are fully functional and can return to their full functionality after the resolution of ongoing inflammatory insults. Herein we investigated the consequences of inflammation from GVHD on Lgr5+ISCs in multiple well-defined clinically relevant models of gastro-intestinal acute graft-versus-host disease (GI GVHD). Methods: We utilized single cell RNA (scRNA) sequencing to assess transcriptomics, Assay of transposase-accessible chromatin sequencing (ATAC-seq) to assess epigenomics, and functional metabolomics of ISCs in clinically relevant in vivo models of GVHD after major histocompatibility complex (MHC)-disparate BALB/c→C57BL/6 (B6) and MHC matched minor mismatched C3H.sw→B6 models of allogeneic SCT. Ex vivo intestinal organoids cultures, mitochondrial, and functional biochemical assays were utilized to determine the biological relevance of the changes observed from the ‘omic’ analyses and further validated them in vivo by developing novel Lgr5 +ISC specific succinate dehydrogenase A (SDHA) knock-out mice. Results: We examined the transcriptomes of Lgr5+ISCs with scRNA-seq of the intestinal crypts harvested from MHC-disparate BALB/c→B6 recipients on day +7 after allogeneic SCT. Bioinformatic analyses demonstrated upregulation of interferon and inflammation response genes but significant downregulation of genes involved in mitochondrial function, its complexes including complex II (SDH), ATP metabolic process, OXPHOS, and cytoplasmic translation. To assess the impact of metabolic functional gene changes, we harvested and assessed ISCs in ex vivo organoid cultures from transplanted recipients in the absence of ongoing inflammation. The ISCs harvested from GVHD animals demonstrated significantly reduced regeneration, differentiation and oxygen consumption rates (OCRs) with no change in extracellular acidification rates (ECAR) by Seahorse. FACs analysis confirmed reduction in SDHA component of mitochondrial complex II in Lgr5 +ISCs, demonstrating mechanistic cause for reduction in OXPHOS in ISCs. We next generated and utilized Lgr5 + ISC-specific SDHA KO mice as GVHD recipients and found that demonstrated significantly greater mortality when compared to the WT littermate recipients (P<0.01). Biochemical analyses demonstrated increased levels of succinate, a metabolic intermediary with known epigenetic and inflammatory functions, in ISCs harvested from GVHD animals. We therefore hypothesized that the reduction in ability to form functional organoids ex vivo, in the absence of ongoing inflammation, by the ISCs harvested from GVHD hosts is because of the inflammation epigenetic reprogramming induced by succinate mediated changes in DNA methylation (5-mC) of the ISCs in GVHD recipients. Consistent with the hypothesis greater DNA methylation, with alteration of epigenome by ATAC-seq was observed in ISCs sorted from GVHD recipients. Integrative analyses demonstrated correlation between epigenomic changes and transcriptomic changes. Finally, we analyzed whether the inflammation epigenomic induced changes in the GVHD ISCs with serial ex vivo organoid cultures and in vivo by transfer into secondary hosts. Both ex vivo and in vivo studies demonstrated poor regeneration from GVHD ISCs demonstrating retention of maladaptive memory in ISCs following their exposure to inflammation during GVHD. Conclusions: GI GVHD induced inflammation causes not only quantitative loss of ISCs but also induced qualitative changes in the surviving ISCs. Inflammation induced OXPHOS deficiency in Lgr5 + ISCs leads to accumulation of succinate that reprograms the epigenome and restrains their subsequent regeneration potential.

Introduction: The severity of T cell-mediated gastrointestinal graft-versus-host disease (GI-GVHD) correlates with a decrease in the gut microbiome diversity, loss of obligate anaerobic bacteria and alterations in levels of salutary metabolites like short chain fatty acids (SCFAs). However, it is unknown whether the intestinal anatomic geography of the microbiome and its metabolites impacts GI GVHD severity. Herein, we investigate the pattern of the gut microbiome and metabolites from four distinct anatomical sites of intestines after allogeneic stem cell transplant (allo-SCT) via shotgun metagenomics and untargeted mass-spectrometry. Methods: To determine the composition of the gut microbiome and gut metabolites of mice after allo-SCT, we utilized contemporaneous analyses of shotgun metagenomic sequencing and untargeted mass spectrometry on the gut contents of mice 7 or 21 days after major histocompatibility complex (MHC)-disparate BALB/c→C57BL/6 (B6) allogeneic SCT. We investigated the microbial community composition and gut metabolites from four distinct gut locations (terminal ileum, cecum, transverse colon, descending colon) and performed integrative analysis to assess for novel pathways that may regulate GVHD biology. For shotgun metagenomics analyses, reads were depth normalized with BBnorm v.38.96 and assembled per-sample with MEGAHIT v.1.2.9. Prodigal v.2.6.3 was used to find genes in each bin. KofamScan v.1.3.0 was used to assign KEGG ortholog IDs (KO) to translated genes predicted by Prodigal. Community composition profiles were produced with Kraken2 v.2.1.2 and Bracken v.2.6.1. Functional profiles for each sample were determined with the Kraken community composition profiles and Humann3 v.3.0.0, with a GTDB database built with Struo2. Results: Consistent with previous reports from direct stool analyses, our data demonstrated that after allo-SCT, gut microbial diversity is reduced, relative abundance of obligate anaerobes decreases, and relative abundance of facultative anaerobes increases at all the intestinal anatomic sites, but the difference was maximal in ileo-cecal contents. Furthermore, metabolomic analyses reveal a decrease in previously described metabolites such as, SCFAs, bile acids and indoles at these sites. The distinct patterns of change between control and allogeneic samples depended not only on the gut location probed but also correlated with timepoint after transplant (7 days or 21 days) highlighting the importance of probing different gut locations and timepoints. The largest driver of differences between sample groups was (1) gut location (2) time after transplant (3) transplant type. Integrative analyses demonstrated loss of microbial functional genes related to butyrate processing following allo-SCT complementing previous studies that demonstrated reduction in butyrate levels. Further bioinformatic analyses identified novel microbial functional genes and metabolites that may have biological implications. Analyses revealed that after allo-SCT, phenyllactic acid (PLA) levels increased in the transverse colon and distal colon (fig.1). PLA is an anti-microbial compound and has been shown to have immune modulatory properties. Administration of PLA in drinking water of mice after allo-SCT worsened GVHD severity and increased mortality indicating PLA may play a role in inducing dysbiosis and worsening GVHD severity. Conclusion: Contemporaneous analyses of shotgun metagenomic and untargeted mass spectrometry of gut contents after allo-SCT reveal changes in microbial composition and metabolites consistent with previous data from analyses from stool. However, our analysis demonstrates distinct patterns of key metabolites and microbes in between syngeneic and allogeneic depending on gut location and time after transplant. Furthermore, our analyses have identified novel functional genes and metabolites that are implicated in GVHD severity.

China introduced Worldwide Harmonized Light Vehicle Test Procedure (WLTP) in pollutant emission management and fuel consumption type approval test standards for passenger vehicles in 2019 and 2021. The switching of test procedures from the New European Driving Cycle (NEDC) to WLTP will significantly impact carmakers' fuel consumption target and technology compliance strategies. Assessing the impact of WLTP replacing NEDC on fuel consumption and fuel-efficient technology is necessary and urgent. Based on the data of 1038 samples tested under both WLTP and NEDC and the econometric model built in this paper, we analyse the impact of introducing WLTP on fuel consumption and key fuel-efficient technologies. The results show that fuel consumption of gasoline passenger vehicles based on WLTP is 8% higher than that based on NEDC. Switching from NEDC to WLTP has adverse effects on HEV and 48V. It has a slightly beneficial impact on gasoline direct injection (GDI) models and slightly adverse effects on multi-gear automatic transmission (AT) models and models with start-stop.

Promoting new energy vehicles (NEVs) is the key to achieving net-zero emissions in the transportation sector. NEVs' total life cycle CO2 emissions are mainly determined by average vehicle lifespan, annual mileage traveled, energy carbon intensity and energy mix in the production stage. Current studies mainly adopt assumptions about NEVs' average lifespan due to limited available data. This paper expands on the previous studies by examining the NEVs' age and distribution based on the national representative China Compulsory Traffic Accident Liability Insurance for Motor Vehicles (CTALI) database from 2018 to 2020. Then, the survival patterns and lifespan of NEVs are assessed using Weibull distribution. New energy passenger vehicles' life cycle CO2 emissions are further evaluated based on the reshaped representative survival patterns. The results show that there are significant differences in survival patterns between conventional vehicles and NEVs. NEVs generally show a shorter average lifespan compared with conventional vehicles. Among NEVs, the average lifespan of plug-in hybrid electric vehicles (PHEVs) is better than that of battery electric vehicles (BEVs). The survival patterns of several types of electric vehicles (including passenger battery electric vehicles, non-operating light battery electric buses, and light battery electric trucks) do not have a stable period in their first few years of operation. The life cycle assessment results show that the total life cycle CO2 emissions of passenger BEVs and PHEVs are lower than those of conventional vehicles. However, the short lifespan dramatically increases the passenger BEV and PHEV total life cycle CO2 emissions per kilometer, resulting in passenger BEV total life cycle CO2 emissions per kilometer being higher than those of conventional vehicles.

The Parallel Management Regulation of Corporate Average Fuel Consumption and New Energy Vehicle Credits for Passenger Vehicles (dual-credit policy) was released by China in 2017. This is the world's first mandatory new energy vehicle (NEV) policy at the national level. This study analysed the background, details, and rationale of the dual-credit policy from the standpoint of policymakers. Then, we used a comprehensive dataset of passenger vehicles in China to examine the compliance status and characteristics of different auto manufacturers. Possible impacts of the dual-credit policy were also assessed. The results show that independent companies have a better compliance performance than joint ventures and import companies, mainly due to the deployment of more NEVs. The dual-credit policy has accelerated carmakers' (especially joint ventures) product introduction plan for NEVs. The policy also accelerated the market share and technological progress (including the e-range and electricity consumption rate of battery electric vehicles) of NEVs. However, the rate of improvement of the average fleet fuel consumption rate (FCR) has not significantly accelerated compared with that available in the past. We made some recommendations for the next phase of dual-credit policy after examining the compliance performance from 2016 to 2019.