Review on recent progress in on-line monitoring technology for atmospheric pollution source emissions in China.

Emissions from mobile sources and stationary sources contribute to atmospheric pollution in China, and its components, which include ultrafine particles (UFPs), volatile organic compounds (VOCs), and other reactive gases, such as NH3 and NOx, are the most harmful to human health. China has released various regulations and standards to address pollution from mobile and stationary sources. Thus, it is urgent to develop online monitoring technology for atmospheric pollution source emissions. This study provides an overview of the main progress in mobile and stationary source monitoring technology in China and describes the comprehensive application of some typical instruments in vital areas in recent years. These instruments have been applied to monitor emissions from motor vehicles, ships, airports, the chemical industry, and electric power generation. Not only has the level of atmospheric environment monitoring technology and equipment been improving, but relevant regulations and standards have also been constantly updated. Meanwhile, the developed instruments can provide scientific assistance for the successful implementation of regulations. According to the potential problem areas in atmospheric pollution in China, some research hotspots and future trends of atmospheric online monitoring technology are summarized. Furthermore, more advanced atmospheric online monitoring technology will contribute to a comprehensive understanding of atmospheric pollution and improve environmental monitoring capacity.

A Murine Point Mutation of Sgpl1 Skin Is Enriched With Vγ6 IL17-Producing Cell and Revealed With Hyperpigmentation After Imiquimod Treatment.

Sphingosine-1-phosphate lyase is encoded by the Sgpl1 gene, degrades S1P, and is crucial for S1P homeostasis in animal models and humans. S1P lyase deficient patients suffer from adrenal insufficiency, severe lymphopenia, and skin disorders. In this study, we used random mutagenesis screening to identify a mouse line carrying a missense mutation of Sgpl1 (M467K). This mutation caused similar pathologies as Sgpl1 knock-out mice in multiple organs, but greatly preserved its lifespan, which M467K mutation mice look normal under SPF conditions for over 40 weeks, in contrast, the knock-out mice live no more than 6 weeks. When treated with Imiquimod, Sgpl1M467K mice experienced exacerbated skin inflammation, as revealed by aggravated acanthosis and orthokeratotic hyperkeratosis. We also demonstrated that the IL17a producing Vγ6+ cell was enriched in Sgpl1M467K skin and caused severe pathology after imiquimod treatment. Interestingly, hyperchromic plaque occurred in the mutant mice one month after Imiquimod treatment but not in the controls, which resembled the skin disorder found in Sgpl1 deficient patients. Therefore, our results demonstrate that Sgpl1M467K point mutation mice successfully modeled a human disease after being treated with Imiquimod. We also revealed a major subset of γδT cells in the skin, IL17 secreting Vγ6 T cells were augmented by Sgpl1 deficiency and led to skin pathology. Therefore, we have, for the first time, linked the IL17a and γδT cells to SPL insufficiency.