Mechanisms underlying the health effects of desert sand dust.

Mechanisms underlying the health effects of desert sand dust.
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DOI:
10.1016/j.envint.2021.106790
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发表时间:
2021-12
影响因子:
11.8
通讯作者:
Kelly FJ
Kelly FJ
中科院分区:
环境科学与生态学1区
文献类型:
--
作者:
Fussell JC;Kelly FJ

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对52项研究进行了综述,这些研究调查了沙漠灰尘对健康影响的机制。沙漠灰尘可能是炎症和过敏性肺病的危险因素。粘附的化学品、生物和矿物成分是候选活化剂。在城市环境中,沙漠灰尘表面反应可能会增强气溶胶的毒性。荒漠化和气候变化表明,未来全球旱地面积将扩大,干旱风险将增加。因此,人类频繁接触沙漠沙尘并由此对健康产生不利影响的风险可能会不断增加。本综述评估了总共52项实验研究,这些研究试图确定沙漠灰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的暴露剂量,这些研究表明,在远离来源的偏远地点采样的原始沙尘颗粒和沙尘暴颗粒可诱发炎性肺损伤,并加重过敏原诱导的鼻和肺嗜酸性粒细胞增多症。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/髓样分化因子信号传导途径协调作用。研究结果表明,除了参与粘附的化学和生物污染物,矿物成分也可能牵连在人类呼吸系统疾病的发病机制,在粉尘事件。虽然与直径小于2.5 μm的城市颗粒物(PM2.5)的比较表明,富含微生物元素的灰尘- PM2.5的过敏性炎症反应更大,但与非灰尘期间采样的燃烧产生的PM2.5相比,灰尘事件期间产生的气溶胶似乎具有较低的氧化潜力。体外研究结果表明,在风暴期间,大量的悬浮沙漠尘埃可能提供了一个平台,与其表面上的化学物质混合,从而增加了沙尘暴期间PM2.5的生物活性,而矿物尘埃表面反应是大气中有毒有机化学物质的一个未被识别的来源,增强了城市环境中气溶胶的毒性。综上所述,沙漠粉尘对呼吸终点的实验研究在一定程度上阐明了大气沙漠粉尘对人体上呼吸系统和下呼吸系统的作用机制。在这样做的过程中,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上的支持。
52 studies investigating mechanisms behind impacts of desert dust on health are reviewed. Desert dust may be a risk factor for inflammatory and allergic lung diseases. Adhered chemicals, biological and mineralogical components are candidate activators. Desert dust surface reactions may enhance toxicity of aerosols in urban environments. 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 (PM2.5) suggest that allergic inflammatory responses are greater for microbial element-rich dust- PM2.5, aerosols generated during dust events appear to have a lower oxidative potential compared to combustion-generated PM2.5 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 PM2.5 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.
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