Since China’s accession to the World Trade Organization (WTO), its export volume has achieved rapid growth. Meanwhile, the manufacturing of export products has also resulted in a large amount of SO2 emissions in China. To explore the relationship between the export of China’s final use products (ECFuP) and SO2 emissions, this paper first used the Multi-Regional Input–output (MRIO) model to study the SO2 emissions caused by ECFuP during 2003–2011. Then, this paper uses Structural Decomposition Analysis (SDA) to decompose the factors affecting SO2 emission into technical effect, structural effect and scale effect. The results showed that (1) the amounts of China’s SO2 emissions caused by the ECFuP have increased (2003–2007), declined (2007–2009), and increased again (2009–2011). (2) Scale effect is the main factor that causes the increase of SO2 emissions in China; technical effect mainly resulted in a decrease of emissions, whereas structural effect has less impact. Specifically, from 2003 to 2011, scale effect increased domestic SO2 emissions by 2.2 million tons; technical effect and structural effect reduced by 2.4 million tons and 0.5 million tons of emissions, respectively. (3) For different regions, there is a positive correlation between the consumption of the ECFuP and China’s SO2 emissions. Among them, NAFTA (accounting for 33.77%) leads to the largest SO2 emissions, and OTHER EU (5.79%) is the least. (4) From the industrial aspect, some industries with relatively small ECFuP have caused high SO2 emissions. The specific performance is as follows, among the 17 industries, Electricity, Gas and Water Supply (EGW) only occupied 0.6% of the total ECFuP, but it has the largest SO2 emissions (55%); in contrast, while Electrical and Optical Equipment (EOE) occupied 42% of the total ECFuP, its SO2 emissions only accounted for 0.2% of the total. In 2003–2011, the export trade volumes of all the industries increased, but the growth rates of less polluted industries are higher than that of heavy polluted industries. Based on the above findings, the paper also proposed some policy recommendations.

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This study was to explore the effect and mechanism of Probucol on STZ‐induced erectile dysfunction in diabetic rats. Thirty SD male rats aged 12 weeks were given intraperitoneal injection of STZ after fasting for 12 hr. Diabetic rats were haphazardly partitioned under two assemblies and administered 0 or 500 mg/kg probucol by oral gavage to 12 weeks. Control group was intraperitoneally injected with physiological saline, and saline was administered by oral gavage daily. Intracorporeal pressure was used to evaluate erectile function. Levels of proteins were detected using immunohistochemistry and Western blotting. α‐SMA and vWF were detected using immunofluorescence staining. After treatment, erectile function in probucol group was significantly improved. Endoplasmic reticulum stress‐related proteins were expressed higher in DM group than in sham group, while expression of these proteins decreased significantly in probucol group. However, α‐SMA and vWF were expressed at lower levels in DM group than in sham group, and probucol treatment reversed this phenomenon. Finally, Bax and Caspase3 were expressed at higher levels and Bcl‐2 was expressed at lower levels in DM group, while the opposite result was obtained in probucol group. In conclusions, probucol improves erectile function by reducing endothelial dysfunction and inhibiting PERK/ATF4/CHOP pathway in STZ‐induced diabetic rats.