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Fuel standards and gasoline content regulations are widely adopted by policymakers to reduce urban pollution and emission. An important but understudied question for policy design is measuring consumers’ private willingness to pay for higher gasoline standards. The empirical challenge is distinguishing consumers’ preferences over environmental standards from those over other product attributes e.g., price and brand. This paper provides a framework to uncover consumers’ preferences for higher fuel standards and estimates demand responses using high-frequency gas station-level panel data. We exploit unique characteristics of China’s retail gasoline market: government-controlled supply, homogeneous retailers, and highly regulated prices. Policy-induced differences in fuel standards generate spatial discontinuities at regional borders where consumers can freely choose from high or low standard gasoline. Combining difference-in-difference and geographic regression discontinuity, our identification strategy compares sales volume at gas stations on different sides of the border before and after one region experiences an exogenous fuel standard reform. Meanwhile, the reform induces a cost-driven price change that differs from daily price fluctuations. Controlling for this concurrent price change and other confounding factors, our data suggest that the enforcement of higher fuel standards increases sales at gas stations on the treated side of the border by 9.6-14%, which provides evidence that consumers respond strongly to fuel standard improvement. In the preferred specification, we estimate the consumer's WTP for higher fuel standard (III to IV) as 0.288 Yuan/liter, which accounts for about 3.9% of the gasoline price. We also find that consumers of premium gasoline have higher WTP for emission standard improvement than those of regular gasoline. Our findings highlight the importance of considering consumers’ private value from emission standards when designing environmental regulation.

Fcγ receptors (FcI³R) have been proposed to be involved in the pathogenesis of acute rejection (AR) after organ transplantation. However, the mechanisms by which FcγRIIIB mediate this process are still unclear. Previous studies suggested that the FCGR3B gene copy number variation (CNV) is associated with the risk of autoimmune diseases. In this study, we delineated the association of FCGR3B-CNV with end-stage renal disease (ESRD) and risk of rejection post kidney transplantation in 414 kidney transplant recipients and 219 healthy subjects. Our data showed that the percentage of kidney transplant recipients with high copy number of FCGR3B gene was significantly lower than that of healthy controls, suggesting that individuals with low copy of FCGR3B gene are more prone to develop ESRD. Besides, patients with low copy of the FCGR3B gene are associated with susceptibility to AR following kidney transplantation. In mice, transgenic expression of human FcγRIIIB effectively inhibited the AR and improved the function of the transplanted kidney in a model of allogeneic kidney transplantation. This protective effect was associated with an inhibition of T lymphocytes infiltration and Th1 cell immune response. Finally, we showed that FcγRIIIB cross-linking combined with TNF-α treatment in vitro promoted neutrophil apoptosis and was associated with increased activation of cleaved caspase-8 and caspase-3. The combined treatment also increased the arginase-1 expression in neutrophils, which may explain FcγRIIIB-mediated immunosuppression. Funding: This work was supported by the National Fund Committee of China (2012CB517603, 2012AA02A512). Declaration of Interest: No conflicts of interest exist for any authors. Ethical Approval: The study was performed in adherence with the Declaration of Helsinki, and was approved by the Ethics Committee of the First Affiliated Hospital of College of Medicine of Zhejiang University. All patients and healthy controls provided written informed consent.