Desertification and climate change indicate a future expansion of the global area of dry land and an increase in the risk of drought. Humans may therefore be at an ever-increasing risk of frequent exposure to, and resultant adverse health effects of desert sand dust. This review appraises a total of 52 experimental studies that have sought to identify mechanisms and intermediate endpoints underlying epidemiological evidence of an impact of desert dust on cardiovascular and respiratory health. Toxicological studies, in main using doses that reflect or at least approach real world exposures during a dust event, have demonstrated that virgin sand dust particles and dust storm particles sampled at remote locations away from the source induce inflammatory lung injury and aggravate allergen-induced nasal and pulmonary eosinophilia. Effects are orchestrated by cytokines, chemokines and antigen-specific immunoglobulin potentially via toll-like receptor/myeloid differentiation factor signaling pathways. Findings suggest that in addition to involvement of adhered chemical and biological pollutants, mineralogical components may also be implicated in the pathogenesis of human respiratory disorders during a dust event. Whilst comparisons with urban particulate matter less than 2.5 μm in diameter (PM_2.5) suggest that allergic inflammatory responses are greater for microbial element-rich dust- PM_2.5, aerosols generated during dust events appear to have a lower oxidative potential compared to combustion-generated PM_2.5 sampled during non-dust periods. In vitro findings suggest that the significant amounts of suspended desert dust during storm periods may provide a platform to intermix with chemicals on its surfaces, thereby increasing the bioreactivity of PM_2.5 during dust storm episodes, and that mineral dust surface reactions are an unrecognized source of toxic organic chemicals in the atmosphere, enhancing toxicity of aerosols in urban environments. In summary, the experimental research on desert dust on respiratory endpoints go some way in clarifying the mechanistic effects of atmospheric desert dust on the upper and lower human respiratory system. In doing so, they provide support for biological plausibility of epidemiological associations between this particulate air pollutant and events including exacerbation of asthma, hospitalization for respiratory infections and seasonal allergic rhinitis.

荒漠化和气候变化表明未来全球旱地面积将会扩大，干旱风险也会增加。因此，人类频繁接触沙漠沙尘的风险可能不断增加，从而对健康产生不利影响。本综述评估了总共 52 项实验研究，这些研究试图确定沙漠沙尘对心血管和呼吸系统健康影响的流行病学证据的机制和中间终点。毒理学研究主要使用反映或至少接近沙尘事件期间真实世界暴露量的剂量，表明在远离源头的偏远地点采样的原始沙尘颗粒和沙尘暴颗粒会诱发炎症性肺损伤，并加剧过敏原引起的鼻腔炎症。和肺嗜酸性粒细胞增多。细胞因子、趋化因子和抗原特异性免疫球蛋白可能通过 Toll 样受体/骨髓分化因子信号通路来协调作用。研究结果表明，除了附着的化学和生物污染物之外，矿物成分也可能与粉尘事件期间人类呼吸系统疾病的发病机制有关。虽然与直径小于 2.5 μm 的城市颗粒物 (PM _{2.5 ) 的比较表明，富含微生物元素的粉尘 (PM 2.5} ) 的过敏性炎症反应更大，但与燃烧产生的气溶胶相比，粉尘事件期间产生的气溶胶似乎具有较低的氧化电位。在无尘期间采样的PM _{2.5 。}体外研究结果表明，暴风雨期间大量悬浮的沙漠尘埃可能提供与其表面化学物质混合的平台，从而增加沙尘暴期间PM _2.5的生物反应性，而矿物尘埃表面反应是一个未被识别的来源。大气中的有毒有机化学物质，增强城市环境中气溶胶的毒性。综上所述，沙漠沙尘对呼吸终点的实验研究在一定程度上阐明了大气沙漠沙尘对人体上、下呼吸系统的机制影响。在此过程中，他们为这种颗粒空气污染物与哮喘恶化、呼吸道感染住院和季节性过敏性鼻炎等事件之间的流行病学关联提供了生物学合理性支持。