Evaluating the surface water pollution risk of mineral resource exploitation via an improved approach: a case study in Liaoning Province, Northeastern China.

Pollution from mineral exploitation is an important risk factor affecting surface water environment in mineral regions. It is urgent to construct a simple and accurate model to assess the surface water pollution risk from mineral exploitation in the regional scale. Thus, taking a mining province namely Liaoning in northeastern China as the study area, we proposed a framework to simulate the transport process of pollutants from mineral exploitation points to the surrounding surface water based on the "source-sink" theory. In our framework, we adopted the regional growth method (RGM) to extract the potential polluted water area as the certain "sink" considering the influence of the topography, and then applied Minimum Cumulative Resistance (MCR) model to assess the surface water pollution risk from mineral exploitation. The results revealed that: (1) 9.5% of the water areas were located at the potential impact area of MEPs. (2) The total value of resistance surface in Liaoning is relatively low, and gradually decreased from west to east. (3) MEPs in Liaoning had a high risk and seriously threatened the surface water environment, among 2125 MEPs, 733 MEPs (32.99%) were assessed as extremely high risk level, and about 35% of the MEPs were distributed within 10KM buffer zone of surface water. (4) Water pollution risk of MEPs in Dalian, Tieling, Fuxin and Dandong need to be emphasized. (5) Compared to previous studies, we considered the topographical influence before applying MCR model directly, so the results of water pollution risk were more reliable. This study provides a methodological support and scientific reference for the water environment protection and regional sustainable development.

Effects and mechanisms of polycyclic aromatic hydrocarbons in inflammatory skin diseases.

Polycyclic aromatic hydrocarbons (PAHs) are hydrocarbons characterized by the presence of multiple benzene rings. They are ubiquitously found in the natural environment, especially in environmental pollutants, including atmospheric particulate matter, cigarette smoke, barbecue smoke, among others. PAHs can influence human health through several mechanisms, including the aryl hydrocarbon receptor (AhR) pathway, oxidative stress pathway, and epigenetic pathway. In recent years, the impact of PAHs on inflammatory skin diseases has garnered significant attention, yet many of their underlying mechanisms remain poorly understood. We conducted a comprehensive review of articles focusing on the link between PAHs and several inflammatory skin diseases, including psoriasis, atopic dermatitis, lupus erythematosus, and acne. This review summarizes the effects and mechanisms of PAHs in these diseases and discusses the prospects and potential therapeutic implications of PAHs for inflammatory skin diseases.

The key player in the pathogenesis of environmental influence of systemic lupus erythematosus: Aryl hydrocarbon receptor.

The aryl hydrocarbon receptor was previously known as an environmental receptor that modulates the cellular response to external environmental changes. In essence, the aryl hydrocarbon receptor is a cytoplasmic receptor and transcription factor that is activated by binding to the corresponding ligands, and they transmit relevant information by binding to DNA, thereby activating the transcription of various genes. Therefore, we can understand the development of certain diseases and discover new therapeutic targets by studying the regulation and function of AhR. Several autoimmune diseases, including systemic lupus erythematosus (SLE), have been connected to AhR in previous studies. SLE is a classic autoimmune disease characterized by multi-organ damage and disruption of immune tolerance. We discuss here the homeostatic regulation of AhR and its ligands among various types of immune cells, pathophysiological roles, in addition to the roles of various related cytokines and signaling pathways in the occurrence and development of SLE.