期刊
ENVIRONMENT INTERNATIONAL
卷 157, 期 -, 页码 -出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.envint.2021.106790
关键词
Allergic respiratory disease; Asian sand dust; Cardiovascular disease; Desert dust; Inflammation; Microbial materials; Oxidative stress; Toxicology
资金
- World Health Organisation [2019/977968-0]
- National Institute for Health Research (NIHR) Health Protection Research Unit in Environmental Exposures and Health
- Public Health England and Imperial College
- MRC Centre for Environment and Health - Medical Research Council [MR/S0196669/1]
- Wellcome Trust [209376/Z/17/Z]
Research indicates that desert dust particles can cause respiratory disorders, and dust-PM2.5 generated during dust events may induce more severe allergic inflammatory responses.
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 mu m 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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