Health benefits of vehicle electrification through air pollution in Shanghai, China.

Vehicle electrification has been recognized for its potential to reduce emissions of air pollutants and greenhouse gases in China. Several studies have estimated how national-level policies of electric vehicle (EV) adoption might bring very large environmental and public health benefits from improved air quality to China. However, large-scale adoption is very costly, some regions derive more benefits from large-scale EV adoption than others, and the benefits of replacing internal combustion engines in specific cities are less known. Therefore, it is important for policymakers to design incentives based on regional characteristics - especially for megacities like Shanghai - which typically suffer from worse air quality and where a larger population is exposed to emissions from vehicles. Over the past five years, Shanghai has offered substantial personal subsidies for passenger EVs to accelerate its electrification efforts. Still, it remains uncertain whether EV benefits justify the strength of incentives. The purpose of our study is to evaluate the health and climate benefits of replacing light-duty gasoline vehicles (ICEVs) with battery EVs in the city of Shanghai. We assess health impacts due to ICEV emissions of primary fine particulate matter, NOx, and volatile organic compounds, and to powerplant emissions of NOx and SO2 due to EV charging. We incorporate climate benefits from reduced greenhouse gas emissions based on existing research. We find that the benefit of replacing the average ICEV with an EV in Shanghai is US$6400 (2400-14,700), with health impacts of EVs about 20 times lower than the average ICEV. Larger benefits ensue if older ICEVs are replaced, but replacing newer China ICEVs also achieves positive health benefits. As Shanghai plans to stop providing personal subsidies for EV purchases in 2024, our results show that EVs achieve public health and climate benefits and can help inform policymaking strategies in Shanghai and other megacities.

Increased Impact of Aviation on Air Quality and Human Health in China.

China's civil aviation market has rapidly expanded, becoming the world's second-largest. However, the air quality and health impacts caused by its aircraft emissions have been inadequately assessed. Here, we leverage an updated emission inventory of air pollutants with improved temporal and spatial resolution based on hundreds of thousands of flight trajectories and simulate aviation-attributable contributions to ground-level air pollution in China. We find that in 2017, the annual-average aviation-attributed PM2.5 and O3 concentrations were 0.4-1.5 and 10.6-14.5 µg·m-3, respectively, suggesting that aviation emissions have become an increasingly important source of ambient air pollution. The contributions attributable to high-altitude emissions (climb/cruise/descent) were comparable to those at low altitudes (landing and takeoff). Aviation-attributed ambient PM2.5 and O3 exposures are estimated to have caused about 67,000 deaths in China in 2017, with populous coastal regions in Eastern China suffering the most due to the dense aviation activity. We recommend that industrial and policy stakeholders expedite an agenda of regulating air pollutants harmonized with decarbonization efforts for a more sustainable aviation future.

The future air quality impact of electric vehicle promotion and coordinated charging in the Beijing-Tianjin-Hebei region.

The synergetic benefit of air quality improvements together with greenhouse gas (GHG) mitigations from fleet electrification can be maximized if the power used for electric vehicles (EVs) is from renewables. The worth-noting mismatch between renewable power generation and EV fleet charging demand requires appropriate coordination strategy. Here, we analyze the environmental benefits from increased EVs penetration in Beijing-Tianjin-Hebei (BTH) regions by integrating various scenarios of fleet electrification with coordinated charging strategies to examine the air quality improvement and GHG abatement. The study found that fleet electrification could bring substantial reduction on urban PM2.5 in BTH, especially in December by 0.8 ± 0.5 µg/m3. The coordinated charging strategy could further improve the air quality in BTH, albeit smaller than that of fleet electrification itself. PM2.5 reduction benefit from EV adoption could be significantly more pronouncing when ammonia emission reduction was considered, by more than 0.3 µg/m3 in both December and July, validating the great significance of vehicle NH3 emission control and the necessity of prioritizing the electrification of high ammonia emitting fleet. The outcome of this study helps to formulate the effective on-road transportation pollutant abatement strategies and offers technological support for policy makers to conduct more sensible sequence of future fleet electrification process.

Identification of PtdIns(3,4)P2 effectors in human platelets using quantitative proteomics.

After decades in PtdIns(3,4,5)P3's shadow, PtdIns(3,4)P2 has now emerged as a bona fide regulator of important cellular events, including endocytosis and cell migration. New understanding of PtdIns(3,4)P2's cellular roles has been possible via novel approaches to observe and quantify cellular PtdIns(3,4)P2 dynamics, alongside methods to target the kinases and phosphatases governing phosphoinositide turnover. Despite this, the mechanisms by which PtdIns(3,4)P2 orchestrates its cellular roles remain more poorly understood, most notably because, to date, few PtdIns(3,4)P2 effectors have been identified. Here, we develop and apply an affinity-proteomics strategy to conduct a global screen for PtdIns(3,4)P2 interactors in human platelets; a primary cell type with striking PtdIns(3,4)P2 accumulation. Through an integrated approach, coupling affinity capture of PtdIns(3,4)P2-binding proteins to both label-free and isobaric tag-based quantitative proteomics, we identify a diverse PtdIns(3,4)P2 interactome. Included are long-established PtdIns(3,4)P2-binding proteins such as PLEKHA1, PLEKHA2, AKT and DAPP1, and a host of potentially novel effectors, including MTMR5, PNKD, RASA3 and GAB3. The PtdIns(3,4)P2 interactome shows an enrichment of pleckstrin homology (PH) domain-containing proteins, and through bioinformatics and array analyses we characterise the PH domain of MTMR5 and define its phosphoinositide selectivity. The interactome is also diverse in function, including several proteins known to support protein trafficking and cytoskeletal mobilisation. Such proteins have the ability to drive key platelet events, and to fulfil recently-defined roles for PtdIns(3,4)P2 in a wider range of cell types. Moreover, this study will serve as a valuable resource for the future characterisation of effector-driven PtdIns(3,4)P2 function.